1
Q
Front
A
Back
2
Q
What is the general scientific consensus regarding the purpose of sleep?
A
It is still not completely understood. However, we know it is required for the maintenance of many organ systems.
3
Q
What are the consequences of sleep deprivation?
A
It leads to decreased cognitive abilities (e.g., performing worse on exams), impaired regulation of body homeostasis, health risks, and ultimately death.
4
Q
What are specific symptoms of impaired body homeostasis caused by sleep deprivation?
A
Symptoms include having chills or hot spells, and dysregulation of the feelings of satiety and hunger.
5
Q
According to the energy conservation hypothesis, why is sleep needed for the brain?
A
Sleep is needed to replenish glycogen stores.
6
Q
Describe the specific cellular mechanism of energy depletion and replenishment in the brain.
A
- Neurons require glucose to generate ATP. 2. Glucose is supplied to neurons by glial cells called astrocytes. 3. Astrocytes store glucose as glycogen and slowly metabolize these stores during the day to feed neurons. 4. By the end of the day, glycogen stores are depleted. 5. During sleep, brain activity ramps down, allowing glucose shuttled across the blood-brain barrier to replenish the glycogen stores in astrocytes.
7
Q
How does sleep function regarding waste management in the brain?
A
Sleep facilitates the clearance of metabolic waste products. It is easier for the brain to get rid of unwanted waste accumulated during the day when brain activity is reduced.
8
Q
Is the brain entirely inactive/metabolic during sleep?
A
No. In many animals (like rats), the cortex and subcortical areas are highly active during sleep. This activity is often related to cognitive processes rather than just metabolic ones.
9
Q
What is the ‘Consolidation of Memories’ hypothesis?
A
Sleep appears to be required for the consolidation of memories.
10
Q
What evidence supports the hypothesis that sleep is needed for memory consolidation?
A
- Animals that are sleep deprived have a much harder time recalling memories made in the previous wake period. 2. Brain activity patterns during sleep are often very similar to the activity patterns seen during the prior awake period.
11
Q
What are the two primary mechanisms that regulate the sleep/wake state?
A
- The Internal Clock (Circadian rhythm) 2. Light Entrainment
12
Q
From an evolutionary perspective, when is the ‘appropriate time’ for an animal to sleep?
A
When its predators or its prey are not abundant, making it essentially not worthwhile to be alert.
13
Q
What is the specific function of the Internal Clock?
A
It is an intrinsic master system that generates the circadian rhythm, ensuring we are active at certain times of the day and inactive at others.
14
Q
How is the circadian rhythm generated at the cellular level?
A
It is generated by regulatory transcription and translation feedback loops within ‘clock neurons’.
15
Q
Describe the natural sleep/wake pattern of a rat (a nocturnal animal).
A
The rat is active during the night (represented by black bars on activity graphs) and inactive/asleep during the day.
16
Q
What experimental evidence proves that the sleep-wake cycle is regulated by an intrinsic system?
A
When an animal is placed in constant darkness (turning the lights off completely), it still maintains distinct periods of activity and sleep, rather than becoming randomly active.
17
Q
What happens to the circadian rhythm when an animal is deprived of light cues (e.g., constant darkness)?
A
The rhythm shifts slightly. For example, a rat will become active a little earlier and go to sleep a little earlier each day during the 24-hour cycle.
18
Q
What does the ‘shifting’ of the rhythm in constant darkness reveal about the Internal Clock?
A
It reveals that the internal clock is slightly imprecise on its own and requires external cues to stay perfectly on a 24-hour cycle.
19
Q
What is ‘Light Entrainment’?
A
It is the process where the internal clock is synchronized (coupled) with the external light-dark cycle via additional sensory inputs from the retina.
20
Q
Why is Light Entrainment necessary?
A
Because the intrinsic internal clock is imprecise, light entrainment is required to correct the slight daily shifts and keep the sleep/wake cycle aligned with the actual day/night schedule.
21
Q
What characterizes the timing and duration of NREM sleep during a sleep phase?
A
NREM (Non-REM) sleep usually occurs at the beginning of a sleep phase. It is longer during the earlier parts of sleep.
22
Q
What are the physiological characteristics of NREM sleep regarding heart rate, respiration, and metabolism?
A
During NREM sleep, metabolism, heart rate, and respiratory rate are decreased.
23
Q
How deep is NREM sleep and how does it affect waking up?
A
During NREM sleep, the brain is in a state of deep sleep, making it very difficult to wake up from this phase.
24
Q
What does REM stand for and when does it typically occur in the sleep cycle?
A
REM stands for Rapid Eye Movement sleep. It occurs later during the sleep cycle, is intermingled with non-REM sleep, and becomes longer and more frequent later in the sleep phase.
25
How do heart rate, respiratory rate, and metabolic rate during REM sleep compare to the awake state?
They are very similar to the awake state.
26
Which muscles are active and which are inactive during REM sleep?
The eye muscles are very active and move around (frequent eye movements). However, skeletal muscles are inactive, so no other body parts move.
27
How deep is REM sleep compared to NREM sleep?
REM sleep is considered very light sleep. Unlike NREM (which is deep), we can awake fairly easily from REM sleep.
28
Summarize the progression of sleep types over an 8-hour period.
The sleep cycle begins with NREM (deep sleep, low physiologic rates). As the night progresses, NREM sleep is intermingled with REM sleep (light sleep, awake-like physiologic rates), with REM phases becoming longer and more frequent later in the sleep phase.
29
What is Electroencephalography (EEG)?
A non-invasive technique where an array of electrodes is placed on the scalp to measure brain activity.
30
What specific biological signal does an EEG measure?
It measures the field potentials arising from the aggregate activity of cortical neurons located just underneath the skull.
31
Describe the cellular mechanism that creates the electrical field measured by EEG.
When a cortical neuron is activated by excitatory input and fires action potentials, the flow of sodium ($Na^+$) and potassium ($K^+$) ions creates areas in the extracellular space where positive charges outweigh negative ones (or vice versa).
32
Does a single EEG electrode measure the activity of a single neuron?
No. Each electrode measures the aggregate (summed) activity of many neurons.
33
What are the anatomical layers between the cortical neurons and the EEG electrode (from inside out)?
1. Meninges 2. Skull 3. Scalp
34
What characterizes 'Desynchronized' neuronal activity?
Neurons are activated in a staggered, uncoordinated manner (e.g., neuron 1 and 4 might be active, then neuron 2 and 5), rather than firing all at once.
35
What does the EEG trace look like during Desynchronized activity?
It displays small amplitude, high frequency oscillations.
36
Why is the EEG amplitude small during desynchronized activity?
Because the electrical fields generated by individual neurons are not aligned in time, so they do not summate strongly.
37
What characterizes 'Synchronized' neuronal activity?
Neurons fire together at the same time.
38
What does the EEG trace look like during Synchronized activity?
It displays large amplitude, low frequency oscillations.
39
Why is the EEG amplitude large during synchronized activity?
Because the individual electrical fields of the neurons summate (add up) to create a larger signal.
40
In the context of the cortical neurons shown, what types of axons are present?
Afferent axons (bringing signals in) and Efferent axons (sending signals out).
41
Describe the characteristics of EEG oscillations during the Awake state.
The EEG is characterized by low-amplitude, high-frequency oscillations.
42
What does the EEG pattern during the Awake state indicate about cortical neurons?
It indicates that cortical neurons are active in a desynchronized manner.
43
Why is desynchronized neuronal activity necessary during the Awake state?
It allows neurons to process information in parallel, which is required to: 1. Process a variety of sensory information. 2. Relate sensory information to past experiences. 3. Initiate complex movements and behaviors.
44
Describe the characteristics of EEG oscillations during NREM sleep (specifically Stage 4/Slow-wave sleep).
The EEG is characterized by high-amplitude, low-frequency oscillations.
45
What happens to the EEG oscillations as NREM sleep progresses from Stage 1 to Stage 4?
The synchronization increases, leading to progressively higher amplitudes and lower frequencies.
46
What does the synchronized activity during Stage 4 NREM sleep imply about cortical processing?
It implies that very little processing is occurring because synchronized neurons cannot process information in parallel.
47
Which two pathological states exhibit EEG patterns similar to deep NREM sleep (high-amplitude, low-frequency)?
1. Epileptic seizures 2. Coma.
48
Describe the characteristics of EEG oscillations during REM sleep.
The EEG shows low-amplitude, high-frequency oscillations, which look very similar to the EEG potentials recorded during the Awake state.
49
What specific feature distinguishes the REM EEG from the NREM EEG?
During REM sleep, activity is desynchronized (similar to awake), whereas in NREM sleep, activity is synchronized.
50
What cognitive activities are associated with the desynchronized cortical activity seen during REM sleep?
1. Dreaming: People awoken during REM sleep typically report dreaming. 2. Memory Consolidation: This state likely supports the processing required to consolidate memories.
51
Is the cortex responsible for regulating the sleep-wake cycle?
No. Although the cortex displays very different activity patterns during sleep and wakefulness, it is not involved in the actual regulation of these processes. Regulation is performed in other regions of the brain.
52
What are the two primary brain regions involved in the regulation of sleep and wakefulness?
1. The Hypothalamus. 2. The Reticular Activating System (Brainstem).
53
What is the specific function of the Suprachiasmatic Nucleus within the Hypothalamus?
It functions as the internal clock. It has an intrinsic mechanism that ensures the brain undergoes circadian changes in activity.
54
List the four specific regions of the Hypothalamus involved in sleep regulation.
1. Suprachiasmatic nucleus. 2. Preoptic nuclei. 3. Lateral hypothalamic area. 4. Posterior region.
55
What is the Reticular Activating System (RAS), where is it located, and what is its alternate name?
It is a region located in the brainstem. It is sometimes also called the Ascending Reticular Activating System or ARAS.
56
What is the primary function of the Reticular Activating System?
It is of seminal importance in the regulation of wakefulness and arousal. It makes sure that we are awake and alert.
57
Which specific nuclei constitute the Reticular Activating System in the brainstem?
1. Nucleus coeruleus. 2. Cholinergic nuclei. 3. Raphe nuclei.
58
What is the specific location and function of the Suprachiasmatic Nucleus (SCN) within the hypothalamus?
It is located in the hypothalamus and functions as the master regulator of the circadian rhythm (the internal clock). It modulates the activity of other hypothalamic regions involved in sleep regulation.
59
Which neurotransmitters does the Suprachiasmatic Nucleus utilize?
GABA and neuropeptides.
60
Describe the connection between the Suprachiasmatic Nucleus and the Pineal Gland.
The SCN has a direct projection to the pineal gland, which releases the hormone melatonin.
61
What is the function of Melatonin?
At night, melatonin synchronizes the circadian rhythm throughout the body, ensuring autonomic functions (like blood pressure regulation) occur according to the circadian rhythm.
62
What is the primary function of the Preoptic Nuclei (Anterior Hypothalamus) regarding sleep?
It contains GABAergic neurons that facilitate the onset of non-REM sleep (Sleep increases).
63
How do neurons in the Preoptic Nuclei facilitate sleep?
They project to and inhibit neurons that would normally facilitate wakefulness and arousal.
64
What class of drugs affects the Preoptic Nuclei, and what is the mechanism?
Benzodiazepines. They bind to GABA(A) receptors and prolong the action of GABA, facilitating the inhibition of wake-targets (promoting sleep).
65
What is the primary function of the Lateral Hypothalamic Area?
It tends to facilitate wakefulness and alertness (Wakefulness increases).
66
Which neurotransmitter is released by the Lateral Hypothalamus?
Orexin (also called Hypocretin).
67
What disorder is associated with the Lateral Hypothalamus and Orexin?
Narcolepsy.
68
Describe the mechanism and symptoms of Narcolepsy.
It is caused by mutated/dysfunctional orexin receptors which compromise signaling. Patients fall asleep at random times and have REM-like sleep episodes during the day, including cataplexy (inability to move). This shows orexin normally suppresses REM sleep in favor of wakefulness.
69
What is the specific nucleus located in the Posterior Hypothalamus and what neurotransmitter does it release?
The Tuberomammillary nucleus. It releases Histamine.
70
What is the function of Histaminergic neurons in the Posterior Hypothalamus?
They are active during wakefulness and stimulate alertness (Wakefulness increases).
71
How do Antihistamines affect sleep/wakefulness?
While used for allergies/inflammation in the periphery, if they cross the blood-brain barrier, they inhibit transmission at histaminergic synapses in the CNS, causing drowsiness.
72
What neurotransmitter is released by the Cholinergic Nuclei in the brainstem?
Acetylcholine (ACh).
73
What is the firing pattern and function of Cholinergic Nuclei?
They are active during Wakefulness and REM sleep (REM sleep increases), and they suppress non-REM sleep.
74
How do Cholinergic neurons affect the EEG pattern?
They project to the thalamus and innervate thalamocortical neurons. The release of ACh desynchronizes these neurons, causing the EEG to switch from a synchronized to a desynchronized pattern.
75
What neurotransmitter is released by the Raphe Nuclei (e.g., dorsal raphe) in the brainstem?
Serotonin.
76
What is the firing pattern and function of the Raphe Nuclei regarding sleep stages?
They facilitate wakefulness (Wakefulness increases) and decrease REM sleep (REM sleep decreases). They are active during wakefulness, decrease activity during non-REM, and are virtually silent during REM sleep.
77
How do SSRIs (used for depression) affect sleep patterns?
Because Serotonin suppresses REM sleep, patients taking SSRIs (Selective Serotonin Re-uptake Inhibitors) often show a selective suppression of REM sleep.
78
What neurotransmitter is released by the Nucleus Coeruleus in the brainstem?
Norepinephrine.
79
What is the function of the Nucleus Coeruleus regarding sleep and behavior?
It facilitates wakefulness and specifically increases alertness. It decreases REM sleep (REM sleep decreases).
80
What drug is related to the Nucleus Coeruleus and what disorder does it treat?
Methylphenidate (Ritalin). It treats ADHD.
81
What is the mechanism of Methylphenidate (Ritalin)?
It is a norepinephrine re-uptake inhibitor. It causes a general rise in norepinephrine levels in the brain, allowing patients to better focus on tasks.
82
What are the six specific topics covered under the study of Integrative Functions regarding Emotions and Goal-Directed Behaviour?
1. Neural system regulating emotions and goal-directed behaviour 2. Function of the hypothalamus 3. Role of the amygdala 4. Function of the mesolimbic dopaminergic pathway 5. Psychoactive drugs and addiction 6. Affective disorders
83
What is the primary function of the Limbic System regarding external stimuli?
It recognizes extrinsic cues (rewards or aversive stimuli) and generates Goal-Directed Behaviour and Emotions.
84
How is Goal-Directed Behaviour regulated by stimuli?
It is reinforced by rewards and diminished or suppressed by aversive stimuli.
85
What two types of needs does Goal-Directed Behaviour subserve? Give examples of each.
1. Primary needs: e.g., feeding, running away from predators. 2. Acquired desires: e.g., discussing politics.
86
When the Limbic System initiates a response to a cue, what two types of processes are triggered?
1. Voluntary motor responses (behaviour). 2. Autonomic processes (and hormonal responses).
87
In the specific example of seeing a nice-looking hamburger (a reward), what is the Voluntary Motor response?
'Grab before somebody else comes along! Chew!' (Grab the hamburger and start chewing).
88
In the specific example of seeing a nice-looking hamburger, what is the Autonomic response?
'Activate gastric system! Salivate!' (Salivation and initiation of peristalsis/digestion).
89
How are Emotions defined in the context of the Limbic System?
They include conscious experiences or inner feelings (e.g., happiness, sadness, anger, anxiety) as well as outward expressions and autonomic/hormonal responses.
90
In the specific example of sighting a bear (an aversive stimulus), what is the Voluntary Motor response?
'Freeze!' (Stop all movement in hopes the bear doesn't notice).
91
In the specific example of sighting a bear, what is the Autonomic response?
1. Raise blood pressure and heart rate. 2. Decrease cutaneous blood flow (make skin pale).
92
In the specific example of Politics (an acquired desire/stimulus), what physiological responses are triggered?
1. Raise blood pressure and heart rate. 2. Increase cutaneous blood flow (flushing/agitation). 3. 'Get agitated!'.
93
Within the modern view of the Limbic System, what is the primary role of the Hypothalamus?
It acts as the output hub of the limbic system.
94
What are the three distinct ways the Hypothalamus regulates the body's response to emotions?
1. Initiates changes in the tone of the Autonomic Nervous System (ANS). 2. Elicits changes in hormonal release from the pituitary gland. 3. Elicits somatic motor responses through the reticular formation.
95
How does the Hypothalamus regulate the Autonomic Nervous System (ANS)?
It changes the tone of the ANS by altering the relative balance between the sympathetic and parasympathetic nervous systems. This is done by projecting to preganglionic sympathetic and parasympathetic neurons.
96
What are the physiological consequences of the Hypothalamus altering ANS tone?
It leads to alterations in heart rate, blood pressure, respiration, and cutaneous blood flow.
97
How does the Hypothalamus control hormonal responses to emotion?
It controls the hormonal release from the pituitary gland.
98
What is the purpose of the somatic motor responses elicited by the Hypothalamus?
They generate the outward expression of emotion. Examples include making an excited face or assuming a defensive body posture.
99
Which brainstem structure does the Hypothalamus project to in order to elicit somatic motor responses?
The Reticular Formation.
100
What specific tract conveys signals from the Reticular Formation to spinal cord interneurons?
The Reticulospinal tract (an extrapyramidal tract).
101
Are we typically aware of the somatic motor responses (like facial expressions) generated by this pathway?
No. We are normally not even aware of them; we do not intend to make these expressions or postures.
102
Where is the Amygdala located?
It is a bilateral structure nestled within the anterior-medial portion of the temporal lobe.
103
What specific types of sensory input does the Amygdala receive?
It receives a variety of inputs including visual, auditory, somatosensory, and olfactory input.
104
Describe the 'dual nature' of the sensory input received by the Amygdala.
1. Unprocessed input: Comes directly from the thalamus. 2. Processed input: Comes from the sensory cortices.
105
What specific type of information does the Limbic Cortex provide to the Amygdala?
It provides contextual information.
106
What is the main function of the Amygdala?
To look for sensory stimuli that should elicit fear-related behaviour in response to aversive stimuli.
107
What are Innately Aversive stimuli? Give examples.
Stimuli that naturally create a fear response without prior learning (e.g., pain, taste, smell). Examples include the sight of a predator or the angry face of a roommate.
108
What is a Conditioned Fear Response?
It is the activation of the Amygdala by initially neutral or innocuous sensory stimuli (e.g., visual, auditory) that have been associated with a fearful or fear-inducing situation.
109
Describe the steps of a classical fear conditioning experiment with a rat.
1. Aversive Stimulus: An electric foot shock is delivered, creating a fear response where the rat freezes (exhibits freezing behaviour). 2. Pairing: The shock is paired with an innocuous stimulus, such as a light going on just before the shock. 3. Association: The Amygdala learns to associate the light with the shock. 4. Result: Turning on the light alone (without the shock) initiates the fear response.
110
Once the Amygdala detects an aversive or conditioned stimulus, which three regions does it send output signals to?
1. Hypothalamus. 2. Reticular formation. 3. Limbic cortex.
111
What is the physiological purpose of the Amygdala signaling the Hypothalamus?
To elicit both somatic motor responses and changes in autonomic function that make it easier to cope with the aversive stimulus.
112
What is the primary function of the Mesolimbic Dopaminergic Pathway?
To generate reward-oriented behaviour.
113
Which specific brain structures form the central components of this pathway?
1. The Ventral Striatum (specifically the Nucleus Accumbens). 2. The Ventral Pallidum. 3. The Ventral Tegmental Area (VTA).
114
How do the Ventral Striatum and Ventral Pallidum function together regarding goal-directed behaviour?
They act as a brake on the initiation of all goal-directed behaviour.
115
Describe the specific mechanism of the 'brake' provided by the Ventral Pallidum.
1. Neurons in the Ventral Pallidum are GABAergic (inhibitory). 2. They project to and inhibit neurons in the Thalamus (specifically the mediodorsal nucleus). 3. This inhibition is tonic (long-lasting/sustained), preventing thalamic neurons from exciting cortical regions.
116
How is the tonic inhibition of the Thalamus overcome (the process of De-repression or Disinhibition)?
1. Neurons in the Ventral Striatum are activated. 2. These striatal neurons are also GABAergic and inhibit the neurons in the Ventral Pallidum. 3. Inhibiting the inhibitor (pallidum) leads to disinhibition of the Thalamus, allowing it to activate the Cortex.
117
What two types of signals are required to activate neurons in the Ventral Striatum?
1. Intent signal: From the forebrain (Limbic Cortex, Hippocampus, or Amygdala) signaling the intent for a behaviour. 2. Facilitatory signal: Dopaminergic input from the Ventral Tegmental Area (VTA).
118
Under what conditions are dopaminergic neurons in the Ventral Tegmental Area (VTA) activated?
They are active during situations that are pleasant or rewarding, or when we anticipate that a behaviour will result in a reward.
119
Why is dopamine from the VTA necessary for this pathway?
It signals emotional reward (or anticipation) and is needed to maximally activate neurons in the Ventral Striatum, facilitating the de-repression of the thalamus.
120
How does this pathway explain the difficulty in initiating non-rewarding tasks (like doing dishes) versus rewarding ones (like eating cake)?
The pathway is wired to initiate behaviour only when facilitated by the reward signal (dopamine). Without the reward signal, it is physically harder to overcome the 'brake' and initiate the behaviour.
121
How does the neural circuit of the mesolimbic pathway compare to the motor system?
The circuitry is very similar: 1. Inhibitory Output: In the motor system, the Globus Pallidus inhibits the thalamus; here, the Ventral Pallidum inhibits the thalamus. 2. Input: Both require cortical input and a facilitatory dopamine signal. 3. Dopamine Source Difference: In the motor system, dopamine comes from the Substantia Nigra; here, it comes from the Ventral Tegmental Area.
122
What is the general definition of Psychoactive Drugs?
They are chemical substances that change our mood, our perception, our cognitive processes, our behaviour, and our consciousness.
123
What is the common site of action for all psychoactive drugs?
The Mesolimbic Dopaminergic Pathway.
124
What is the common physiological effect of all psychoactive drugs on this pathway?
They all act by increasing the activation of the ventral striatum (specifically via dopamine signaling).
125
Which specific drug is mentioned as being structurally related to dopamine?
Methamphetamine.
126
What are the two mechanisms by which drugs structurally related to dopamine (like amphetamines/cocaine) function?
1. They activate dopamine receptors directly. 2. They inhibit the clearance of dopamine by blocking its re-uptake into neurons.
127
How do Opiates enhance dopaminergic signaling if they are not structurally related to dopamine?
They inhibit GABAergic neurons (interneurons) in the Ventral Tegmental Area (VTA). This removes the inhibition on dopaminergic neurons, leading to increased dopamine release in the ventral striatum.
128
How does Alcohol affect the mesolimbic pathway?
It acts very similarly to opiates, by inhibiting GABAergic neurons in the VTA.
129
How does Nicotine enhance dopaminergic signaling?
It directly activates dopaminergic neurons in the VTA, causing an increased release of dopamine.
130
Besides the short-term increase in dopamine, what is the long-term effect of psychoactive drugs on the brain?
They reduce the ability of striatal neurons to respond to cortical input (decreased excitability).
131
What are the behavioral consequences of the long-term reduction in striatal neuron responsiveness?
It leads to behavioural changes and an intense craving to continue the use of the psychoactive drug (Addiction).
132
What are the two main types of affective (mood) disorders?
1. Unipolar depression. 2. Bipolar spectrum disorder (also known as Manic depression).
133
What is the lifetime incidence of Unipolar Depression in men and women?
* Women: 10% to 25%. * Men: 5% to 12%.
134
What are the specific symptoms characterized by Unipolar Depression?
* Pervasive low mood. * Loss of interest in favorite activities. * Preoccupation with feelings of worthlessness and hopelessness. * Poor concentration and memory. * Withdrawal from social activities. * Insomnia. * Suicidal tendencies.
135
Describe the alternating episodes experienced in Bipolar Spectrum Disorder.
Periods of depression (with symptoms similar to unipolar depression) alternate with episodes of Mania.
136
What are the symptoms of a Manic episode in Bipolar disorder?
* Euphoria. * Increased psychomotor activity. * Disinhibited social behavior. * Sometimes psychosis (hallucinations or delusions).
137
What are the general causes of affective disorders?
They are complex and encompass both genetic as well as environmental (social) factors.
138
Based on functional magnetic resonance imaging (fMRI), which brain regions show altered neuronal activity in patients with affective disorders?
1. The Limbic Cortex. 2. The Amygdala. 3. Certain areas in the Frontal Cortex.
139
What does the Monoamine Theory of Depression posit?
It posits that the cause of the disease is a relative lack of serotonin (5HT), norepinephrine (NE), and dopamine (DA) signalling in the brain.
140
What observation forms the basis/evidence for the Monoamine Theory?
The observation that pharmacological interference with either the breakdown or the clearance (re-uptake) of monoamines leads to amelioration of the symptoms.
141
How do Monoamine Oxidase Inhibitors (MAOIs) treat depression?
They inhibit the enzyme monoamine oxidase, which catalyzes the rate-limiting step of monoamine breakdown. This blocks the breakdown of serotonin, dopamine, and norepinephrine.
142
What is the downside of using MAOIs?
Because monoamines have a host of different functions, MAOIs have many side effects.
143
How do Tricyclic Antidepressants work?
They block the re-uptake of serotonin and norepinephrine. Their efficacy is comparable to MAOIs.
144
How do Selective Serotonin Re-uptake Inhibitors (SSRIs) work?
They specifically interfere with the uptake of serotonin. This is the most recent advancement in treatment.
145
What evidence (the 'Lag Phase') makes the Monoamine Theory difficult to fully accept?
While drugs change monoamine levels in the brain in a matter of days, patients do not experience a difference in symptoms for 3 to 4 weeks. This suggests the simple 'lack of monoamines' hypothesis is insufficient and the mechanism is more complex.
146
What are the six specific topics covered in the section on Cognition?
1. Definition of cognition. 2. Role of association cortices in cognition. 3. Cortical areas involved in language processing. 4. Symptoms and causes of schizophrenia. 5. Subcortical circuits regulating cognitive processes. 6. Memory: Categorization and brain regions involved.
147
What is the comprehensive definition of Cognition?
Cognition subsumes all mental actions or processes that serve to acquire knowledge or understanding through thought, experience, and our senses.
148
What specific intellectual functions and requirements does cognition encompass?
* Perception and attention. * The formation of knowledge and memory. * Recognizing objects. * Storing information on novel stimuli and their relation to familiar objects. * Judgment and reasoning. * Comprehension and problem solving. * Decision making and planning of appropriate responses. * Comprehension and production of language.
149
What two types of knowledge do cognitive processes utilize?
They use both existing knowledge and new knowledge that is being made using our senses.
150
Why are humans usually better at cognition than other non-human primates or mammals?
Because humans have a significantly larger amount of associational cortical areas, resulting from the dramatic expansion of the cortex during the evolution of the human species.
151
How is the Associational Cortex defined?
It includes all cortical areas that are not primary sensory areas or motor cortex.
152
What proportion of the whole human cortex is comprised of Associational Cortex?
About four-fifths (4/5) of the whole cortex.
153
What are the three primary sources of our scientific understanding of associational cortical areas?
1. Studying deficits elicited by localized lesions of the associational cortex in humans. 2. Electrophysiological recordings in non-human primates. 3. Functional MRI (fMRI) studies in humans.
154
What are the three primary functions of the Frontal Association Cortex?
Problem solving, planning, and social behaviour.
155
Who was Phineas Gage and what injury did he sustain?
He was a railroad construction engineer in the 19th century who experienced a traumatic brain injury where a metal rod impaled his skull and drove all the way through his prefrontal cortex while working with explosives.
156
What functions remained unaltered in Phineas Gage after his accident?
His general intelligence and his memory.
157
What specific 'Executive Function' deficits did Phineas Gage exhibit after the injury?
* His social behaviour was completely changed. * His judgment was impaired. * His social skills deteriorated (he became impatient and mean). * He started lying (which he hadn't done before). * He was unable to plan his daily life or work projects (unable to continue construction work).
158
What are the primary functions of the Parietal Association Cortex?
Attention and perceptual awareness.
159
What syndrome results from lesions (e.g., stroke) to the Parietal Association Cortex?
Contralateral Neglect Syndrome.
160
Describe the symptoms of Contralateral Neglect Syndrome.
Patients can describe surroundings on the side ipsilateral (same side) to the lesion but are unable to pay attention to whatever is present on the contralateral (opposite) side.
161
How is Contralateral Neglect Syndrome illustrated in drawing tasks (as seen in the slide)?
When asked to copy a model (e.g., a clock or a house), the patient's copy completely omits details on one side (e.g., the left side numbers of a clock are missing).
162
What anatomical fact explains why the neglect is on the contralateral side?
All sensory afferents cross the midline of the brain; whatever is sensed with the right half of the body ends up in the left cortical hemisphere, and vice versa.
163
What is the primary function of the Temporal Association Cortex?
Recognition of objects.
164
What disorder results from lesions to the Temporal Association Cortex?
Agnosia (the inability to recognize familiar objects).
165
How does Agnosia (Temporal lesion) differ from Neglect (Parietal lesion)?
In Agnosia, patients are aware of the stimulus/object (they can see it), they just cannot recognize or identify it.
166
What is Prosopagnosia and where is the lesion located?
It is the inability to recognize faces. It is caused by a lesion specifically in the lower right temporal association cortex.
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What abilities are retained in patients with Prosopagnosia?
* They can identify people by their gait or voice. * They can describe facial features (shape of nose/mouth, eye color).
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What is the specific deficit in Prosopagnosia despite being able to describe features?
They are unable to put a name to the face.
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In the experiment shown, what four tasks was the test subject asked to perform to study language processing?
1. Hearing words. 2. Seeing words. 3. Speaking written words. 4. Generating words.
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What technique was used to measure brain activity during this experiment?
Functional Magnetic Resonance Imaging (fMRI).
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What physiological change does fMRI measure, and how does it relate to brain activity?
It measures changes in blood flow. It exploits the fact that blood flow is very tightly coupled with neuronal activity (active areas have increased blood flow).
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Does language processing utilize a single brain area?
No. It utilizes many associational areas. Different tasks (speaking, seeing, hearing, generating) activate very different areas of the brain.
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Aside from association areas, which primary cortices are activated when seeing or hearing a word?
* Seeing a word: Activates the Primary Visual Cortex. * Hearing a word: Activates the Primary Auditory Cortex.
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Where is Wernicke's Area located?
In the Temporal Association Cortex.
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What is the primary function of Wernicke's Area?
Language comprehension.
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Describe the symptoms of a patient with a lesion in Wernicke's Area.
* Generation: They can still generate language, find words, and construct elaborate sentences (speech is fluent). * Content: What they say doesn't make any sense to others. * Comprehension: They have difficulties understanding the speech of others or reading text.
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Where is Broca's Area located?
In the Frontal Cortex.
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What is the primary function of Broca's Area?
To generate language.
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What is the specific term for the deficit caused by a lesion in Broca's Area?
Expressive Aphasia.
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Describe the symptoms of a patient with a lesion in Broca's Area.
* Generation: They have difficulty forming words and sentences (it takes a long time). They struggle to find appropriate words and with grammatical construction. * Comprehension: They are still able to understand other people and have no issues reading books or newspapers.
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What does it mean for a cognitive function to be lateralized?
It means the function is more dominantly processed in one of the hemispheres than in the other.
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Which cortical hemisphere is dominant for language generation and processing?
The left cortical hemisphere.
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What are the two specific fiber tracts that connect the two hemispheres of the brain?
1. The Corpus Callosum. 2. The Anterior Commissure.
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Why do some patients have their corpus callosum surgically severed (transected)?
To treat intractable epilepsy. The dissection preserves one hemisphere from epileptic seizures generated on the other side.
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In a patient with a severed corpus callosum, what happens when they hold an object (e.g., a key) in their right hand?
They are able to name the object (e.g., 'Key').
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In a patient with a severed corpus callosum, what happens when they hold an object (e.g., a key) in their left hand?
They are unable to name the object.
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Why can't a split-brain patient name an object held in the left hand? (Describe the pathway).
1. Sensory afferents cross the midline at the level of the brainstem. 2. Information about the object ends up in the right somatosensory cortex (contralateral hemisphere). 3. Due to the severed corpus callosum, the right somatosensory cortex has no connection to the speech centers (Wernicke's and Broca's areas) on the left side.
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Does this inability to name objects apply only to touch (somatosensory information)?
No. It also applies to visual information. If an object appears in the left visual field (processed by the right hemisphere), the patient cannot name it.
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What overall conclusion about brain function is drawn from these split-brain observations?
These observations show that language processing is lateralized and mainly occurs in the left half of the brain.
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What is the general role of subcortical areas in cognition?
While associational cortical areas are important, many subcortical areas also play an important part in modulating cognition, as illustrated by diseases like schizophrenia [Text].
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What are the three categories of symptoms associated with Schizophrenia?
1. Positive symptoms. 2. Negative symptoms. 3. Cognitive symptoms.
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Describe the Positive symptoms of Schizophrenia.
Hallucinations (visual or auditory) and paranoid delusions.
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Describe the Negative symptoms of Schizophrenia.
Apathy, lack of emotion, and social anxiety (which makes social interaction difficult).
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Describe the Cognitive symptoms of Schizophrenia.
Disorganized thoughts, difficulty completing tasks, difficulty in planning, and difficulty in judgment [Text].
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What broad factors contribute to the causes of Schizophrenia?
Genetic, developmental, and social factors.
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What statistic illustrates the genetic component of Schizophrenia?
If an individual has an identical twin with schizophrenia, there is a 40 percent chance that they will develop the disorder as well [Text].
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What specific developmental and environmental factors are linked to Schizophrenia?
* Premature birth [Text]. * Complications during pregnancy [Text]. * Social stress and isolation during childhood [Text]. * Substance abuse during adolescence [Text].
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How is Schizophrenia classified regarding its development and onset?
It is a neurodevelopmental disorder resulting from aberrant development during adolescence. It usually manifests during adolescence or young adulthood [Text].
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What structural changes in the brain are associated with Schizophrenia?
Structural changes in the frontal cortex, specifically altered function and activation of frontal cortical areas [Text].
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What is the Dopamine Hypothesis of Schizophrenia?
It posits that the symptoms of schizophrenia are due to an increased activity of the dopaminergic system.
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What pharmacological evidence regarding agonists supports the Dopamine Hypothesis?
Dopamine receptor agonists can cause hallucinations and delusions.
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What pharmacological evidence regarding antagonists supports the Dopamine Hypothesis?
Neuroleptics (dopamine receptor antagonists) can reduce the positive symptoms of schizophrenia.
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Which specific structures of the Basal Nuclei act as a 'brake' on cognitive processes?
The Nucleus Caudatus (the anterior part of the striatum) and the Globus Pallidus.
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What is the specific function of the Nucleus Caudatus and Globus Pallidus regarding thoughts and planning?
They act as a brake on all cognitive processes, preventing the selective initiation of thoughts unless activated.
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How does the Globus Pallidus enforce this 'brake' on cognition?
By inhibiting neurons in the Thalamus.
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Which specific nuclei of the Thalamus are inhibited by the Globus Pallidus in the cognitive circuit?
The Mediodorsal (MD) and Ventral Anterior (VA) nuclei.
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What happens when these Thalamic neurons are inactive (repressed)?
No cognition happens because they cannot project to associational cortical areas to initiate cognitive processes.
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What is the mechanism to initiate a cognitive process (release the brake)?
Neurons in the Caudate Nucleus (Striatum) must be activated, which then inhibit the neurons in the Globus Pallidus (disinhibition).
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What two types of signals are required to activate the neurons in the Caudate Nucleus?
1. Cortical Input: Signals from the Prefrontal Cortex indicating the intent to initiate a cognitive process. 2. Modulatory Input: A facilitatory dopaminergic signal.
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What are the sources of the dopaminergic signal for the cognitive circuit?
1. The Ventral Tegmental Area (VTA). 2. The Substantia Nigra pars compacta (SNc).
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How does the cognitive control circuit compare to the circuits controlling movement and goal-directed behaviour?
The circuit logic is very similar (Cortical input + Dopamine -> Striatum -> inhibits Pallidus -> disinhibits Thalamus -> Cortex), but the specific parts of the basal nuclei differ [cite: text].
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Summary of the Cognition Circuit Components:
* Cortical Input: Prefrontal Cortex. * Striatum Component: Caudate Nucleus. * Dopamine Source: VTA and SNc. * Thalamic Target: Mediodorsal and Ventral Anterior nuclei.
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What is the general definition of Memory?
The ability of the brain to store information from the past and to store experience.
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What are the two Qualitative categories of memory?
1. Declarative memory. 2. Non-declarative (procedural) memory.
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Describe Declarative Memory and give an example.
It is available to consciousness and can be expressed in language. * Examples: The birthday of a friend or the phone number of a parent.
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Describe Non-declarative (Procedural) Memory and give an example.
It is generally not available to consciousness (difficult to describe) and involves skills like motor coordination. * Example: Knowing how to ride a bike.
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What are the Temporal categories of memory?
1. Working memory (short-term). 2. Long-term memory.
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How long does Working Memory last and what is required to keep it?
It lasts only seconds to minutes. Unless used over and over again (repetition), it will slip from memory because it has not yet been transferred to long-term memory.
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Where is the Hippocampus located and what is its primary function regarding memory?
It is located in the medial temporal lobe of the cerebrum. It is intimately involved in the formation and consolidation of declarative memories.
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Who was Patient H.M. and why was his hippocampus removed?
He was a patient in the 1950s/60s who suffered from intractable epilepsy originating in his hippocampi. The surgery involved removing his hippocampi to stop the seizures.
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What abilities remained intact in Patient H.M. after surgery?
* He recovered well and had normal brain functions in many respects. * Sensory and motor abilities were fine. * Most cognitive behaviour was indistinguishable from before. * Retrograde memory: He could still remember events from before his surgery (childhood and adolescence).
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What specific memory deficit did Patient H.M. suffer from?
A pronounced Anterograde Amnesia: an inability to form any new declarative memory after his surgery.
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What major scientific conclusion about the Hippocampus was drawn from Patient H.M.'s case?
That the hippocampus is required for the formation of declarative memory, but it is not the side of their storage (since he retained old memories).
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What behavioral test is used to study Declarative (Spatial) Memory in mice?
The Morris Water Maze.
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Describe the Morris Water Maze task.
A mouse is placed in a tank of opaque water and must find a submerged platform. Over multiple trials, the mouse learns to memorize the location and finds it faster.
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What happens to mice that lack the gene for the NMDA-type glutamate receptor in the Morris Water Maze?
They are unable to learn the location of the submerged platform, suggesting NMDA receptors are important for forming new declarative memories.
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Why is the NMDA receptor called a 'Coincidence Detector'?
Because its opening requires two simultaneous events: 1. The release and binding of glutamate on the extracellular surface. 2. The depolarization of the postsynaptic membrane (to open the ion channel).
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What ion enters the postsynaptic neuron once NMDA receptors are activated?
Calcium ions ($Ca^{2+}$).
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What physiological process is initiated by Calcium signaling through NMDA receptors?
Long-Term Potentiation (LTP).
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What is Long-Term Potentiation (LTP)?
A long-lasting increase in the size of excitatory postsynaptic potentials at the synapse where the NMDA receptor is activated.
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What is the prevailing hypothesis regarding the cellular basis of declarative memory?
That Long-Term Potentiation (LTP) at glutamatergic synapses is required for the formation of declarative memories.
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Besides NMDA receptors, what other molecule is essential for LTP and memory formation?
Calcium/calmodulin-dependent kinase II (CaMKII).
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According to case studies like H.M., what is the specific role of the Hippocampus in declarative memory?
It is required for the formation of declarative memories, but it is not the site of their storage.
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Is the Hippocampus required for Non-declarative memory?
No.
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Where is Short-term Declarative memory processed/located?
The Hippocampus.
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Where is Long-term Declarative memory stored?
In a variety of cortical regions, especially the associational cortical areas.
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Why does a specific lesion within the cortex not eradicate already formed declarative memories?
Because declarative memory is stored in a parallel fashion, in several associational cortices at the same time.
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Where is Short-term Non-declarative (procedural) memory located?
The sites are unknown, but presumably widely distributed.
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Which brain structures are involved in Long-term Non-declarative (procedural) memory, specifically for motor learning?
1. Cerebellum 2. Basal Nuclei (Basal Ganglia) 3. Motor Cortex (and Premotor Cortex)
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Summary: Compare the brain regions for Long-term Declarative vs. Long-term Non-declarative memory.
* Declarative: Variety of Cortical Regions (Association cortices). * Non-declarative: Cerebellum, Basal Ganglia, and Premotor Cortex.
