PSL300 > Nervous System 2 > Flashcards

Nervous System 2 Flashcards

Week 2 (73 cards)

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1
Q

What is the function of the Blood-Brain Barrier (BBB)?

A

Protects the brain and spinal cord from general blood circulation, maintaining a stable environment for neurons.

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2
Q

Why must the ionic composition around neurons be carefully controlled?

A

To prevent changes in excitability (e.g., excess K⁺ → depolarization → Na⁺ channel inactivation → no action potentials).

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3
Q

Why can’t neurotransmitters float freely in the brain’s extracellular fluid?

A

They would confuse signaling; BBB prevents random entry.

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4
Q

What are the two main BBB barriers?

A

Blood vessels ↔ Interstitial fluid; (2) Blood vessels ↔ CSF.

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5
Q

How does interstitial fluid compare to CSF?

A

Nearly identical composition; free diffusion between them.

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6
Q

Why can’t dopamine be injected to treat Parkinson’s?

A

Dopamine doesn’t cross the BBB.

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7
Q

What is given instead of dopamine in Parkinson’s treatment?

A

L-DOPA, which crosses BBB and is converted into dopamine.

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8
Q

Why does MSG sometimes cause symptoms outside the brain?

A

It doesn’t cross the BBB well, but activates glutamate receptors in the peripheral nervous system.

Makes us very thirsty after consuming a lot of it

However some people also complain of stiff neck, because MSG cannot readily cross the BBB, but can active glutamate receptors outside the brain and peripheral nervous system

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9
Q

Where is the BBB intentionally broken?

A

Hypothalamus, pituitary gland, and circumventricular organs.

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10
Q

Why is the BBB broken in some areas?

A

To allow hormone release or chemical/metabolite sensing from the bloodstream.

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11
Q

What protects the brain and spinal cord?

A

Skull, backbone, meninges (dura, arachnoid, pia).

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12
Q

What is the subarachnoid space filled with?

A

Cerebrospinal fluid (CSF).

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13
Q

What is meningitis?

A

Infection of the meninges (viral or bacterial).

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14
Q

Meningitis

A

made up of the following three connective tissues (cranial meninges for the brain and spinal meninges for the spinal cord)

Dura mater (very tough membrane, sac containing the brain and the spinal cord) Sits closest to the skull

Arachnoid membrane (much more delicate tissue)

Pia mater (lies right on top of the brain; tethered to Arachnoid by Arachnoid ‘Trabeculae’)

Between the arachnoid membrane and Pia matter there is a Subarachnoid space (filled with CSF)

The brain floats in to protect from mechanical stress

Note that liquid itself is not compressible but, the membrane around the membrane is

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15
Q

What does the reticular formation regulate?

A

Consciousness, alertness, sleep-wake cycles.

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16
Q

How do brain blood vessels differ from body blood vessels?

A

Brain vessels have tight junctions (no gaps), forming the BBB

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17
Q

What produces most CSF?

A

Choroid plexus

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18
Q

Pathway of CSF circulation?

A

Lateral ventricles → 3rd ventricle → Aqueduct of Sylvius → 4th ventricle → central canal → subarachnoid space (spinal cord) → venous sinus

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19
Q

CSF is found in the

A

Ventricles

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20
Q

How does CSF return to circulation?

A

Via arachnoid villi into venous sinus.

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21
Q

Choroid Plexus

A

Choroid Plexus produces most of the CSF (but not all, some are produced in the capillaries inside the brain)

Made up of epithelial cells connected by tight junctions

Choroid Plexus produces CSF continuously (550 ml/day) to circulate

It is a cleansing mechanism

Choroid Plexus is a dense network of capillaries ballooning out into the ventricular wall with tight junction so that everything has to be transported

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22
Q

A lumbar puncture (spinal tap) is a diagnostic, therapeutic procedure for?

A

collect sample of cerebrospinal fluid (CSF) for analysis

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23
Q

What do astrocytes do at synapses?

A

Remove neurotransmitters & provide energy substrates to neurons.

provide a bridge between neurons and blood vessels

Remove neurotransmitters because they are sitting right at the synapse

Provide energy substrates for neurons and more

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24
Q

What is the metabolic role of astrocytes?

A

Perform glycolysis → produce lactate → neurons use lactate for ATP.

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25
How do astrocytes regulate blood flow?
Detect glutamate at synapses → Ca²⁺ wave → prostaglandin (PGE₂) release → vasodilation → ↑ blood flow. Astrocytes have connection with the neuron at the synapse and when they detect increased signaling, they can send a metabolic signal outward to BV (opposite to nutrient flow), signaling neuronal activity level Glutamate in synapses triggers Ca2+ release within astrocytes; Ca2+ wave travels through astrocytes and triggers prostaglandin (PGE2) release at end-foot PGE2 causes vasodilation > increased blood flow
26
What is a receptor potential?
A graded change in membrane potential due to an external sensory cue (not from a presynaptic neuron).
27
How do sensory receptors usually respond to stimuli?
They depolarize upon receiving energy input (touch, light, etc.), except photoreceptors which hyperpolarize.
28
How do receptor proteins generate receptor potentials?
They change shape in response to energy → open ion channels or trigger G-protein cascades. When the receptor protein changes shape, it can either: Directly open ion channels (e.g. cation channels > leads to depolarization of the membrane) Enzyme is activated via G-protein coupling > leading to production of 2nd messenger (cAMP, cGMP, InP3) > lots of 2nd messenger > amplifying the signal
29
What happens when a chemical stimulus binds to a metabotropic receptor?
G-protein activates an enzyme → second messengers (cAMP, IP₃, cGMP) → amplification → ion channel modulation.
30
What is the advantage of metabotropic signaling?
Amplification of signals → one stimulus produces a large cellular response.
31
Classic example of a metabotropic receptor?
Olfactory receptor → odorant binds → G-protein → adenylyl cyclase → cAMP → ion channels open → depolarization. Note that the receptor potential is not an action potential but a graded potential (like PSP) So it travels passively to the trigger zone Because we are generating current indirectly through the metabotropic mechanism, this will result in the amplification of the signal, making the olfactory cells very sensitive
32
What are the 2 main stages of amplification in metabotropic signaling?
(1) One receptor activates many G-proteins, (2) Each enzyme produces many 2nd messengers.
33
Why does metabotropic amplification make neurons sensitive?
A small signal (one odorant molecule) can generate a big, long-lasting response.
34
Why is smell unique compared to other senses?
Olfactory signals bypass the thalamus, going directly to the olfactory cortex.
35
What bone allows olfactory nerve fibers to reach the brain?
The cribriform plate (thin, sieve-like bone). Damage → loss of smell.
36
Two categories of sensory cell transmission?
(1) Sensory cell generates its own AP, (2) Sensory cell releases neurotransmitters without an AP.
37
Where is the “trigger zone” for action potentials in sensory neurons?
At the branch point (first excitable patch of membrane).
38
How do taste receptor cells transmit signals?
They generate receptor potentials → Ca²⁺ influx → vesicle release (no AP).
39
The sensory cell itself does not have to generate its own action potential as long as it can release neurotransmitters ... why?
The depolarizing current doesn't produce any AP > travel throughout the membrane and at the other end > they depolarize the membrane sufficiently > influx of Ca++ ions and trigger exocytosis vesicles > sensory cell is releasing vesicles and not producing an AP If the sensory cell could release transmitters then the next cell in line will simply pick this up and act as the postsynaptic neuron, firing an action potential So the depolarization in the first order neuron (the sensory cell that does not generate an action potential will not itself produce an action potential, but instead will release neurotransmitters by opening Ca++ channels
40
What is adaptation?
Decay of membrane potential during sustained stimulus.
41
lowly vs. rapidly adapting receptors?
lowly adapting → sustained response (magnitude). Refers to receptor potential being sustained for the duration of the stimulus So as long as you maintain the stimulus, some receptor potential remains Interested in overall magnitude of the stimulus Rapidly adapting → respond to changes in stimulus (velocity). Receptor potential elicited by change in stimulus energy, decays to zero when stimulus is constant The receptor potential is elicited by change in the stimulus energy Upward change, or a downward change The receptor potential decays to 0 when the stimulus is constant
42
What is habituation?
Weaker responses to repeated identical stimuli over time.
43
How is stimulus intensity coded?
Greater stimulus → larger receptor depolarization → more NT release or higher AP frequency. Greater stimulus results in greater change in the receptor potential The greater the intensity, the greater the change in the receptor potential – greater receptor depolarization Results in greater frequency or more neurotransmitter release The greater the depolarization > the faster the membrane will be brought up from hyperpolarization to generate a new spike The Impulse frequency will always be limited by the refractory period
44
Why is AP frequency limited?
Refractory period caps maximum discharge rate.
45
How do neurons code above this ceiling?
Recruitment of additional, higher-threshold sensory neurons.
46
What is the “labeled line” strategy?
Activity in a specific pathway = a specific modality (e.g., vision, hearing, touch).
47
What is population coding?
Stimulus quality encoded by the ratio of activity across multiple receptor types.
48
What is a receptive field?
The spatial territory where stimulation activates a single sensory neuron.
49
What happens when a neurotransmitter binds to a postsynaptic receptor?
The receptor protein changes shape → effect depends on receptor type.
50
What are the two main types of postsynaptic receptors?
Ionotropic (direct ion channel opening) and Metabotropic (G-protein/2nd messenger cascade).
51
What determines the effect of a neurotransmitter?
The receptor, not the transmitter itself.
52
What is a post-synaptic potential (PSP)?
A graded change in postsynaptic membrane potential caused by receptor activation.
53
How long does a PSP last?
20–40 ms (as long as transmitter is present).
54
EPSP vs IPSP ion selectivity?
EPSP: cations (Na⁺, K⁺) → depolarization. - Excitatory post-synaptic potential IPSP: Cl⁻ or K⁺ → hyperpolarization - Inhibitory post-synaptic potential
55
Example of an ionotropic receptor for ACh?
Binding of acetylcholine to nicotine receptors changes the shape of these proteins and opens the diffusion channel This channel is highly specific for cations Opening these channels results in the generation of EPSP Note ; opening these channels and binding is fast
56
Main ligands for ionotropic receptors?
Acetylcholine (Ach) - binds to nicotine receptors Glutamate GABA – usually inhibitory, IPSP Glycine
57
How do benzodiazepines act on GABA?
They are GABA agonists → enhance inhibition → ↓ neuronal excitability.
58
How do metabotropic receptors work?
Ligand binds → G-protein activation → enzyme activity → ↑ or ↓ 2nd messengers (cAMP, cGMP, IP₃)
59
How do metabotropic effects differ from ionotropic?
Slower, involve 2nd messengers, effects can be metabolic or modulate ion channels indirectly.
60
Example of a metabotropic receptor?
β-adrenoreceptor for noradrenaline → G-protein → adenylyl cyclase → ↑ cAMP → phosphorylates Ca²⁺ channels → ↑ contractility. Is a metabotropic receptor β-receptor is a metabolic receptor for Noradrenalin (NA) Binding of NA to β-receptor activates adenylyl cyclase via G-protein alteration Adenylyl cyclase increases production of cAMP(2nd messenger) CAMP then activates kinases which phosphorylate membrane Ca++ channel This phosphorylation of the Ca++ channel > increase in Ca++ influx (important in heart muscle, increases contractility)
61
What do beta-blockers do?
Beta-blockers Beta-blockers block the interaction of noradrenaline to its beta-receptor, resulting in the decrease of Ca++ availability Calcium is involved in the contractility of the heart therefore, decreases in the Ca++ results in decreased contractility
62
Ligands for metabotropic receptors?
ACh (muscarinic), peptides (Substance P, β-endorphin, ADH), catecholamines (NA, dopamine), serotonin, ATP, adenosine, NO, CO
63
Where are PSPs generated?
In dendrites & soma (inexcitable membrane).
64
Where is the first site for action potential generation?
Trigger zone (axon hillock, initial segment)
65
What is PSP spread
When a postsynaptic potential (PSP) (EPSP or IPSP) is generated at a synapse (usually on a dendrite), that electrical signal spreads or travels along the membrane of the neuron — typically toward the soma (cell body) and possibly the axon hillock (where action potentials start).
66
Why is summation needed?
A single EPSP is rarely enough to reach threshold at the trigger zone.
67
Types of PSP summation?
Spatial (many EPSPs at once, from different synapses) and Temporal (repeated EPSPs from same synapse over time).
68
Where are IPSPs often located?
On the soma, close to the trigger zone
69
How do IPSPs inhibit EPSPs?
Open Cl⁻ channels → clamp membrane near resting potential → shunt depolarization. PSP involves the opening of the Cl-channel There are more Cl- ions on the outside than on the inside, because they were repelled by the negatively charged proteins The equilibrium potential for Cl-is very close to the resting MP (-70 mV) Therefore at rest, opening of the Cl-channel would result in little change However, when the membrane is depolarized, opening of the Cl-channel will bring the MP back down to -70 mV The net effect of Cl-is basically to ‘clamp’ the MP, which is preventing excitation, thus preventing depolarization > inhibitory effect These IPSPs are very strategically located and they completely block any signal coming from EPSPs simply by positioning right on the soma
70
Why are IPSPs often more precise/important than EPSPs?
Location near trigger zone makes them strategically effective at blocking firing.
71
What is a spike train?
Continuous stream of APs from strong, prolonged synaptic input.
72
How is depolarization block avoided during spike trains?
After-hyperpolarization (via K⁺ channels) resets Na⁺ channels for reactivation.
73
Why is after-hyperpolarization critical?
Restores excitability, allowing repeated APs during sustained depolarization.
PSL300
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