Which regions of the cat brain are sufficient for the expression of emotional behaviour?
- remove cortex but leave cerebellum, brain stem, hypothalamus
- Sham Rage - angry at anything
- as above but also remove hypothalamus
- no sham rage
- Bard’s cats
- realised hypothalamus was an integrating centre for this particular type of emotion: fear
- also for a lot of autonomic functions
- fear responses are very much directed at survival and homeostasis
How can emotional systems develop?
e. g.
- between the ages of four and six, predominant fears include kidnappers, robbers, ghosts and mosters
- at six years, fears of bodily injury, death and failure develop
- these may continue into early adolescence
- at ten or eleven years of age, fears regarding social comparison, physical appearance, personal conduct and school examinations may predominate
How can emotional systems become dysfunctional?
abnormal experiencing of anxiety can occur in a variety of ways, commonly they are classified as follows:
- generalised anxiety disorder (GAD)
- panic attack
- panic disorder
- phobias
- obsessive compulsive disorder
- post-traumatic stress disorder
What are symptoms of a Panic Attack?
- pounding heart
- chest pains
- light-headedness or dizziness
- nausea or stomach problems
- flushes or chills
- sweating
- shortness of breath or a feeling of smothering or choking
- tingling or numbness
- shaking or trembling
- feelings of unreality
- terror
- a feeling of being out of control or going crazy
- fear of dying
- a lot are associated with some sort of dysregulation of autonomic function
- some somatic
- cognitive
What are nervous system components that organise expression of emotional experience?
emotional expression
- descending “extrapyramidal” (not the corticospinal part of cortex) projections from “limbic” (origin of emotional control of muscles) centres of ventral-medial forebrain and hypothalamus
medial (aminergic, dopamine etc)
- gain setting
- sets the tone for the brain
- more noradrenaline, outward looking
- less, inward looking
- rhythmic reflexes
- inputs on brainstem reticular formation and moror neuron pools
lateral
- specific emotional behaviours
- inputs on motor neuron pools
motor neuron pools
- autonomic preganglionic neurons
- activation of smooth muscle and glands
or
- motor neurons cranial nerve nuclei and ventral horn
- muscle contraction and movement
What are pyramidal and extrapyramidal contributions to facial expressions?
- can tease out the difference between emotional activation of the muscles and the somatic/voluntary activation
e. g. in someone with a particular facial motor paresis
- volunatry smile - can only lift half of the lips into smile
- response to humour: no problem smiling on both halves of face
or emotional motor paresis
- voluntary smile is fine
- response to humour: only half the face
- each has a disruption in either voluntary pathway OR emotional pathway
What are elements of the so-called limbic lobe?
- edge of the cortex
- midline
- gets thinner - 5, 4 or even 3 layers
- cm or so above the corpus callosum right on the midline is called the cingulate gyrus
- emotional response to pain
- feeling of thirst
- screaming etc
- parahippocampal gyrus
What is modern conception of the limbic system?
- don’t just have fear for a single moment
- persistance of neural activity after the stimulus
- must be some sort of circuit
- Pates circuit (spelling?)
- all this activity whizzing round
- hippocampus, hypothalamus, projections up to other parts of the brain
- is this how emotion is sustained ?
- almost certainly wrong
- where is fear coordinated?
- amygdala (subcortical nucleus in the temporal lobe)
- it’s really the connections between the amygdala and the cingulate cortex (and other cortical areas) that really the context and coordination of emotion, and the expression of emotion is downstream of things like hypothalamus, autonomic brain stem
What is the amygdala?
- most important region of the brain regarding fear
- named because it looks like an almond?
- at least three main divisions:
- basal-lateral group
- medial group
- central group
- sits just below cerebral cortex in medial temporal lobe
core of expression and experience of fear
What are the interactions of the amygdala?
orbital and medial prefrontal cortex amygdala (basal lateral nuclei) –> ventral basal ganglia (and/or) –> mediodorsal nucleus of the thalamus orbital and medial prefrontal cortex
cortex is a really a circuit that connects to itself via basal ganglia and thalamus
e.g. activated when people asked to make judgements of trustworthiness
What are pathways in the rat brain that mediate association of auditory and aversive somatic sensory stimuli?
Auditory pathways –>
medial geniculate nucleus –>
auditory cortex and amygdala
auditory cortex –> amygdala
other projections (including somatic sensory pathways) –> amygdala
amygdala –> output to circuits that influence somatomotor and autonomic activity
auditory fear conditioning
receive electric shock to the foot
- avoidance etc
associate a tone with the shock
pavlovian conditioning
generates the full response
don’t need auditory cortex to get fear conditioning but you do need the auditory pathway (unless differentiation between tones is needed)
What is a model of associative learning in the amygdala relevant to emotional function?
Inputs: primary reinforccers
- touch, taste, pain
Inputs: neutral sensory stimuli
- visual, auditory stimuli related to an object
converge on the same neuron
Outputs:
- orbital and medial prefrontal cortex
- implicit motor actions
- explicit conscious processing to obtain rewards, avoid punishers and implement long-term plan
- hypothalamus and brainstem
- visceral motor effector systems to prepare body for action
What receptors are activated by glutamate?
NMDA receptor and AMPA receptor
- these two receptors each with distinct physiological properties often coexist at the same synapse
- weak stimulation of the presynaptic neuron causes release of glutamate from the synaptic terminal
- binds to both receptors
- both are permeable to sodium and potassium ions
- weak stimulation normally activates only AMPA receptors, resulting in a slight depolarisation of the post synatpic neuron (partial depolarisation -35mV)
- when glutamate binds to the NMDA receptor and slightly depolarised or membrane voltages, very few ions flow through the channel
- this low conductance occurs because the pore of the channel is blocked by Mg ions
- prevents other ions from passing freely through the channel
- under such conditions the EPSP will be mediated entirely by the AMPA receptors
- given a stimulus of sufficient strength and frequency, AMPA receptors can depolarise the membrane sufficiently to expel the magnesium from the NMDA channel
- NMDA now actively responds to glutamate
- admitting not only sodium ions but large amounts of calcium as well
- the calcium acts as an important second messenger, activating many important signalling cascades in the post synaptic neuron
e. g. CAM –> activates protein kinases such CaMKII - cam kinase phosphorylates AMPA receptors increasing their conductance to sodium ions
- also promotes movement of AMPA receptors from intracellular stores into the membrane
- more receptors available to stimulte the spine
- in addition to these post synaptic effects, calcium may also facilitate the release of transmitters for the axon terminal via retrograde signals such as nitric oxide
- as a result of the increase in the number of AMPA receptors, the response to a stimulus of a given strength will be stronger than it was before the NMDA receptors were activated
“synaptic enhancement”
- this physiological mechanism is throught to underlie long term potentiation
What is homosynaptic?
tetanic activity at a synapse will make it more effective
What is heterosynaptic?
- activation of a synapse at a process can associate two synapses
- when one synapse was activated it became strengthened
- but the one near by didn;t change
- not the case in the amygdala
- when a strong activation occurs in one neuron, changes synapse that carried tone information as well
- if tone information is occuring at the same time as the stimulus, will also be strengthened –> heterosynaptic –> associative LTP
neurons that fire together, wire together
What is Urbach-Wiethe disease?
- bilateral loss of amygdala
- brain damage controls behave just like undamaged controls
- patient with no amygdala: intelligent and perceptive, couldn’t recognise fear
- don’t know what it is like to be afraid
- experienced every other emotion, just not fear
Can we ‘treat’ fear?
one drug seems to be amazingly effective at reducing fear
- benzodiazepine drugs extremely effective
- good at dealing with symptoms of panic attacks etc
- binds to a site on the GABA receptor
- ethanol
- incredible complexity of mechanisms and yet sometimes single little things can change the whole behaviour of a system quite coherently
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