The Corticolimbic Circuit: Anatomy Flashcards
two main functions of the corticolimbic circuit?
reaction and recognition
input to amygdala
- thalamus
- sensory cortices (which receive information from the thalamus)
what kind of information does the thalamus provide to the amygdala?
low-resolution sensory information
what kind of information do the sensory cortices provide to the amygdala?
high-resolution sensory information
output of amygdala
hypothalamus
brainstem
substantia innominata
insula
hippocampal formation
PFC
general amygdala info
bilateral in structure and function
deep subcortical structure
13 different amygdala nuclei
parts of amygdala
(input) –> BLA –> ICMs –> CeA –> (output)
Thalamus in relation to amgydala
input from the world & sends information to the amygdala BLA
parts of thalamus
ventral posterior (touch/ taste)
medial geniculate nucleus (hear)
lateral geniculate and pulvinar (vision)
what about smell and the thalamus?
smell is separate, it doesn’t go through the thalamus but straight from olfactory bulb to BLA
visual information from the thalamus
magnocellular layers of the pulvinar get information from the rods (dorsal pathway) –> “where”
cones (ventral stream) are for the sensory cortex –> “what”
high vs. low road
low road: faster processing, but more crude, motive movement
high road: what/ where
* better that low road is faster bc its more adaptive (more cautious)
example of high vs. low road
if walking on trail and see something long in the distance, may initially think its a snake and act accordingly, but quickly realize its a stick (but if it was a snake, you would have been safe)
better to look like a fool nc its a stick than risk getting bit by a copperhead
white matter pathways & recognition speed
more white matter pathways between the pulvinar and amygdala increases the speed in recognizing something as a threat or not a threat
hypothalamus and amygdala
output (HPA stress response axis)
HPA access stress response
- central nucleus of amygdala
- PVN of hypothalamus
- anterior lobe of pituitary
- ACTH
- adrenal gland
- (which stimulates response of hormone cortisol to bloodstream)
—–> which goes back and influences PVN again
stress response implications
- more glucose production in the liver
- more blood flow
- greater vasoconstriction (less bleeding)
- immune suppression
chronic stress
bad bc immune suppression normal stress response, can be really damaging
how to minimize stress output?
interesting study over impact of oxytocin
- there are oxytocin receptors on the lateral division of the CeA that can inhibit stress output
brainstem and amygdala
(output) sympathetic arousal
targets the sympathetic nervous system and increases arousal to meet immediate challenges
parts of brainstem
- midbrain
- pons
- medulla
midbrain parts
periaqueductal gray – “freeze response”
dorsal raphe nucleus – “release of serotonin”
ventral tegmental area – “release of dopamine”
neuromodulators
(dorsal raphe nucleus, ventral tegmental area, locus coeruleus)
because modulate activity in amygdala by releasing hormones
pons parts
(NRPC) nucleus reticularis pontis caudalis – “increase startle response”
parabrachial nucleus – “increase breathing rate”
locus coeruleus – “increase serotonin”
startle response
increase sensitivity to input leads to an exaggerated response
medulla parts
dorsal motor nucleus of vagus nerve – “increases heart rate”
periaqueductal gray
avoidance – fight/ flight – immobility
If you freeze, you may not have to fight, if you’re not seen (momentary default)
substantia innominata and amygdala
(output) alertness
substantia innominata parts
BNST and NBM (influence CeA)
NBM (of the substantia innominata)
releases acetylcholine, because of projections of the CeA driving the NBM
BNST (of the substantia innominata)
same direct targets of central nucleus, creates background awareness
what is the impact of acetylcholine on response? (in the substantia innominata)
it reduces the threshold for firing and increases sensitivity to threat (more susceptible to input)
POTENTIATION
what are the two pathways from CeA as a result of the substantia innominata?
- NBM –> indirect pathway
insula, hippocampal formation, PFC, posterior fusiform gyrus - direct pathway
hypothalamus, brainstem, NBM
study on rodents and BLA in substantia innominata
injected neurons in BLA with a tracker to see the major target of CeA
found BNST is a redundancy of info tracking, so it can maintain levels of activation and arousal so amygdala can respond to threats as they arise
Insula and the amygdala
(output) interoception
awareness of bodily adjustments begin in insula
information to insula
BLA sends information with axons directly to insula, which projects to the anterior insula
- creates representation of somatosensory and interoceptive projections from the body
implications of insula
creates change in body temperature, blood pressure, etc. changes in sensory input (ex. butterflies in stomach)
“we’re afraid because we run from the bear”
hippocampal formation and the amygdala
(output) contextual memory
memory of where/ when a change has occurred (context of threat/ situation)
hippocampal formation’s two impacts
- excitatory projects from BLA allows amygdala to protentiate activity of the HF and indirectly increase acetylcholine by projects of CeA to NBM
- HF creates a break for HPA access negative feedback to end its own signaling (directly inhibits PVN)
prefrontal cortex and the amygdala
(output) attention & regulation-inhibition
PFC and information
BLA has direct projections to PFC medial right hemisphere
two functions of PFC and amygdala
- Converging information for conscious awareness
- reappraisal (stop threat response)
conscious awareness of PFC
subjective evaluation
amygdala –> vmPFC –> dmPFC –>dACC
convergence of information into the vmPFC creates conscious awareness of our experiences
projections from BLA increase sensitivity of vmPFC neurons to input
PFC lateral surface
dlPFC: planning
vlPFC: reappraisal
PFC reappraisal
reappraisal back through the amygdala (can inhibit) – you survived, can stop the threat response now
NBM –> vmPFC –> dmPFC –> BLA –> ICMs –> CeA
can inhibit through ICMs or BLA to CeA
Michael’s video
he was scared before he even came out so flooded with cortisol, freezes then falls (fear-potentiated startled response)
- everything else stops except his response to that threat
- lots of acetylcholine so ready to fire
- he was an effective regulator, jumps back up (reappraisal)
“let’s get back under control here”
The ____ functions as the primary input structure of the amygdala.
BLA
The ____ nucleus of the thalamus relays visual information to the amygdala.
pulvinar
CeA projections to the _____ facilitate fear-potentiated startle.
NRPC
The _____ PAG mediates freezing in response to threat.
Vl (ventrolateral)
aka, periaqueductal gray
Greater density of ______ receptors in the lateral division of the CeA contributes to prosocial and affiliative behaviors.
oxytocin
Through the integration of inputs from multiple structures, the vmPFC facilitates the ______ of our experiences.
subjective evaluation
