Cortical modulation of sympathetic nervous outflow Flashcards
What happens to your heart rate and blood pressure when you are angry or scared?
angry- increases bp and hr - so being angry is bad for you
fear- bp is increased from normal but is much less than when you are angry
emotions can alter your bp and hr
Why is transynaptic viral labelling better than imaging to determine the areas involved in changes in cardiovascular control during different emotions ?
because although imaging can show you the areas that are active during different emotions, you cant directly show that the area is linked to cardiovascular control
Why is transynaptic viral tracing so useful?
it is crucial for mapping and determining pathways
PRV is a commonly used retrograde tracer- taken up into terminals and then its transported up to cell body where it replicates and goes along axon to enter the next neurone in the pathway
it can help determine which sympathetic effectors are influenced by which cortical regions
What does the adrenal gland, stellate ganglion and coeliac ganglion regulate?
adrenal gland- regulates adrenal medulla
stellate ganglion- regulates the heart
coeliac ganglion- regulates the gastrointestinal tract
When they injected PRV into the adrenal gland what labelling was seen in cortical regions?
the infra limbic cells had been labelled and cells in the dorsal part of the agranular insular cortex
ILC- mainly labelling was in layer 5
Ald- labelling was mainly in layers 2 and 5
When they injected PRV into the stellate ganglion what labelling was seen in cortical regions ?
there was labelling in the ILC and also in the Ald but less in the Ald than for the adrenal gland
When they injected PRV into the coeliac ganglion what labelling was seen in cortical regions ?
much fewer cells were labelled in the ILC and Ald, therefore the ILC and Ald are clearly more involved in cardiac functions compared to gut functions
What experiment was carried out to determine if the medial PFC was influencing the sympathetic nervous system ?
injected KCl into the medial PFC and this caused depolarisation and caused a large decrease in blood pressure, therefore the mPFC is involved in cardiovascular control
they also injected an anterogade tracer into the mPFC to work out where the cells project to
What anterograde tracer was used and what was shown to determine link between mPFC and sympathetic outputs?
PHA-L was injected into the mPFC (mainly Cg3 area however it could have been taken up by dendrites of adjacent neurones) and it was taken up by cell bodies and transported down axon of cells to determine those labelled in the pathway
Where was the anterograde tracer injected into the mPFC found ?
there were PHA-L labelled axons in the central autonomic area of the spinal cord - axons were labelled in laminae 1, above central canal region
surprisingly they didn’t find many labelled neurones in the lateral horn which is where preganglionic axons predominantly live
boutons were labelled- they are enlarged parts of the axon containing synaptic vesicles and machinery to release transmitters
What did they see about the tracer when they used electron microscopy?
showed that the labelled structures are synaptic terminals - they make asymmetric synapses which are associated with excitatory synapses
they synapsed with specialised structures which researches suggested could be interneurones
What did the injection of a retrograde tracer into the spinal cord confirm ?
it confirmed there is a direct projection to the spinal cord from the medial PFC
injected retrograde tracer into spinal cord and it was taken up by terminals - then they allowed it to travel back up axon to cell body to then label other neurones in the pathway and this demonstrated labelling in the pre limbic cortex area
What did they do to determine if there were any other projections from the mPFC?
injected the retrograde tracer, WGA-HRP, into medullary nuclei which are known to influence the sympathetic nervous system - NTS, rVLM, cVLM
once they had injected into these areas they left the tracer to infect the previous neurones in the pathway which demonstrated labelling in the mPFC therefore mPFC must project to these medullary nuclei
Bacon & Smith didn’t see any terminals in the RVLM when they injected PHA-L into the PFC but Gabbott and others reported projections to the RVLM from the mPFC. Why could these differences arise?
injected into slightly different areas in the prefrontal cortex
if they massively excited cells with glutamate/KCl(particularly glutamate) then excitotoxicity could have occurred and killed the cells
If outputs from the mPFC to the spinal cord are excitatory how can these cause a decrease in bp ?
it could be that they excite inhibitory neurones which then act on sympathetic preganglionic neurones to reduce their activity so blood pressure is reduced
