They observed distinct coding of hunger and thirst within SFO/MnPO and AgRP neurons is an exciting observation. SFO-activation induced drinking in the quenched state, in conjunction with insular responses, powerfully demonstrates the interoceptive function of this neural circuit
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Analysis & exclusion of arousal-related and time-related factors differentiated the findings from 1) insula's role in mapping autonomic arousal (see our most recent fMRI paper https://www.ncbi.nlm.nih.gov/pubmed/28726799 ) & 2) time perception, which has also been linked to insula (
@marcwittmann)Prikaži ovu nit -
The inability to predictably model all recorded insular cortex neurons (Fig 2B/C) is not that surprising to me. It may reflect the fact that insular cortex is more polymodal than V1, as it will likely be mapping signals from cardiac, respiratory, GI, GU, chemosensory sources etc.
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Given cross-species differences in insular cortex cytoarchitecture, I wonder if the ability to model insular neurons heavily depends on where you measure from. Mouse analogs to posterior vs. anterior insula? Simultaneous recordings?
@sarah_stern@anna_beyeler@henry_c_evrardPrikaži ovu nit -
Some speculation: the additional SFO input during quenched/sated states may represent a non-gustatory influence on control of eating behavior, i.e. a potential mechanism by which allostatic regulation could occur. The exaggerated responses across both conditions is hard to ignore
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The findings could have implications for both the acquisition and extinction of associative learning in psychiatric disorders. What if disordered eating could be partially explained by SFO- and AgRP-induced hyperpolarization of insular neurons during quenched/sated states?
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