Peripheral neurons, CRH, and sickness behavior

jnmaciuch said:
I suppose a mouse could be jumpy and non-mobile but that seems a bit weird.
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I saw plenty of jumpy mice being non-mobile when I used to do animal experiments. Freezing still is a usual response to fear. But admittedly that isn't 'lethargy'. And maybe the local adrenergic signals are nothing to do with a systemic adrenergic response. I do think it is becoming complicated though! Not that that is a bad thing. I suspect we need to discover in what way we have been oversimplifying things, in order to see the wood for the trees.
 
Jonathan Edwards said:
But admittedly that isn't 'lethargy'.
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The people I’ve talked to that do mouse models of Covid say it’s pretty distinctive. They call it “loafing” or “ragdolling.” Apparently theyre the easiest mice to handle by far.

Jonathan Edwards said:
And maybe the local adrenergic signals are nothing to do with a systemic adrenergic response. I do think it is becoming complicated though! Not that that is a bad thing. I suspect we need to discover in what way we have been oversimplifying things, in order to see the wood for the trees.
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I might be misremembering something read a long time ago, but I’m pretty sure that ACTH is increased in prolonged sepsis. Plus cortisol spikes alongside the first burst of cytokines as a negative feedback mechanism during regular infection. So it doesn’t seem surprising that CRH activation happens in infection, just that the connection to sickness behavior is surprising.

Maybe the sickness behavior mechanism just cancels out the expected jumpiness of HPA-axis activation. It makes perfect sense from an evolutionary standpoint—keep the immunoregulatory mechanism, but make sure that the animal still collapses in a corner away from other animals.
 
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