Role of the Basal Forebrain Neurons in Cortical Activation and Behavioural State Regulation

Re: Symposium 388

Robert W. McCarley, M.D.
mccarley@mediaone.net

On Fri Dec 4, grover wrote
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>Dr,. McCarley: Hope you are enjoying the meeting.  Great poster. I am a bit confused.   "This site-specific accumulation of AD during prolonged wakefulness suggests that the sleep-promoting effects of AD may be mediated by an AD inhibition of the BF cholinergic arousal system."   You also indicate that AD agonist infusion in the region promotes wakefulness.  To me this suggests that AD-receptor activation promotes wakefulness rather than the other way around.  Can you clarify how you arrive at this conclusion?
>
HI,
thanks for your interest.
We say:
"Local perfusion of an A1 receptor agonist inhibits the discharge of wake-active BF neurons."....so the agonist inhibits wake-promoting neurons, and is thus compatable with DECREASING WAKE. (this is in single unit experiment)

iN MORE GLOBAL MICRODIALYSIS PERFUSION EXPERIMENTS, WE SAY,
"Furthermore, in preliminary experiments, BF perfusion of A1 antagonist(CPT) increased W (Figure 5; paired t (4)=6.2, p<.005) and decreased sleep, effects opposite of BF perfusion with AD agonists (NBTI or AD itself), and suggesting that the A1 receptor may mediate the NBTI & AD (300uM) effects already seen."

SO, basically there are two experiments, one inhibiting W promoting neurons (agonist) and one infusing antagonist to decrease behavioral wakefulness.
Hope this clarifies things.
Best,
Bob McCarley

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