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Dr. Bob is Robert Hsiung, MD,
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Posted by Jimmyboy on September 21, 2007, at 15:12:05
Ok, I feel kind of dumb here, but I have been reading some things about how one theory of bipolar depression is an abnormality in the binding or function of muscarinic receptors, which are involved with acetylcholine. Can someone explain this to me if they have any knowledge about this?
Thanks
JB
Posted by Phillipa on September 21, 2007, at 21:45:17
In reply to Muscarinic receptors and bipolar, posted by Jimmyboy on September 21, 2007, at 15:12:05
Jimmyboy you're feeling dumb? I'm dumber than you as I don't understand the full question you asked. Phillipa
Posted by linkadge on September 21, 2007, at 22:20:46
In reply to Re: Muscarinic receptors and bipolar » Jimmyboy, posted by Phillipa on September 21, 2007, at 21:45:17
Hard to say exactly. I don't know enough. I know they are involved in certain forms of emotional processing.
Excessive cholinergic function at certain receptors can cause depression, irritability, racing mind, anxiety, hyperactive REM sleep, excessivly reflective states of mind, inability to live in the moment, inability to let go of certain thoughts/feelings, chronic fatigue, seizures, list goes on.
Some of the above are anecdotal however.
Why does cholinergic function become excessive? Who knows. Excessive brain content of acetylcholine, low acetycholinsterase, receptor supersensitivity, low content of certain monoamines, stress.
Linkadge
Posted by Phillipa on September 21, 2007, at 22:32:58
In reply to Re: Muscarinic receptors and bipolar, posted by linkadge on September 21, 2007, at 22:20:46
The Monster stress sounds like me Phillipa
Posted by rina on September 22, 2007, at 1:47:17
In reply to Muscarinic receptors and bipolar, posted by Jimmyboy on September 21, 2007, at 15:12:05
In the bulbectomised rat model of depression, a decrease in cortical muscarinic receptors occurs that returns to control values following treatment with antidepressants (Earley et al, 1994).
The anticholinergic activity of the tricyclic antidepressants is usually associated with their unacceptable peripheral side-effects and most second-generation antidepressants lack such side-effects.
Possible support for a cholinergic hypothesis of depression is that the cholinesterase inhibitor pyridostigmine, when administered to drug-free patients with depression, causes an enhanced activation of the anterior pituitary glands, as shown by the release of growth hormone (O'Keane et al, 1992).
This suggests that the muscarinic receptors are supersensitive in patients with depression. Janowsky et al (1986) postulated that depression arises as the result of an imbalance between the central noradrenergic and cholinergic systems; in depression, the activity of the former system is decreased and, conversely, in mania it is increased.
As most antidepressants enhance noradrenergic function, it is hypothesised that the reduction in cholinergic activity is a consequence of the increase in noradrenergic activity.
This is the end of the thread.
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