Posted by SLS on April 20, 2006, at 6:53:04
In reply to Re: Drugs versus Psychotherapy - Backlash? » linkadge, posted by zeugma on April 20, 2006, at 6:11:52
"The decreased binding of [3H]nisoxetine to NETs in the LC in major depression may reflect a compensatory downregulation of this transporter protein in response to an insufficient availability of its substrate (norepinephrine) at the synapse."
That's very interesting. I would love to know if there is any biological precedence for their conclusion that the transporter would downregulate in the absence of neurotranmitter. Has this phenomenon been documented elsewhere? I can't imagine that no one has measured the amounts of NE to be found in the LC of suicide victims.
Can you think of a dynamic in circuitry that would explain this?
I gotta think about this one.
I see that the authors have published other papers studying NE and 5-HT function in major depression and Alzheimers. They all seem to corroborate each other and indicate that dimished neurotransmission is accompanied by reductions in transporter and increases in autoreceptors and the enzymes that produce neurtransmitter.
Ah. I get it. I suppose there must be a certain amount of neurotransmitter in the synaptic cleft to maintain a partial depolorization (prevent a static hyperpolarization) of the postsynaptic membrane.
- Scott
poster:SLS
thread:629584
URL: http://www.dr-bob.org/babble/20060417/msgs/635149.html