Posted by DSCH on August 19, 2003, at 14:42:29
In reply to Dsch, Re: Hmmmmmmmmm, posted by McPac on August 19, 2003, at 12:31:20
OK, definition time...
Two neurons are seperated by a synaptic gap. Neurotransmitters transfer information across the gap. There is some storage within the neuron from which these molecules get released and receptors they plug into on the far side to transfer the message.
Some of the molecules released from storage to relay a message are sucked back into the same storage space before they can cross the gap. This is called 'reuptake'. A REUPTAKE INHIBITOR is supposed to reduce the chances of this ocurring, thus causing an increase in signal conveyed across the gap.
A RELEASE AGENT stimulates the neuron to release more molecules of a given type from storage each time a message needs to be conveyed and thus increases the signal that way. Note if the storage is running low, this isn't going to accomplish much, so your results from this sort of drug are limited by your processing of amino acids to synthesize the neurotransmitters in the first place.
These two types focused on the upstream side of the synaptic gap. Downstream, where the receptors are, you can do two other things. You can introduce molecules that will temporary bind into given types of receptor(s) and stimulate it (thus acting as a stand-in for the associated neutrotransmitter molecule) and these are called AGONISTS and increase signal. Or you can use a molecule that will also temporarily bind into given types of receptor(s), but not stimulate it and also shield the receptor from being stimulated by the upstream neuron's own molecules while it is bound in. You can decrease signal with these and they are called ANTAGONISTS.
Agonist and Antagonists effects vary depending upon what sort of activity occurs if a particular class or classes of receptors is stimulated/blocked-off.
In the case of Remeron (according to SLS's chart), it is an antagonist of the following receptor types: NE-alpha2, 5-HT2a, 5-HT2c, 5-HT3, and H1. The only one I am familar with is H1, which is for histamine. You'd be less likely to have an asthma or allergy attack on Remeron but also tend to be sedated as histaminergic neurons in the hypothalamus help to regulate the sleep/wake cycle and stimulate the pre-frontal cortex to full attention. I'm not sure what those others do though. I'm afraid I'm out of my current knowledge range at that point. :-p
Hope that helps.
poster:DSCH
thread:250201
URL: http://www.dr-bob.org/babble/20030818/msgs/252200.html