Neurotransmission serotonergic neurons

Moore, R.Y. The anatomy of central serotonergic neuron systems in the rat brain. In Jacobs, B.L., and Gelperin, A., eds. Serotonin Neurotransmission and Behavior. Cambridge, MA MIT Press, 1981. pp. 35-71. 

When compared with the selective serotonin reuptake inhibitors (SSRIs), mirtazapine may show an earlier onset of action (although data are currently not well established). Mirtazapine has also been found to be efficacious in the treatment of elderly patients with depression. Mirtazapine has been shown to be effective in the treatment of panic disorder, social phobia, and post-traumatic stress disorder. In one study, mirtazapine combined with citalopram in obsessive-compulsive patients induced an earlier response when compared with citalopram plus placebo. It was suggested that antagonism of presynaptic a2-adrenergic receptors does not enhance serotonin neurotransmission directly, but rather disinhibits the norepinephrine activation of serotonergic neurons and thereby increases serotonergic neurotransmission by a mechanism that may not require a time-dependent desensitization of receptors. 

Local application of 8-OH-DPAT in the raph4 nuclei reduces the firing rate of serotonergic neurons by acting on the somatodendritic autoreceptor. This in turn leads to a reduction of the serotonergic neurotransmission, i.e. less serotonin is released in the synaptic cleft. It is not known which of the postsynaptic receptors is critically involved in the mediation of LLR. As far as we know, no local application studies have been performed in the major projection areas of the serotonin system. 

Unlike aniracetam, pramiracetam does not appear to interact with dopaminergic, serotonergic, or adrenergic neurotransmission (72). The agent inhibits prolylendopeptidase in certain brain areas, but its inhibition constant, iC, is only 11 ]lM (69). The absence or weak activity of this compound with various neuronal systems appears to make it less likely to be of significant therapeutic value than other members of this class of agents. 

The acute effects of ethanol and other sedative-hypnotics are mediated by actions at a number of receptor systems. For example, ethanol inhibits several excitatory receptor systems, including N-methyl-D-aspartate (NMDA) receptors, kainate receptors, and Ca channels. In addition, ethanol enhances the action of GABA at GABA receptors and appears to modulate serotonergic neurotransmission. Although a component of ethanol reinforcement is mediated by the activation of mesocorticolimbic dopamine neurons, activation of these neurons may not be necessary for ethanol reinforcement, as ethanol remains reinforcing in the absence of these neurons (Samson and Harris, 1992 Koob, 2000b). 

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