As already mentioned a number of 5-HT autoreceptors regulate 5-HT release by post- or presynaptic mechanisms. However there are a number of other neurotransmitters involved in the regulation of 5-HT. The serotonergic system densely innervated large portions of the brains and is co-localized with many other neurotransmitter systems. It has been shown that there are both alpha-1 and alpha-2 adrenergic heteroreceptors acting on serotonergic neurons. The alpha-1 heteroreceptors are located on the cell bodies of serotonergic nuclei, and it has been shown that noradrenaline activates these alpha-1 adrenoreceptors resulting in an inhibition of the firing of 5-HT neurons. This has been shown in many brain regions (Hjorth et al, 1995). The alpha-2 heteroreceptor is restricted to terminal areas where they directly regulate serotonin release (Tao & Hjorth, 1992; de Boer et al, 1996). Inhibitory alpha-2 adrenoceptors on the NE neuroterminals form part of a feedback control mechanism. Mirtazapine, an antagonist at alpha-2 adrenoceptors, does not enhance 5-HT neurotransmission directly but disinhibits the NE activation of 5-HT neurons and thereby increases 5-HT neurotransmission by a mechanism that does not require a time-dependent desensitization of receptors.
GABA receptors are also known to regulate the release of serotonin.
GABAA receptors are present in the MRN and DRN nuclei and decrease the firing activity of the serotonergic neurons located there. GABAB receptors are located on the DRN and also in terminal areas such as the nucleus accumbens. Activation of these GABAB receptors results in the decrease in 5-HT release in terminal areas and decreases the overall 5-HT neuronal firing in the DRN (Tao & Auerbach, 2000).
Dopaminergic D2 receptors have been found to be involved in serotonin release. This was illustrated using a selective D2 agonist (LY 171,555) and
observing the increased concentration of serotonin. Upon administration of D2
antagonists (raclopride) the increase in serotonin levels was annulled (Ferre et al, 1993; 1994).
It has been reported that presynaptic glutamatergic receptors (AMPA/
kainate) are located on serotonergic neurons (Ghersi et al, 2003; Pittaluga et al, 1997), and can mediate the firing and release of the serotonergic neuron.
Similarly, histamine receptors have been located on serotonergic neurons and have been shown to be involved in the regulation of firing and release of 5-HT (Schwartz et al, 1991; Barbara et al, 2002).
As investigations into the interactions of the various neurotransmitter systems continue, there will no doubt be further evidence for alternate neurotransmitter receptors being localized on serotonergic neurons, which can directly mediate the firing of the 5-HT neuron, or neurotransmitter release from the serotonergic terminals. The involvement of many of these receptors in the modulation of serotonin and their role in depression as well as its treatment are further discussed in chapter 3.
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