Limbic system serotonin action

The biology of the monoamines is described in detail elsewhere. In simple terms, they facilitate transmission in neural pathways that originate in nuclei of the brainstem and have descending projections to the autonomic nervous system and widespread ascending projections to sites in the limbic system and cortex. These pathways modulate many aspects of behavioural function as well as anxiety responses. Of the three monoamines, the role of serotonin in anxiety is best understood, but the picture is complex as increased serotonergic activity may be anxiogenic or anxiolytic depending on the site of action (Bell and Nutt 1998). 

It is believed that although antipsychotic medications block norepinephrine, serotonin, and acetylcholine, their primary action is as central dopamine antagonists (Galenberg, 1991 Meyer Quenzer, 2005). That is, these drugs block central dopamine receptors, particularly the Dj subtype, and thus inhibit dopaminergic neurotransmission in the brain. The postsynaptic receptor blockade in the limbic system is thought to reduce the schizophrenic symptoms. 

Serotonin (5-hydroxytryptamine, 5-HT) occurs in the intestinal wall, where it regulates motility and secretion in blood platelets, where it modulates platelet aggregation and vascular blood flow and in the CNS, where it acts as a neurotransmitter in areas of the midbrain. At least seven different receptors for serotonin have been characterized, which mediate a wide variety of different physiological effects. Depression and anxiety are thought to be the result of actions on 5-HTia receptors in the brain limbic system. Following release from neurons by a depolarizing action potential at central synapses, the activity of 5-HT is terminated by neuronal reuptake. This is performed by a synaptic membrane amine transporter protein, specific for 5-HT, which also co-transports sodium and chloride ions to repolarize the neuronal membrane. 

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