Distribution and Physiological Function of the Serotonergic Neuron

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In the CNS, serotonergic neurons are limited to a group of brain-stem reticular formation nuclei, the raphe nuclei. Dahlstrom and Fuxe (1964) originally described nine sero-tonergic cell groups, which they named B1 through B9. Most of these groups are associated with the raphe nuclei and the reticular region of the lower brain stem from which they project rostro-caudally, and thus to virtually all areas of the CNS receive serotonergic inputs. The serotonergic neurons in the midbrain and pontine dorsal and median raphe project to higher brain centers: cerebral cortex, cerebellum, hippocampus, thalamus, hypothalamus, and basal ganglia. In contrast, serotonergic cell bodies in the ventral medulla, caudal pons, and pontomesencephalic reticular formation provide long descending projections to the spinal cord. The origins of the serotonergic projections to the dorsal horn are the neurons of the raphe magnus and adjacent reticular formation and are involved mainly in pain sensation. The serotonergic neurons that terminate in the ventral horn arise primarily from the raphe obscurus and raphe pallidus nuclei and facilitate motor activity. The pre-ganglionic sympathetic neurons of the intermediolateral column in the thoracic cord also receive serotonergic input, mostly from the ventrolateral medulla, and are involved in blood pressure regulation and perhaps other autonomic functions. The pathways from the midbrain raphe to the prefrontal cortex may mediate depressive and cognitive effects of serotonin. The pathway from the midbrain raphe to basal ganglia likely underlies the role of serotonin in the pathophysiology of obsessive-compulsive disorder (OCD). This pathway also is thought to be related to the regulatory action of serotonin on locomotion. The regulatory functions of serotonin on emotions, anxiety, and memory are thought to be related by the pathway from the raphe to the limbic cortex. The pathway from midbrain raphe to hypothalamus might mediate the effects of serotonin on appetitive behaviors. Sexual function mediated by serotonin might be related to the descending pathways from the raphe to the spinal cord. Moreover, the serotonergic system has been implicated in the regulation of circadian rhythms through its actions on the suprachiasmatic nucleus (SCN). Recent data suggest that along with excitatory amino acids, serotonin may be important in the neutral pathway that mediates the transmission of photic information to the circadian system. Recently, it has been demonstrated that the serotonergic system also has a link to neuroadaptive changes that occur in substance dependence. For example, extracellular serotonin levels decreased dramatically during cocaine withdrawal.

The action of serotonergic neurons, as a whole, is complex, and it is difficult to understand how specific changes in serotonin neurotransmission affect specific behaviors or neurological functions. This issue becomes even more challenging by the molecular cloning of more than 14 serotonin receptor subtypes, each with its own expression pattern, coupling mechanism, and pharmacological profile. Moreover, serotonergic nerve terminals may contain other neuro-transmitters, such as acetylcholine (ACh), noradrenaline (NE), substance-P(SP), enkephalins, thyrotropin-releasing hormone (TRH), calcitonin gene-related peptide (CGRP), and postraglandins. The physiological response to seroton-ergic innervation reflects the nature of the postsynaptic receptors. The 5-HT1B, and 5-HT1D receptors are autorecep-tors, and they regulate further release of 5-HT through inhibition of adenyl cyclase. These receptors are both so-matodendritic and terminal autoreceptors. The somato-dendritic autoreceptors suppress cell firing and are believed to play a role in collateral inhibition among seroton-ergic neurons. These autoreceptors also lead to reduction in serotonin synthesis and release in the areas to which the cells project by inhibiting neuronal activity. In contrast, terminal autoreceptors are not believed to influence cell firing but instead inhibit serotonin release, and possibly also synthesis from the nerve terminals. Most serotonergic synapses are inhibitory, though some are excitatory.

The involvement of the serotonergic system in motor function in vertebrates was indicated initially by its dense axon terminal innervation of motoneurons in both the brain stem and spinal cord. Secondary motor structures, such as the basal ganglia, substantia nigra, and habenula, also receive significant serotonergic input as noted. Administration of serotonergic agonists produces a motor syndrome in rats: head shakes, hyperreactivity, tremor, hindlimb abduction, lateral head weaving, and reciprocal forepaw treading. Extracellular recordings in conjunction with mi-croiontophoresis of serotonin onto motoneurons in the rat facial motor nucleus or in the spinal cord ventral horn showed that when serotonin interacts with excitatory influences on motoneurons, it produces a strong facilitation of neuronal activity (via 5-HT2 receptors). Administration of serotonergic agonists directly into the trigeminal nerve in cats produced an increase in the amplitude of the elec-tromyography (EMG) of both the masseter muscle and an externally elicited jaw-closure reflex.

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