Neurons in the brain that communicate using serotonin
Serotonergic pathways
A serotonin pathway identifies aggregate projections from neurons which synthesize and communicate the monoamine neurotransmitter serotonin.[citation needed] These pathways are relevant to different psychiatric and neurological disorders.[1][2][3]
The anterior dorsal raphe primarily projects to the cortex, neostriatum, amygdala and SN, while the caudal division of the dorsal raphe projects to the latter three. The highest density of cortical innervation is in layer 1.
Projections into the hippocampus are the most dense in the subiculum, followed by Ammon's horn and the Dentate gyrus. Projections into the VTA modulate firing rate, increasing the rate with lower activity, and depressing it with higher activity.
Given the wide area that the many serotonergic neurons innervate, these pathways are implicated in many functions, as listed above. The caudal serotonergic nuclei heavily innervate the spinal cord, medulla and cerebellum. In general, manipulation of the caudal nuclei(e.g. pharmacological, lesion, receptor knockout) that results in decreased activity decreases movement, while manipulations to increase activity cause an increase in motor activity. Serotonin is also implicated in sensory processing, as sensory stimulation causes an increase in extracellular serotonin in the neocortex. Serotonin pathways are thought to modulate eating, both the amount as well as the motor processes associated with eating. The serotonergic projections into the hypothalamus are thought to be particularly relevant, and an increase in serotonergic signaling is thought to generally decrease food consumption (evidenced by fenfluramine, however, receptor subtypes might make this more nuanced). Serotonin pathways projecting into the limbic forebrain are also involved in emotional processing, with decreased serotonergic activity resulting in decreased cognition and an emotional bias towards negative stimuli.[5] The function of serotonin in mood is more nuanced, with some evidence pointing towards increased levels leading to depression, fatigue and sickness behavior; and other evidence arguing the opposite.[6]
^Helton, Sarah G.; Lohoff, Falk W. (1 January 2015). "Serotonin pathway polymorphisms and the treatment of major depressive disorder and anxiety disorders". Pharmacogenomics. 16 (5): 541–553. doi:10.2217/pgs.15.15. ISSN1744-8042. PMID25916524.
^Jacobs, edited by Christian P. Müller, Barry (2009). Handbook of the behavioral neurobiology of serotonin (1st ed.). London: Academic. pp. 309–367. ISBN9780123746344. {{cite book}}: |first1= has generic name (help)CS1 maint: multiple names: authors list (link)
^Andrews, Paul W.; Bharwani, Aadil; Lee, Kyuwon R.; Fox, Molly; Thomson Jr., J. Anderson (1 April 2015). "Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response". Neuroscience & Biobehavioral Reviews. 51: 164–188. doi:10.1016/j.neubiorev.2015.01.018. PMID25625874. S2CID23980182.
