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Serotonergic Modulation of Retinal Input to the Mouse Suprachiasmatic Nucleus Mediated by 5-HT1B and 5-HT7 Receptors
Bret N. Smith
Department of Anatomy and Neurobiology, Program in Molecular, Cellular, and Integrative Neurosciences, Colorado State University, Fort Collins, CO 80523-1760, USA; Department of Cell and Molecular Biology, 2000 Stern Science Center, Tulane University, New Orleans, LA 70118, USA.
Patricia J. Sollars
F. Edward Dudek
Gary E. Pickard
Department of Anatomy and Neurobiology, Program in Molecular, Cellular, and Integrative Neurosciences, Colorado State University, Fort Collins, CO 80523-1760, USA
Serotonin (5-HT) and 5-HT receptor agonists can modify the response of the mammalian suprachiasmatic nucleus (SCN) to light. It remains uncertain which 5-HT receptor subtypes mediate these effects. The effects of 5-HT receptor activation on optic nerve–mediated input to SCN neurons were examined using whole-cell patch-clamp recordings in horizontal slices of ventral hypothalamus from the male mouse. The hypothesis that 5-HT reduces the effect of retinohypothalamic tract (RHT) input to the SCN by acting at 5-HT1B receptors was tested first. As previously described in the hamster, a mixed 5-HT1A/1B receptor agonist, 1-[3-(trifluoromethyl)phenyl]-piperazine hydrochloride (TFMPP), reduced the amplitude of glutamatergic excitatory postsynaptic currents (EPSCs) evoked by selectively stimulating the optic nerve of wild-type mice. The agonist was negligibly effective in a 5-HT1B receptor knockout mouse, suggesting minimal contribution of 5-HT1A receptors to the TFMPP-induced reduction in the amplitude of the optic nerve–evoked EPSC. We next tested the hypothesis that 5-HT also reduces RHT input to the SCN via activation of 5-HT7 receptors. The mixed 5-HT1A/7 receptor agonist, R(+)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide (8-OH-DPAT), reduced the evoked EPSC amplitude in both wild-type and 5-HT1B receptor knockout mice. This effect of 8-OH-DPAT was minimally attenuated by the selective 5-HT1A receptor antagonist WAY 100635 but was reversibly and significantly reduced in the presence of ritanserin, a mixed 5-HT2/7 receptor antagonist. Taken together with the authors' previous ultrastructural studies of 5-HT1B receptors in the mouse SCN, these results indicate that in the mouse, 5-HT reduces RHT input to the SCN by acting at 5-HT1Breceptors located on RHT terminals. Moreover, activation of 5-HT7 receptors in the mouse SCN, but not 5-HT1A receptors, also results in a reduction in the amplitude of the optic nerve–evoked EPSC. The findings indicate that 5-HT may modulate RHT glutamatergic input to the SCN through 2 or more 5-HT receptors. The likely mechanism of altered RHT glutamatergic input to SCN neurons is an alteration of photic effects on the SCN circadian oscillator.
Key Words: serotonin • 5-HT receptors • 5-HT7 receptors • suprachiasmatic nucleus • retinohypothalamic tract • circadian rhythms • 8-OH-DPAT • 5-HT1B receptor knockout
Journal of Biological Rhythms, Vol. 16, No. 1,
25-38 (2001)
DOI: 10.1177/074873040101600104
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