title: Melatonin receptor activation increases glutamatergic synaptic transmission in the rat medial lateral habenula.
abstract: Melatonin (MLT) is secreted from the pineal gland and mediates its physiological effects through activation of two G protein-coupled receptors, MT1 and MT2 . These receptors are expressed in several brain areas, including the habenular complex, a pair of nuclei that relay information from forebrain to midbrain and modulate a plethora of behaviors, including sleep, mood, and pain. However, so far, the precise mechanisms by which MLT control the function of habenula neurons remain unknown. Using whole cell recordings from male rat brain slices, we examined the effects of MLT on the excitability of medial lateral habenula (MLHb) neurons. We found that MLT had no significant effects on the intrinsic excitability of MLHb neurons, but profoundly increased the amplitude of glutamate-mediated evoked excitatory post-synaptic currents (EPSC). The increase in strength of glutamate synapses onto MLHb neurons was mediated by an increase in glutamate release. The MLT-induced increase in glutamatergic synaptic transmission was blocked by the competitive MT1 /MT2 receptor antagonist luzindole (LUZ). These results unravel a potential cellular mechanism by which MLT receptor activation enhances the excitability of MLHb neurons. The MLT-mediated control of glutamatergic inputs to the MLHb may play a key role in the modulation of various behaviors controlled by the habenular complex.
authors.affiliation: Department of Pharmacology and Toxicology, University at Buffalo, State University of New York, Buffalo, New York.|Research Institute on Addictions, University at Buffalo, State University of New York, Buffalo, New York.
authors.forename: Katherine M
authors.initials: KM
authors.lastname: Evely
authors.affiliation: Department of Physiology and Biophysics, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, New York.
authors.forename: Randall L
authors.initials: RL
authors.lastname: Hudson
authors.affiliation: Department of Pharmacology and Toxicology, University at Buffalo, State University of New York, Buffalo, New York.
authors.forename: Margarita L
authors.initials: ML
authors.lastname: Dubocovich
authors.affiliation: Department of Pharmacology and Toxicology, University at Buffalo, State University of New York, Buffalo, New York.|Research Institute on Addictions, University at Buffalo, State University of New York, Buffalo, New York.
authors.forename: Samir
authors.initials: S
authors.lastname: Haj-Dahmane
mesh_terms: D000818:Animals; D019706:Excitatory Postsynaptic Potentials; D018698:Glutamic Acid / Q000378:metabolism*; D019262:Habenula / Q000378:metabolism* / Q000502:physiology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D044094:Receptors, Melatonin / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism* / Q000502:physiology; D014363:Tryptamines / Q000494:pharmacology
chemical_list: D044094:Receptors, Melatonin; D014363:Tryptamines; C057154:luzindole; D018698:Glutamic Acid
keywords: EPSC; glutamate synapse; habenula; melatonin; melatonin receptor