Neuronal Gap Junction Coupling May Mediate a Fast Copulatory Neuromuscular Circuit


Meeting Abstract

P2.152  Monday, Jan. 5  Neuronal Gap Junction Coupling May Mediate a Fast Copulatory Neuromuscular Circuit SERRANO-VELEZ, J. L.; TORRES-VAZQUEZ, I.; RIVERA-RIVERA, N. L. ; FRASER, S. E.; YASAMURA, T.; DAVIDSON, K. G. V.; RASH, J. E.; LAUDER, G. V.; ROSA-MOLINAR, E.*; Univ. of Puerto Rico-Rio Piedras; Univ. of Puerto Rico-Rio Piedras; Univ. of Puerto Rico-Rio Piedras; California Institute of Technology; Colorado State Univ.; Colorado State Univ.; Colorado State Univ.; Harvard Univ.; Univ. of Puerto Rico-Rio Piedras ed@hpcf.upr.edu

During development, gap junctions are thought to disappear as chemical synapses form, with one study concluding that switching from electrical to chemical synapses requires activation of a major class of ionotropic glutamate receptors expressed throughout the vertebrate central nervous system (CNS), N-methyl D-aspartate receptor 1 [NMDAR1]. Using neural tract tracing, confocal microscopy, and freeze-fracture replica immunogold labeling in the spinal cord of an adult sexually dimorphic teleost fish Gambusia, we show large numbers of gap junctions within dendrodentritic mixed synapses between apical dendrites of coupled motor neurons and interneurons. Dendrodendritic mixed synapses are a hallmark of motor systems evolved for high-speed oscillatory neural synchronization, such as the fast neuromuscular circuit controlling the torque-thrust movement (20 ms) we identified in male Gambusia copulation. Gap junctions within mixed synapses between coupled motoneurons and interneurons were heavily labeled by antibodies to connexin 35 (Cx35), the teleost homolog of connexin 36 (Cx36) found in mammals. Postsynaptic densities [PSDs] within the mixed synapses were glutamatergic. Work reported here demonstrates that functional electrical and chemical synapses persist in mixed synapses in the adult CNS, shows that collaboration between NMDA receptor activation and gap junction coupling is possible, and suggests persistent electrical communication may have a central role in fast neuronal circuits. Supported by NIH grant 5 U54 NS 39405-08 (NINDS).

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