title: Neuronal coupling via connexin36 contributes to spontaneous synaptic currents of striatal medium-sized spiny neurons.
abstract: Gap junctions provide a means for electrotonic coupling between neurons, allowing for the generation of synchronous activity, an important contributor to learning and memory. Connexin36 (Cx36) is largely neuron specific and provides a target for genetic manipulation to determine the physiological relevance of neuronal coupling. Within the striatum, Cx36 is more specifically localized to the interneuronal population, which provides the main inhibitory input to the principal projection medium-sized spiny neurons. In the present study, we examined the impact of genetic ablation of Cx36 on striatal spontaneous synaptic activity. Patch-clamp recordings were performed from medium-sized spiny neurons, the primary target of interneurons. In Cx36 knockout mice, the frequencies of both excitatory and inhibitory spontaneous postsynaptic currents were reduced. We also showed that activation of dopamine receptors differentially modulated the frequency of GABAergic currents in Cx36 knockout mice compared with their wild-type littermates, suggesting that dopamine plays a role in altering the coupling of interneurons. Taken together, the present findings demonstrate that electrical coupling of neuronal populations is important for the maintenance of normal chemical synaptic interactions within the striatum.
authors.affiliation: Mental Retardation Research Center, University of California at Los Angeles, Los Angeles, California 90095, USA.
authors.forename: Damian M
authors.initials: DM
authors.lastname: Cummings
authors.forename: Irene
authors.initials: I
authors.lastname: Yamazaki
authors.forename: Carlos
authors.initials: C
authors.lastname: Cepeda
authors.forename: David L
authors.initials: DL
authors.lastname: Paul
authors.forename: Michael S
authors.initials: MS
authors.lastname: Levine
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D000962:Antimalarials / Q000494:pharmacology; D002450:Cell Communication / Q000187:drug effects / Q000502:physiology*; D017630:Connexins / Q000378:metabolism*; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D004298:Dopamine / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D017629:Gap Junctions / Q000187:drug effects / Q000378:metabolism; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D015767:Mefloquine / Q000494:pharmacology; D051379:Mice; D018345:Mice, Knockout; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D026941:Sodium Channel Blockers / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D000097004:Gap Junction delta-2 Protein
chemical_list: D000962:Antimalarials; D017630:Connexins; D004298:Dopamine; D015767:Mefloquine; D026941:Sodium Channel Blockers; D013779:Tetrodotoxin; D000097004:Gap Junction delta-2 Protein