Nitric oxide controls oscillatory activity in thalamocortical neurons.
Nitric oxide (NO) is considered a diffusible messenger involved in neuronal communication, although the post-synaptic target cells of NO action and the associated biological function in the CNS are still a matter of controversy. Within the discrete pattern of NO-synthesizing neurons in the brain, NO synthase is specifically colocalized with the cholinergic brain stem-thalamic system, which is thought to regulate the state-dependent activity of the thalamocortical circuit. Here we report evidence indicating that the release of NO onto thalamocortical neurons results in an alteration in voltage dependence of the hyperpolarization-activated cation conductance, probably mediated via the cGMP system. NO selectively dampens oscillatory neuronal activity, indicating a rapidly diffusing signaling mechanism that controls the functional state of the thalamocortical network.
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Abteilung Neurophysiologie Medizinische Fakultät Rhur-Universität, Bochum, Germany.
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D000818:Animals; D002412:Cations / Q000378:metabolism; D002415:Cats; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D006152:Cyclic GMP / Q000378:metabolism; D004594:Electrophysiology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D009474:Neurons / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism*; D013788:Thalamus / Q000166:cytology / Q000378:metabolism / Q000502:physiology*
D002412:Cations; D009569:Nitric Oxide; D006152:Cyclic GMP