title: Population synaptic potentials evoked in lumbar motoneurons following stimulation of the nucleus reticularis gigantocellularis during carbachol-induced atonia.
abstract: The effect of electrical stimulation of the medullary nucleus reticularis gigantocellularis (NRGc) on lumbar spinal cord motoneurons was studied in the decerebrate cat using sucrose-gap recordings from ventral roots. The NRGc was stimulated ipsi- and contralaterally before and during atonia elicited by the microinjection of carbachol into the pontine reticular formation. Prior to carbachol administration, the NRGc-induced response recorded from the sucrose-gap consisted of two consecutive excitatory population synaptic potentials followed by a long-lasting, small amplitude inhibitory population synaptic potential. Following carbachol injection, the same NRGc stimulus evoked a distinct, large amplitude inhibitory population synaptic potential, whereas the excitatory population synaptic potentials decreased in amplitude. In addition, after carbachol administration, the amplitude of the monosynaptic excitatory population synaptic potential, which was evoked by stimulation of group Ia afferents in hindlimb nerves, was reduced by 18 to 43%. When evoked at the peak of the NRGc-induced inhibitory response, this potential was further decreased in amplitude. Systemic strychnine administration (0.07-0.1 mg/kg, i.v.) blocked the NRGc-induced inhibitory population synaptic potential and promoted an increase in the amplitude of the excitatory population synaptic potentials induced by stimulation of the NRGc and group Ia afferents. These data indicate that during the state of carbachol-induced atonia, the NRGc effects on ipsi- and contralateral spinal cord motoneurons are predominantly inhibitory and that glycine is likely to be involved in this inhibitory process. These results support the hypothesis that the nucleus reticularis gigantocellularis is part of the system responsible for state-dependent somatomotor inhibition that occurs during active sleep.
authors.affiliation: Department of Physiology, University of California, Los Angeles 90024.
authors.forename: J
authors.initials: J
authors.lastname: Yamuy
authors.forename: I
authors.initials: I
authors.lastname: Jiménez
authors.forename: F
authors.initials: F
authors.lastname: Morales
authors.forename: P
authors.initials: P
authors.lastname: Rudomin
authors.forename: M
authors.initials: M
authors.lastname: Chase
mesh_terms: D000818:Animals; D001479:Basal Ganglia / Q000502:physiology*; D002217:Carbachol / Q000008:administration & dosage / Q000494:pharmacology*; D002415:Cats; D003655:Decerebrate State / Q000503:physiopathology; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D008845:Microinjections; D009046:Motor Neurons / Q000502:physiology*; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D011149:Pons; D012890:Sleep / Q000502:physiology; D013116:Spinal Cord / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D013331:Strychnine / Q000494:pharmacology; D013569:Synapses / Q000502:physiology*
chemical_list: D002217:Carbachol; D013331:Strychnine