title: Activity of locus coeruleus neurons in amygdala kindled rats: role in the suppression of afterdischarge.
abstract: Kindling is a model of epilepsy. The mechanisms of kindling development are unknown but may involve attenuation of noradrenergic neurotransmission. Single unit recordings, pharmacologic and lesion techniques were used to test the hypothesis that the increased seizure duration of kindled rats is the consequence of an inactivation of noradrenergic neurons in the locus coeruleus (LC). No difference was found between unkindled (naive) and kindled rats in the firing rates of recorded LC neurons either between or during seizures in the paralyzed, ventilated condition. Moreover, in naive rats, frank destruction of the LC did not lengthen seizure duration. We conclude that the lengthened seizure duration of kindled rats, in the paralyzed, ventilated conditions, is not the consequence of inactivation of the LC since the firing rate of recorded LC neurons in kindled rats was not decreased and since destruction of the LC in naive rats did not lengthen seizure duration. If attenuation of noradrenergic neurotransmission does contribute to the kindling phenomenon, then the LC is not likely to be the site at which this attenuation occurs.
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000679:Amygdala / Q000503:physiopathology*; D000818:Animals; D004146:Dioxanes / Q000494:pharmacology; D004569:Electroencephalography; D019329:Idazoxan; D007696:Kindling, Neurologic; D008125:Locus Coeruleus / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000503:physiopathology
chemical_list: D004146:Dioxanes; D009638:Norepinephrine; D019329:Idazoxan