Down-regulation of norepinephrine sensitivity after induction of long-term neuronal plasticity (kindling) in the rat dentate gyrus.
Actions of norepinephrine (NE) in the dentate gyrus were examined before and after kindling-induced epilepsy, neuronal plasticity produced by daily high-frequency stimulation. NE, acting on beta 1-receptors, depolarized granule cells, increased input resistance, firing and influx of Ca2+ in response to repetitive stimulation, and elicited long-lasting potentiation of synaptic potentials. In addition, NE acting via alpha 1-receptors, attenuated Ca2+-dependent regenerative potentials. After kindling-induced plasticity, there were marked reductions in all these effects of NE on granule cells, changes likely to influence kindling-induced seizures, protecting against further enhancement of excitability once plasticity is in place.
Stanton
P K
PK
Department of Biophysics, Johns Hopkins University, Baltimore, MD 21218.
Mody
I
I
Heinemann
U
U
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000503:physiopathology*; D007696:Kindling, Neurologic; D008297:Male; D009473:Neuronal Plasticity; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D002118:Calcium; D009638:Norepinephrine