Effect of desipramine on spontaneous activity of hippocampal CA1 neuron after transient cerebral ischemia in rats.
OBJECTIVE
To study the spontaneous firing of CA1 neurons in rat hippocampus after transient cerebral ischemia and the effect of desipramine (Des) on the post-ischemic electric activity of CA1 neurons.


METHODS
Single-unit extracellular recordings were performed in rats on d 3 after 10 min of cerebral ischemia by occlusion of 4 arteries. Des and saline were injected into a tail vein. The histological changes of CA1 neurons was assessed by the neuronal density of the CA1 sector.


RESULTS
The spontaneous firing rate of CA1 neurons on d 3 after ischemia was enhanced in comparison with the control value. Des (0.2 and 0.4 mg.kg-1, i.v., n = 5 & 6, respectively) reduced dose-dependently the increase of firing rate with maximal inhibition by 6 min (58% & 85%) to 9 min (69% & 94%) (vs vehicle group, P < 0.01). About 50% cells in CA1 region showed necrotic changes.


CONCLUSIONS
Des antagonized the hyperexcitability of CA1 neurons after cerebral ischemia.
Zhu
Z T
ZT
Department of Pharmacology, Nanjing Railway Medical College, China.
Zhang
X X
XX
Liu
J
J
Jin
G Z
GZ
D000818:Animals; D000929:Antidepressive Agents, Tricyclic / Q000494:pharmacology*; D003891:Desipramine / Q000494:pharmacology*; D004594:Electrophysiology; D006624:Hippocampus / Q000502:physiology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D009474:Neurons / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley
D000929:Antidepressive Agents, Tricyclic; D003891:Desipramine