[Role of central neuronal nicotinic receptor in the inhibitory effect of isoflurane on synaptic long-term potentiation in hippocampal slices of rats].
OBJECTIVE
To determine effect of central neuronal nicotinic receptor on synaptic long-term potentiation (LTP) in the CA1 area of rats hippocampal slices.


METHODS
Brain slice preparation transverse hippocampal slices were obtained from male Sprague-Dawley rats that were ether-anesthetized and decapitated. The hippocampus was rapidly removed, and slices were prepared in ice-cold artificial cerebrospinal fluid (ACSF), oxygenated with 95% O2 - 5% CO2. Seventy-seven slices were randomly divided into 11 equal groups (n = 7 each): group LTP; group isoflurane 0.125; group isoflurane 0.25; group isoflurane 0.5; group nicotine 0.1; group nicotine 1.0; group nicotine 10.0; group nicotine 1.0 + isoflurane 0.25; group nicotine 10.0 + isoflurane 0.25; group mecamylamine; group mecamylamine + isoflurane 0.125. One recording electrode was positioned in the pyramidal cell layer of the CA1 area of rats hippocampal slices to simultaneously record evoked population spikes (PS). For LTP induction, high-frequency stimulation (HFS) conditioning pulses (100 Hz/s) were applied to the Schaffer collateral-commissural pathway of hippocampus using a bipolar stimulating electrode. The changes of PS amplitude after HFS were analyzed in each group.


RESULTS
The PS amplitude of the rats hippocampal slices in group LTP after HFS was significantly increased by (52 +/- 12)% compared with that of pre-HFS indicating the successful induction of LTP. Compared with group LTP, the PS amplitudes decreased significantly in group isoflurane 0.125, 0.25 and 0.5 after HFS (P < 0.01) and increased significantly in group nicotine 1.0 and 10.0 (P < 0.01), but the PS amplitudes in group nicotine 0.1 was not significantly changed after HFS (P > 0.05). The PS amplitudes after HFS in group nicotine 1.0 + isoflurane 0.25 and group nicotine 10.0 + isoflurane 0.25 was dramatically increased compared with the value of group isoflurane 0.25 (P < 0.01), but did not differ significantly from group LTP (P > 0.05). The PS amplitudes after HFS in group mecamylamine has no significant difference compared with the value of group isoflurane 0.125, but it was significantly lower than that in group LTP (P < 0.01). The PS amplitudes after HFS in group mecamylamine + isoflurane 0.125 significantly decreased compared with the value of group isoflurane 0.125 and group LTP (P < 0.05 or P < 0.01).


CONCLUSIONS
The inhibition of LTP induction may contribute to isoflurane-induced deficits in memory, and the underlying mechanism is involved in the inhibition of nicotinic acetylcholine receptor activation in hippocampus of rats.
Feng
Chun-Sheng
CS
Department of Anesthesiology, First Hospital of Jilin University, Changchun 130021, China.
Wang
Yun
Y
Ma
Hai-Chun
HC
Yue
Yun
Y
D000818:Animals; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology*; D066298:In Vitro Techniques; D007530:Isoflurane / Q000494:pharmacology*; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D009434:Neural Pathways; D009474:Neurons; D051381:Rats; D017207:Rats, Sprague-Dawley; D011978:Receptors, Nicotinic / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects*
D011978:Receptors, Nicotinic; D007530:Isoflurane