The effect of nicotine on motoneurones of the immature rat spinal cord in vitro

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Abstract
1 Nicotine [(–)-nicotine di(+)-tartrate 1–50 μm] produced depolarization of motoneurones as recorded from ventral roots of immature (1–5 day old) rat hemisected spinal cord preparations. This action of nicotine was accompanied by marked desensitization which persisted for at least 2 h following a 2 min application. 2 Ventral roots sectioned from the spinal cord, which were sensitive to glycine, failed to respond to nicotine. 3 Blockade of regenerative electrical activity with tetrodotoxin produced a mean reduction of 39% in the response to 10 μm nicotine. 4 In order to avoid desensitization, blocking agents were tested for their ability to suppress the initial response to a 2 min application of 10 μm nicotine (0.58 mV ± 0.07 s.e.mean, 21 preparations) in 4 or more naive preparations. Responses to nicotine (10 μm) were significantly reduced by 10 μm hexamethonium and were abolished by 250 μm hexamethonium but were resistant to the following antagonists:- atropine (1 μm), phentolamine (2 μm), strychnine (10 μm), kynurenic acid (2mm) and a mixture of bicuculline (50 μm) and picrotoxin (50 μm). 5 It is concluded that the depolarizing responses to nicotine may be due to the presence of nicotinic receptors either on the motoneurone membrane or on nerve terminals adjacent to motoneurones which release an unidentified neurotransmitter.