The effect of chronic nicotine and withdrawal on intra-neuronal dynamics of acetylcholine and related enzymes in a preganglionic neuron system of the rat
التفاصيل البيبلوغرافية
العنوان:
The effect of chronic nicotine and withdrawal on intra-neuronal dynamics of acetylcholine and related enzymes in a preganglionic neuron system of the rat
The effect of chronic nicotine treatment, given in the drinking water for 8–10 weeks in a dose equivalent to that of a heavy cigarette smoker, and of withdrawal 2 days on acetylcholine (ACh), choline acetyltransferase (CAT) and ACh-esterase (AChE) activities in the preganglionic cervical nerve and the superior cervical ganglia (SCG) of rats, were studied. Control rats were housed and handled as the nicotine rats. After cutting the preganglionic nerve 7–19 h before dissection, ACh, CAT and AChE accumulated in the nerve part proximal to the cut (relative to the nerve cell bodies in the spinal cord). A clearance of these substances was observed in the nerve distal to the cut. This indicates that all 3 substances are transported proximo-distally in this preganglionic cholinergic nerve. In the SCG, ACh was decreased already by 7 h (to about 60%), while CAT and AChE-activities were lowered to 60% and 80%, respectively, at 19 h after cutting the nerve. Chronic nicotine treatment caused an increased ACh accumulation (by about 35 %) and a decreased CAT accumulation (by about 20%) in the cut nerve, while the ganglionic levels of all 3 substances were essentially unchanged. Withdrawal of nicotine for 2 days prior to the final experiments caused a reduced ACh-accumulation (by about 30%) in the nerve and normalized the CAT accumulation. The AChE-activity of intact nerve was markedly increased to about 175% of control, and the transportable fraction of AChE (clearance distal to the cut) was about twice as large as in control. In the SCG withdrawal caused marked changes in the ACh content, which was decreased to 62% of control. CAT-activity was increased to 117% of control while AChE was unchanged. Our hypothesis to explain the results is that chronic nicotine treatment and in particular withdrawal of nicotine may cause marked alterations in the activity of the preganglionic neuron. This may induce changes in the intra-axonal transport of the 3 substances and an increased turnover of ACh in the nerve terminals of the SCG after withdrawal of nicotine.
