Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea‐pigs

Abstract

1 The effect of acute and chronic (16 days) administration of nicotine on cortical acetylcholine (ACh) release, gross behaviour and brain nicotinic binding sites was investigated in rats and guinea-pigs.2 The drug, injected either subcutaneously (0.45-0.90mgkg-1) or intracerebroventricularly (1, 3 and 5 ig) increased the cortical ACh release, in a dose-dependent manner, through mecamylaminesensitive receptors for 1-2 h in both species. 3 Chronic treatment significantly increased basal ACh release in the rat and slightly lowered it in the guinea-pig, but the response to a challenging dose of nicotine was proportionally maintained in both species. 4 The number of nicotinic receptors was four times higher in the rat than in the guinea-pig and was not dependent on the radioligand used ([3H]-nicotine or [3H]-ACh, in the presence of atropine) to determine this. The nicotinic binding sites showed an apparent increase in chronically treated rats but no change in guinea-pigs. 5 Tolerance to the inhibitory effect of the drug, assessed with the T maze test, was found in the rat. No apparent change in gross behaviour was detected in the guinea-pig. 6 It is concluded that chronic nicotine treatment causes evident tolerance to its inhibitory effect on behaviour in the rat, but no adaptation to its excitatory properties on the cholinergic brain structures in rats and guinea-pigs.

Cerebral Cortical Vasodilatation Mediated by Nicotinic Cholinergic Receptors: Effects of Old Age and of Chronic Nicotine Exposure

“…injection of nicotine at a dose of 30 mg/kg. This result is in agreement both with a nicotine-induced activation of the neurons of the Meynert nucleus, and with the finding that nicotine induces ACh release from the cerebral cortex in anesthetized cats 17) and in conscious rats, 18) and also from synaptosomes obtained from the rat cerebral cortex. 19,20) The nicotine-induced ACh release in the cortex may produce cortical vasodilation, by activation not only of the nicotinic, but also of the muscarinic receptors.…”

Effect of acute and subchronic nicotine treatment on cortical efflux of [3H]‐d‐aspartate and endogenous GABA in freely moving guinea‐pigs

“…In fact, the facilitation of [3H]-D-aspartate is short-lived while the inhibition of GABA release is long lasting. Considering the different time courses of nicotine effects on the release of other putative transmitters (Imperato et al, 1986;Nordberg et al, 1989) a complex neurochemical (and behavioural) picture arises. This may explain the biphasic nicotine influence on locomoter activity of the rat (inhibition followed by facilitation, see Freeman et al, 1987;Clarke & Kumar, 1983) as well as the increased alertness and decreased anxiety, the two overlapping stages of behavioural and subjective signs caused by nicotine in smokers (Pomerleau, 1986).…”

“…Nicotine is known to increase the firing rate of many neuronal pools and to enhance the release of a number of putative neurotransmitters, by interacting with receptors located on the cell bodies and/or nerve terminals (see Nordberg et al, 1989). However, only a few investigations have been devoted to analyzing effects of nicotine on the amino acid transmitters.…”

Tobacco Tar Components That Stimulate Nerve Growth Factor (NGF) Synthesis/Secretion of Mouse Astroglial Cells in Culture

“…3 ,4) Patients with AD or Parkinson's disease are lacking acetylcholine or dopamine, respectively, and as a results the cholinergic neurons or dopaminergic neurons are damaged in these disease. Nicotine, one of the major components of tobacco tar, stimulates the in vitro and in vivo release of acetylcholine 5 ) and dopamine, 6,7) and nicotine has an improving effect on juvenile Parkinsonism. 2 ) What functions nicotine has in the brain and how nicotine correlates with neurotrophic factors that are essential for neuronal survival are ofgreat interest.…”