PubMed · 9634390
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N M Weinberger, J S Bakin. 1998-05-22. Research on auditory cortex plasticity.. https://doi.org/10.1126/science.280.5367.1171e
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Using indo-1 microspectrofluorometry, we examined the effects of cholinergic agonists on the concentration of intracellular Ca(2+) ions ([Ca(2+)](i)) in spiral ganglion neurons, isolated from rat cochleae at different stages of post-natal development (from P3 to P30). Extracellular application of acetylcholine (ACh) or carbamylcholine generated a rapid and transient increase in [Ca(2+)](i). The ACh concentration-response curve indicated an apparent dissociation constant (K(d)) of 8 microM and a Hill coefficient of 1.0. Removing extracellular free Ca(2+) did not suppress the ACh-induced Ca(2+) responses suggesting an intracellular Ca(2+)-release mechanism. When we compared the cholinergic response at different stages of postnatal development, there were no significant differences on the aspect of the Ca(2+) response and the percentage of responsive neurons, which ranged between 50 and 65% per cochlear preparation. The application of muscarine triggered reversible Ca(2+) responses similar to those observed with ACh, with an apparent K(d) of 10 microM and a Hill coefficient of 1.0. The cholinergic-induced Ca(2+)pirenzepine. Nicotine (10 to 100 microM) did not evoke Ca(2+) responses and the nicotinic antagonist curare (10 microM) did not block the ACh-evoked responses. The present study is the first direct demonstration of functional muscarinic receptors (mAChRs) in spiral ganglion neurons. These mAChRs activated by the cholinergic lateral efferent system may participate in the regulation of the electrical activity of the afferent auditory fibers contacting the inner hair cells.
Soman, an anticholinesterasic neurotoxic drug, induces epileptic seizures during severe intoxication. The neuropathological lesions then observed are linked to the appearance of these seizures, but their trigger conditions still remain unknown and a great variability between animals is observed. We have developed a technique allowing, in freely moving rats, the in vivo determination of three sets of neurophysiological data, before and during a soman intoxication. For the same rat, we associated cortical acetylcholinesterase (AChE) activity by microdialysis with both the assay of extracellular acetylcholine (ACh) concentrations and electroencephalographic (EEG) recording and power spectrum analysis (gamma band). Data have been analyzed to define the critical parameters which lead to the epileptic fit. Although we found thresholds for seizure occurrence, AChE inhibition having to be over 65% and ACh over 200-fold the baseline, these two criteria are not sufficient to predict the appearance of seizures. Only animals with no increase of energy in the gamma band early after soman poisoning will then exhibit an epileptic fit. Gamma band energy is modulated by noradrenergic activity and might be related to the sympathetic response to stress. So we can hypothesize, that the variation of energy in gamma band after intoxication, which might be related to stress adaptation strategy, may determine whether or not the animal will exhibit an epileptic fit.
Repeated treatment with psychostimulant drugs causes long-lasting behavioral sensitization and associated neuroadaptations. Although sensitization induced by a single psychostimulant exposure has also been reported, information on the behavioral and neurochemical consequences of a single psychostimulant exposure is sparse. Therefore, to evaluate whether behavioral sensitization evoked by single and repeated psychostimulant pretreatment regimens represent the same neurobiological phenomenon, the time-dependent expression of behavioral, neurochemical, and neuroendocrine sensitization after a single exposure to amphetamine was investigated in rats. A single exposure to amphetamine (5 mg/kg, i.p.) caused context-independent sensitization of the locomotor effects of amphetamine, which intensified over time. Thus, sensitization to amphetamine was marginal at 3 d after treatment and more evident after 1 week, whereas 3 weeks after treatment, profound sensitization, as well as cross-sensitization, to cocaine was observed. Amphetamine pretreatment caused an increase in the electrically evoked release of [(3)H]dopamine from nucleus accumbens, caudate putamen, and medial prefrontal cortex slices and of [(14)C]acetylcholine from accumbens and caudate slices. The hyperreactivity of dopaminergic nerve terminals appeared to parallel the development of locomotor sensitization, i.e., whereas hyperreactivity of accumbens dopaminergic terminals increased between 3 d and 3 weeks after treatment, the hyperreactivity of medial prefrontal dopaminergic terminals decreased. Pre-exposure to amphetamine also sensitized the hypothalamus-pituitary-adrenal axis response to amphetamine at 1 and 3 weeks, but not at 3 d after treatment. Because these data closely resemble those reported previously for repeated amphetamine pretreatment, it is concluded that a single exposure to amphetamine is sufficient to induce long-term behavioral, neurochemical, and neuroendocrine sensitization in rats.