Neuroscience
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The activity-dependent induction of immediate-early genes is commonly used to map activated neuronal networks. In a previous analysis of the cortico-basal ganglia circuits, we have shown that a cortical stimulation produces Fos protein expression in the striatum and the subthalamic nucleus, with a pattern which conforms to the anatomical organization of cortical projections [Sgambato V. et al. (1996) Neuroscience 81, 93-112]. In the present study, we examined the effects of a unilateral blockade of the corticostriatal transmission on c-fos and zif 268 messenger RNA expression evoked in the substantia nigra pars reticulata and the subthalamic nucleus following stimulation of the ipsilateral motor cortex. ⋯ The lack of immediate-early gene induction strongly contrasted with the neuronal discharges evoked in these nuclei by the cortical stimulation. Comparison between the cortically evoked neuronal activities and the pattern of immediate-early gene expression suggests that the induction of immediate-early genes in the basal ganglia mainly reflects the level of synaptic activity rather than the frequency of discharge of the postsynaptic neurons. Moreover, the results stress that modifications of immediate-early gene expression observed in the basal ganglia after an acute or a chronic interruption of the corticostriatal transmission are not superimposable.
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A few hours after peripheral axons of cutaneous afferent neurons have been transected, some of their novel endings become excitable by physical or chemical stimuli. It has been assumed that these axon endings preferentially respond to those stimuli which have excited their previous receptive endings. We studied the prevalence of sensory properties among 784 unmyelinated sural nerve fibres which had been axotomized 2-24 h before, by applying mechanical and thermal forces to the nerve lesion site. ⋯ The distribution of sensory properties among acutely axotomized sural nerve C-fibres is therefore largely similar to the recently published distribution of receptor types among intact sural nerve C-fibre afferents. Thus, the hypothesis that responses of axotomized afferent fibres reflect their original receptive properties is corroborated. Knowledge of underlying transduction mechanisms may lead to specific pharmacological tools for suppression of ectopic discharges in unmyelinated axotomized afferents, which probably contribute to neuropathic pain states.
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This study was carried out in order to examine the effects of acute or chronic L-DOPA treatment on striatally expressed FosB- and JunB-like proteins in a rat model of Parkinson's disease. Rats with a unilateral, near-total 6-hydroxydopamine lesion of the ascending mesostriatal projection received either an acute challenge or a one-week treatment with 10 mg/kg/day methyl L-DOPA (combined with 15 mg/mg benserazide), and were killed at either 3 h or two days post-injection. Both acute and chronic L-DOPA treatment caused a pronounced, persistent increase in the number of FosB-like immunoreactive cells in the dopamine-denervated striata (five- and seven-fold increase, respectively, above the levels found in lesioned but non-drug-treated controls), but the two treatment groups differed markedly with respect to both the average amount of staining per cell, which was two-fold larger in the chronic L-DOPA cases, and the anatomical distribution of the labeled cells. ⋯ However, JunB did not exhibit prolonged expression kinetics, and was somewhat down-regulated in the chronically compared with the acutely L-DOPA-treated rats. The present results show that L-DOPA administration produces a long-lasting increase in the levels of FosB-, but not JunB-like immunoreactivity in the dopamine-denervated striatum. More importantly, these data show that striatal induction of FosB- and JunB-like proteins by chronic L-DOPA treatment exhibits both regional and compartmental specificity.
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Microinjection of a cholinergic agonist, carbachol, into the pontine reticular formation of chronically instrumented intact or acutely decerebrate rats and cats has been used extensively to study rapid eye movement sleep mechanisms. In this study, we sought to develop a reduced carbachol model of rapid eye movement sleep-like neural events exhibiting multiple physiological markers of this state, and allowing for the use of invasive electrophysiological techniques. Accordingly, we investigated whether pontine carbachol could produce rapid eye movement sleep-like motor atonia and electrocortical changes in urethane-anaesthetized rats. ⋯ This shows that complex and stereotyped neuronal events underlying both ascending and descending signs of rapid eye movement sleep can be pharmacologically activated under general anaesthesia. Such a reduced preparation may be useful for studies into the central neuronal mechanisms underlying generation of rapid eye movement sleep; particularly for studies requiring techniques that are difficult to implement in intact, naturally sleeping animals. The acceleration of the respiratory rate observed only when carbachol induced electroencephalogram desynchronization suggests that neural events associated with electrocortical changes contribute to the respiratory rate increases observed in natural rapid eye movement sleep.
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Cataplexy, a symptom of narcolepsy, is a loss of muscle tone usually triggered by sudden, emotionally significant stimuli. We now report that locus coeruleus neurons cease discharge throughout cataplexy periods in canine narcoleptics. ⋯ Our results are consistent with the hypothesis that locus coeruleus activity contributes to the maintenance of muscle tone in waking, and that reduction in locus coeruleus discharge plays a role in the loss of muscle tone in cataplexy and rapid-eye-movement sleep. Our results also show that the complete cessation of locus coeruleus activity is not sufficient to trigger rapid-eye-movement sleep in narcoleptics.