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EN
The pedunculopontine tegmental nucleus (PPN) is anatomically connected with dopminergic cells in the ventral mesencephalon, which are known to participate in the regulation of various adaptive appetitive behaviours.In present experiment we studied a possible involvment of PPN in feeding elicited by the stimulation of the ventral tegmental area (VTA).It was found that bilateral electrolytic lesionong of the PPN affected VTA-elicited feeding.However, the effects were diverse and showed dependence on the localization of the lesion within the PPN area.Lesions localized anteriorly in the PPN impaired VTA feeding whereas those involving the middle portion of the nucleus facilitated electrically elicited food ingestion.A precise alignment of the lesion and the area activated at the site of stimulation appeared crucial for the effect of the lesion.The results indicate that PPN belongs to the central feeding circuitry and it contains both activating and inhibiting elements directed to the ventral tegmental area.
EN
It was found previously that unilateral electrolytic and 6-OHDA lesions of the ventral tegmental area (VTA) and unilateral intra-VTA injection of bicuculline resulted in facilitation of behavioral responses evoked by electrical stimulation of the symmetrical VTA area in the contralateral hemisphere. We postulated that ?the contralateral facilitation effect?, which may reflect the yet unexplored mechanism of immediate compensation after acute unilateral brain injury, is attributable to the A10 DA neurons and their regulatory inputs. The present study was aimed at examining the possible involvement of NMDA-mediated glutamatergic transmission in VTA in the ?contralateral facilitation effect?. The behavioral model of the VTA stimulation-induced feeding in rats was used. Latency to eat was measured as a function of stimulation frequency before and after unilateral intra-VTA injection of non-competitive NMDA receptors antagonist, MK-801, (doses 0.0, 1.25 and 2.5 mg). MK-801 caused a dose-dependent augmentation of feeding evoked by stimulation of the contralateral VTA, which manifested as a decrease in the reaction frequency threshold and a leftward shift of the latency/frequency curve. Dose 2.5 mg replicated the facilitatory effect of electrolytic and 6-OHDA lesions. The results are interpreted in terms of MK-801-evoked depression of excitatory glutamatergic tone over A10 DA cells and compensatory increase in DA release in the contralateral hemisphere.
EN
Despite resembling each other in many respects, dopaminergic neurons of the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) exhibit dissimilar responses to nicotine in vivo. To investigate this in an in vitro model, the acute effects of nicotine on the firing of SNc and VTA neurons were compared in transverse juvenile rat midbrain sections (300-350 m) using extracellular recording. Levels of nicotine comparable with those encountered in smokers (0.2-1.0 _M, 3 min) not only increased firing rate, but also evoked prolonged irregular firing, as indicated by the increase in the coefficient of variation of discharge frequencies. Pre- and postsynaptic nicotinic cholinergic receptors (nAChRs) were involved, as both effects persisted, although at an attenuated level, in low Ca2+/high Mg2+. Only thenicotine-induced elevation of firing rate was sensitive to the glutamate receptor antagonists APV and CNQX, implying that enhanced glutamate release and glutamate receptor activation are involved in the effects of nicotine on discharge frequency but not pattern. Furthermore, nicotine (1.0 _M) exerted a greater increase in the firing frequency of VTA neurons relative to SNc neurons, suggesting that the differential effects on the two populations previously reported in vivo were due to a difference in the postsynaptic nAChR response and/or local synaptic circuits. Low concentrations of nicotine can thus profoundly modulate the activity of dopaminergic mesencephalic neurons through a local action within the ventral midbrain in vitro, and, similarly to in vivo conditions, evoke stronger effects in the VTA.
EN
It was found previously that unilateral destruction of the ventral tegmental area (VTA) facilitated behavioral responses (exploration, eating) induced by electrical stimulation of the contralateral VTA. The same effect occurred after unilateral injections of pharmacological agents, which led to a decrease in dopaminergic transmission in the VTA. While trying to explain the mechanism behind this 'contralateral facilitation effect' in the present experiment we examined whether augmentation of function of the contralateral hemisphere would be reflected in cortical and hippocampal EEG changes in conscious rats. Unilateral, cytotoxic lesion of the VTA caused a bilateral decrease in neocortical and hippocampal EEG power during both exploratory sniffing and eating. Depression involved all the frequency bands in the prefrontal cortex, mainly in the hemisphere contralateral to the VTA lesion. In the hippocampus the depression was slightly more intense ipsilaterally, also involving all the frequency bands although to different degrees. The results indicate that the VTA is involved in the regulation of cortical and hippocampal activity during VTA-dependent behavioral activation, and that the 'contralateral facilitation effect' is concomitant with lateralized changes in EEG activity.
EN
Unilateral lesions of the ventral tegmental area (VTA) facilitate behavioral responses (feeding and exploration) induced by electrical stimulation of the VTA in the contralateral hemisphere. It was hypothesized that this facilitation may result from a lesion-induced compensatory increase in dopamine transmission in the intact hemisphere. In the present study we tested on the functional level the hypothesis that the activity of bilateral mesocorticolimbic systems is inversely related. For this purpose we compared the effect of unilateral subthreshold activation with the effect of subsequent unilateral lesion of VTA on feeding response evoked by electrical stimulation of the contralateral VTA. In male Wistar rats implanted with bilateral VTA electrodes stimulation-induced feeding was tested in a latency to feed - -stimulation frequency curve-shift paradigm. One electrode was used for induction of feeding reaction and the other electrode was used for concurrent stimulation (with the subthreshold current) and subsequent electrolytic lesioning of the contralateral VTA. It was found that both contralateral stimulation and subsequent lesion performed through the same electrode facilitated a feeding response that manifested as a decrease in the reaction's threshold and a leftward shift of the latency-frequency curve. The paradoxical similarity of the effects of the stimulation and lesion is discussed in terms of functional organization of the mesocorticolimbic system and adaptive changes in dopaminergic transmission.
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