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issue 3
201-206
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
Seventeen dogs were trained in a three-choice auditory spatial delayed response task, guided by auditory stimulus, at a 10 s delay to a criterion of 90% correct responses in 90 consecutive trials. Four dogs then received bilateral anterior temporal lobe lesions (AT), 6 dogs received hippocampal lesions (H), and 7 dogs served as controls (C). Group C reached postoperative criterion immediately while groups AT and H needed additional training. When subsequently tested at longer delays and with distractions, the group H animals performed more poorly than either the AT or C animals. Further, the group H dogs were again impaired when they retrained at a 10 s delay. In the second phase, the group H and AT animals received a second lesion forming a group (HAT) with bilateral lesions to both the hippocampus and the anterior temporal lobe. Unexpectedly, dogs from group HAT were unimpaired in either postoperative retraining or during performance task and distractions. The results emphasize the importance of the hippocampus in spatial delayed response with an acoustic cue. Effect of combined lesions after extensive training is discussed. Data might support the view, that the hippocampus plays time limited role in memory storage.
EN
Restricted electrolytic lesions of the lateral hypothalamus (LH) evoke sleeplessness in the rat. The present study was aimed to analyze a possible anatomical substrate of the LH hyposomnia within the hypothalamus. In a group of electrolytically lesioned LH rats the intensity of sleep disturbances, assessed on the basis of EEG records from the neocortex and the hippocampus, was confronted with the localization and the extent of destruction of the LH area and with the topography of known fiber systems of the medial forebrain bundle (MFB). In separate experiments the effects of the destruction of LH cell bodies by means of bilateral ibotenic acid (IBO) injections and inhibition of LH neuronal elements by bilateral muscimol (MUSC) administration were also tested. It was found that pronounced hyposomnia follows electrolytic but not IBO lesions of the LH/MFB area. The effective LH damage might have been localized at every level of its antero-posterior axis, from the preoptic area up to the posterior hypothalamus, suggesting involvement of fiber system(s) rather than a localized group of neuronal pericaria. The most effective lesions transsected projections descending from the preoptic/anterior hypothalamic area, olfactory structures, ventral striatum and the central amygdaloid nucleus as well as fibers connecting LH with the brainstem reticular formation, many of them using GABA as a neurotransmitter. Bilateral MUSC injections caused a dose-dependent, bicuculline-reversible, increase in waking time, most pronounced at a dose of 50 ng, which ressembled the effect of the electrolytic lesion. These results indicate that LH hyposomnia is not attributable to the damage to the intrahypothalamic neurons and suggest the participation of GABA-ergic transmission in LH in waking-sleep regulation.
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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