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E Jurkowlaniec

Publications and source records attributed to E Jurkowlaniec.

13 recordsLinked to original sources

Microinjection of procaine into the pedunculopontine tegmental nucleus suppresses hippocampal theta rhythm in urethane-anesthetized rats.

It was found that the cholinergic component of the pedunculopontine tegmental nucleus (PPN) is involved in the generation of theta rhythm in the hippocampus. However, it is still not known how important PPN is in the brainstem theta-generating system, where the nucleus reticularis pontis oralis is regarded as a primary generator. In the present experiment, performed on urethane-anesthetized rats, we studied the effect on the tail pinch-elicited hippocampal theta of unilateral inactivation of PPN by means of direct procaine microinjection. Procaine induced ipsilateral suppression of theta rhythm, manifested as desynchronization of hippocampal EEG, a shift of the fast Fourier transformation (FFT) power peak toward lower frequencies, and a reduction of FFT peak magnitude at theta band. Hippocampal field activity returned to normal (both its FFT peak frequency and magnitude) within 30 min after the injection. The results obtained indicate that PPN is critical for hippocampal theta generation but it may not be involved in encoding theta frequency.

Anesthetics, Intravenous↗

Anatomical correlates of the lateral hypothalamic influence on waking-sleep relationship in the rat.

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 medical 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.

Animals↗

Effect of lateral hypothalamic lesion on sleep-waking pattern and EEG power spectra in the rat.

Bilateral, electrolytic lesion of the lateral hypothalamus (LH) in rats produces hyposomnia and qualitative EEG changes which are difficult to assess by conventional visual inspections of electroencephalograms. In the present study the spectral analysis of EEG was applied in LH-lesioned rats and confronted with a standard visual scoring method. One-hour samples of hippocampal and cortical EEG were taken from the light part of the circadian cycle before and after electrolytic or sham LH damage. In half of the LH-lesioned rats a power spectral analysis was performed using a Fast Fourier Transform routine at 1 Hz bands from 0.5 to 25 Hz; in the other half, as well as in the sham-lesioned group, EEG records were visually scored for the amount of waking, slow wave sleep and paradoxical sleep. Significant hyposomnia effects were found in LH-lesioned rats. Power spectral analysis of hippocampal EEG revealed a significant increase in power density at 4-6 Hz and a reduction at 7-10, 14-17, 19-22 and 23-24 Hz. In neocortical EEG there was a significant increase in power density at 5-6 Hz band and a reduction at 7-8 Hz. The results are discussed in the context of the effects of selective destruction of the specific neurotransmitter systems occupying the LH area.

Animals↗

Daily pattern of EEG activity in rats with lateral hypothalamic lesions.

The experiment was aimed to further elucidate the phenomenon of sleep suppression observed earlier after electrolytic lesions of the lateral hypothalamus (LH). In male Wister rats the amounts of waking (W), slow wave sleep (SWS) and paradoxical sleep (PS) were counted in 1 h samples of EEG taken from the light and dark parts of the circadian cycle, as well as in the whole 12 h diurnal records before lesioning and after electrolytic or sham lesions of LH. Significant increase of W with a simultaneous reduction of SWS and PS was found in 1h and 12h diurnal records; no effect of the lesion on nocturnal EEG was observed. The results suggest that lesion-induced sleep suppression concerns the light part of the day when rats are naturally less active, and that 1h samples of diurnal EEG may be sufficient to diagnose LH insomnia. No correlation was found between the magnitude of waking-sleep disturbances and the intensity of ingestive impairments (aphagia, adipsia, body weight loss) evoked by LH lesions which suggests that LH insomnia may be a result of disruption of a mechanism directly involved in the regulation of waking-sleep cycle rather than a secondary effect of other lesion-induced impairments.

Animals↗

Disturbances in sleep-waking pattern and cortical desynchronization after lateral hypothalamic damage: effect of the size of the lesion.

The effect of electrolytic lesions of varying size within the anterior part of the lateral hypothalamus (LH) on neocortical activity and quantitative sleep-waking relations was studied in male Wistar rats. It was found that extensive LH lesions caused simultaneously an abolishment of cortical desynchronizing reactions and an electroencephalographic insomnia. More restricted damage left the qualitative pattern of cortical EEG unchanged, but still produced substantial reduction in the amount of sleep. Pronounced EEG disturbances coexisted with relatively mild behavioral deficits. It is concluded that a constellation of the LH syndrome symptoms is critically dependent on the variations of lesion parameters.

Animals↗

Differential effect of the damage to the lateral hypothalamic area on hippocampal theta rhythm during waking and paradoxical sleep.

Hippocampal theta rhythm was analyzed in rats subjected to bilateral, electrolytic lesions of the lateral hypothalamic (LH) region at different levels of its rostro-caudal axis. It was found that damage to the LH disturbed the hippocampal theta activity both during waking and paradoxical sleep. The main effect consisted in the lowering of the theta frequency. Typically, a decrease of frequency was accompanied by an increase of amplitude during waking, and an amplitude fall during paradoxical sleep. Extensive lesions increased the amount of rhythmic slow activity during waking and induced long trains of immobility-related theta. The general picture of impairments of the hippocampal theta rhythm in particular subjects depended on the size of the lesion and, to some extent, also on its localization within the LH. It is concluded that LH region contains systems of fibers which transmit impulses from the brain stem reticular formation to the prosencephalic structures generating the rhythmicity of theta.

Animals↗

The effect of lateral hypothalamic lesions on spontaneous EEG pattern in rats.

Neocortical and hippocampal EEG was recorded in ten rats subjected to bilateral lesions of the lateral hypothalamus at different levels of its rostro-caudal axis. In nine rats the damage evoked a marked increase of waking time with a simultaneous reduction of the percentage of large amplitude irregular activity related to slow wave sleep in the first eight postlesion days. There was also a decrease in the amount of paradoxical sleep. Enhanced waking coexisted with behavioral somnolence. The most extensive hypothalamic lesions produced qualitative changes of EEG concerning mainly the frequency of hippocampal theta rhythm. Control lesions within the subthalamic region did not influence either qualitative or quantitative EEG pattern. It is concluded that limited lesions of the lateral hypothalamus did not destroy a sacient number of reticular activating fibers to disturb a cortical desynchronizing reaction. The increased amount of waking pattern may be due to serotonergic deafferentation of the neocortex. Dissociation of behavioral and EEG indices of the level of arousal imply the existence of separate neuronal systems for both aspects of activation.

Animals↗

An attempt to use central dopaminergic stimulation as a reinforcement for T-maze learning in rats.

Two groups of 8 rats with unilateral cannulas aimed at the lateral hypothalamus (LH) or nucleus accumbens (nAcc) were trained in a T-maze to receive intracerebral injections of dopamine as a reinforcement for choosing the proper arm of the maze. Neither in the LH nor in the nAcc groups did dopamine show evident reinforcing properties comparable to those found earlier for noradrenaline.

Animals↗

Intrahypothalamic microinjections of noradrenaline with and without induction of the alimentary drive as a reward in a T maze learning in rats.

Noradrenaline injected into the perifornical region of the anterior part of the lateral hypothalamus in rats can serve as a reinforcement in a T maze learning, whether it induces the activation of the alimentary drive or not. It follows that the main role of noradrenaline in this brain area consists not so much in induction of the alimentary drive as in activation of the very process which is essential for the reinforcement. It is claimed that intrahypothalamic microinjections of noradrenaline evoke pleasurable states which constitute a virtual reinforcement of motivated behavior.

Animals↗

The EEG activity after lesions of the diencephalic part of the zona incerta in rats.

Neocortical and hippocampal EEG activity was recorded in 23 rats subjected to the bilateral electrolytic lesions of the diencephalic zona incerta (ZI). The aim was to find whether damage to ZI can replicate insomnia and disturbances in cortical EEG desynchronization and hippocampal theta rhythm found after lesions of the lateral hypothalamic (LH) area. No effect of the ZI lesions on waking-sleep cycle was found. The amplitude and frequency of cortical waves and hippocampal theta rhythm during waking were changed only in some rats. These changes were small, short-lasting and bidirectional (toward and increase or decrease in different subjects). Both the amplitude and frequency of paradoxical sleep theta were depressed in part of animals. Thus the marked EEG changes after LH lesions can not be attributed to simultaneous damage of the adjacent subthalamic region. However, the ZI seems to constitute a part of a larger system regulating cortical arousal and hippocampal theta rhythm.

Animals↗