Nucleus Reticularis Of Thalamus Research Articles

Abnormal benzodiazepine and zinc modulation of GABA A receptors in an acquired absence epilepsy model

Brain cholesterol synthesis inhibition (CSI) at a young age in rats has been shown to be a faithful model of acquired absence epilepsy, a devastating condition for which few therapies or models exist. We employed the CSI model to study cellular mechanisms of acquired absence epilepsy in Long–Evans Hooded rats. Patch-clamp, whole-cell recordings were compared from neurons acutely dissociated from the nucleus reticularis of thalamus (nRt) treated and untreated with a cholesterol synthesis inhibitor, U18666A. In U18666A-treated animals, 91% of rats developed EEG spike-waves (SWs). Patchclamp results revealed that although there was no remarkable change in GABA A receptor affinity, both a loss of ability of benzodiazepines to enhance GABA A-receptor responses and an increase of Zn 2+ inhibition of GABA A-receptor responses of nRt neurons occurred in Long–Evans Hooded rats previously administered U18666A. This change was specific, since no significant changes were found in neurons exposed to the GABA allosteric modulator, pentobarbital. Taken collectively, these findings provide evidence for abnormalities in benzodiazepine and Zn 2+ modulation of GABA A receptors in the CSI model, and suggest that decreased γ2 subunit expression may underlie important aspects of generation of thalamocortical SWs in atypical absence seizures. The present results are also consistent with recent findings that mutation of the γ2 subunit of the GABA A receptor changes benzodiazepine modulation in families with generalized epilepsy syndromes.

Abnormal benzodiazepine and zinc modulation of GABAA receptors in an acquired absence epilepsy model

Brain cholesterol synthesis inhibition (CSI) at a young age in rats has been shown to be a faithful model of acquired absence epilepsy, a devastating condition for which few therapies or models exist. We employed the CSI model to study cellular mechanisms of acquired absence epilepsy in Long–Evans Hooded rats. Patch-clamp, whole-cell recordings were compared from neurons acutely dissociated from the nucleus reticularis of thalamus (nRt) treated and untreated with a cholesterol synthesis inhibitor, U18666A. In U18666A-treated animals, 91% of rats developed EEG spike-waves (SWs). Patchclamp results revealed that although there was no remarkable change in GABA A receptor affinity, both a loss of ability of benzodiazepines to enhance GABA A -receptor responses and an increase of Zn 2+ inhibition of GABA A -receptor responses of nRt neurons occurred in Long–Evans Hooded rats previously administered U18666A. This change was specific, since no significant changes were found in neurons exposed to the GABA allosteric modulator, pentobarbital. Taken collectively, these findings provide evidence for abnormalities in benzodiazepine and Zn 2+ modulation of GABA A receptors in the CSI model, and suggest that decreased γ2 subunit expression may underlie important aspects of generation of thalamocortical SWs in atypical absence seizures. The present results are also consistent with recent findings that mutation of the γ2 subunit of the GABA A receptor changes benzodiazepine modulation in families with generalized epilepsy syndromes.

Afferent projections to the dorsal thalamus of the rat as shown by retrograde lectin transport. II. The midline nuclei

Afferent projections to midline thalamic cell groups which innervate nucleus accumbens, were identified by the retrograde transport of unconjugated wheat germ agglutinin followed by the identification of labelled cell groups with immunocytochemistry. Large numbers of neurones were labelled in a variety of hypothalamic nuclei; principally in the medial preoptic area, anterior hypothalamic area, ventromedial, periventricular, arcuate and posterior hypothalamic nuclei, and in the supramammillary and lateral hypothalamic areas. Following rostral thalamic injections labelled cells were also found in the lateral septum, bed nucleus of the stria terminalis, and zona incerta. Prominent and localised label was found in the nucleus reticularis of thalamus at its most rostral medial tip. Cortical label was found in the ventral subiculum following rostral injections, and in the perirhinal cortex following mid-thalamic injections. In the brainstem label was found in central grey, laterodorsal tegmental nucleus, raphe, dorsal and ventral parabranchial nuclei and nucleus of the tractus solitarius. The results are discussed in the context of striatal function, particularly the nucleus accumbens, which is a component of the ventral striatum. Thus, the midline thalamic nuclei may provide an interface where a variety of inputs from many limbic regions and hypothalamic nuclei can influence nucleus accumbens function. Comparison of afferents to several thalamic nuclei directly related to striatal function and the prefrontal cortex show, that forebrain thalamic afferents from pallidal and hypothalamic sites, are organised with a clear topography. Some afferents suggest specific routes which may allow the reticular activating system to participate in the regulation of basal ganglia function.

Afferent projections to the parafascicular thalamic nucleus of the rat, as shown by the retrograde transport of wheat germ agglutinin

Afferent projections to the parafascicular nucleus of the rat have been mapped using the retrograde transport of unconjugated wheat germ agglutinin and immunohistochemistry using very short survival times. Retrogradely labelled neurones were found in laminae V and V1 of primary motor cortex, lamina V1 of primary somatosensory cortex, and deep laminae of gustatory cortex; in the reticular thalamic nucleus and zona incerta; and in the caudate-putamen, entopeduncular nucleus, mesencephalic reticular formation and pretectum. Additional label was found in the laterodorsal tegmental nucleus, nucleus tegmenti pedunculopontinus, dorsal and ventral parabrachial nuclei, vestibular nuclei and the lateral cervical, medial and interpositus nuclei of the cerebellum. These results are discussed in the context of the connections of parafascicular nucleus with the motor system, particularly the basal ganglia. Of particular interest are inputs from laterodorsal tegmental nucleus, nucleus reticularis of thalamus, mesencephalic reticular formation, nucleus tegmenti pedunculopontinus, primary motor cortex and deep cerebellar nuclei. These indicate that the parafascicular nucleus lies at an interface between the reticular activating system on the one hand, and the motor system on the other. This result thus enlarges on present concepts of the parafascicular nucleus. Comparison of afferent projections to a variety of non-specific thalamic nuclei, the parafascicular, paraventricular and mediodorsal thalamic nuclei, indicate a remarkable set of topographic parallels from cortical, reticular thalamic, hypothalamic and brainstem sites. These comparisons provide clues as to the organisational principles of these non-specific thalamic nuclei, particularly in the context of the reticular activating system.