Disease relevance of Thalamic Nuclei

• It is possible that selective effects of presynaptic GABAB receptors or GABA release in neocortex and thalamic nuclei of lh/lh mice may contribute to mechanisms underlying absence seizures [1].
• The rats subjected to epileptic seizures showed Evans-blue albumin extravasations especially in the thalamic nuclei, brainstem, occipital, and frontal cortex [2].
• The results indicate that the synaptic organization of GABA-positive profiles in the dorsal superficial subdivision of the MGN nucleus is very similar to that in other thalamic nuclei [3].
• Thionine stains of midbrain coronal sections revealed that, in addition to the loss of neurons seen in several thalamic nuclei following FPI, cell loss in the ipsilateral dorsal lateral geniculate nucleus (dLG) was significantly greater after FPI and hypoxemia than after FPI alone [4].
• Both lesions (via thermocoagulation) and/or neurostimulation (via chronic intracerebral implantation of electrodes) in thalamic nuclei (nucleus ventralis oralis posterior/intermedialis thalami; VOP/VIM) may alleviate rest tremor in PD patients [5].

Psychiatry related information on Thalamic Nuclei

• Involvement of thalamic nuclei in diseases of the nervous system such as Alzheimer's disease and schizophrenia suggests that BuChE could be a potential target for therapeutic intervention in these disorders [6].
• The usefulness of deep brain stimulation (DBS) of thalamic nuclei in Gilles de la Tourette syndrome (GTS) has recently been advocated [7].

High impact information on Thalamic Nuclei

• Using the polymerase chain reaction, we also demonstrate the presence of CNTF and CNTF receptor alpha mRNA in these same thalamic nuclei [8].
• There has been speculation concerning the role that thalamic nuclei play in directing attention to locations in visual space [Crick, F. (1984) Proc. Natl. Acad. Sci. USA 81, 4586-4590] [9].
• We have performed a detailed analysis of Y5 expression in rat brain using in situ hybridization histochemistry with digoxygenin-labeled riboprobes and compared this to expression of Y5 in human brain regions. mRNA for the human Y5 receptor was highly expressed in human hypothalamic and thalamic nuclei [10].
• Here, we report an intense expression of torsinA mRNA in the substantia nigra pars compacta dopamine neurons, the locus ceruleus, the cerebellar dentate nucleus, Purkinje cells, the basis pontis, numerous thalamic nuclei, the pedunculopontine nucleus, the oculomotor nucleus, the hippocampal formation, and the frontal cortex [11].
• We show here by in situ hybridization that GDNF mRNA is expressed in the normal adult rat brain in several targets of substantia nigra neurons, including striatum, nucleus accumbens, thalamic nuclei, olfactory tubercle, hippocampus, cerebellum, and cingulate cortex as well as in the internal granular cell layer of the olfactory bulb [12].

Chemical compound and disease context of Thalamic Nuclei

• Neurochemical changes after morphine, dizocilpine or riluzole in the ventral posterolateral thalamic nuclei of rats with hyperalgesia [13].
• Extensive neurodegeneration in the parietal cortex after L-ephedrine treatment was as pronounced as that previously described for D-amphetamine treatment and also occurred in the intralaminar, ventromedial and ventrolateral thalamic nuclei in rats with severe hyperthermia (peak body temperatures>41.0 degrees C) [14].
• The contribution of the lateral posterior and anteroventral thalamic nuclei on spontaneous recurrent seizures in the pilocarpine model of epilepsy [15].

Biological context of Thalamic Nuclei

• In the present study, we report that CNTF prevents axotomy-induced cell death of neurons in the anteroventral and anterodorsal thalamic nuclei of the adult rat [8].
• The localization of mRNA and binding sites of these receptors in the dorsal horn of the spinal cord, the lateral hypothalamus, the spinal trigeminal nuclei, and the thalamic nuclei supports a role for NPFF in pain modulation [16].
• In addition, rats receiving FG in the PAmp were subjected to audiogenic stress, and the distribution of both FG and the protein product of the immediate-early gene c-fos, Fos, were determined by double immunohistochemistry, to help assess putative functional links between the auditory-responsive thalamic nuclei and PAmp [17].
• Under this condition, application of baclofen decreased the amplitude of the medial lemniscus- and optic tract-evoked excitatory postsynaptic potentials in the two thalamic nuclei investigated [18].
• Among the principal reticulata efferent projections, the ventromedial, ventrolateral, parafascicular, mediodorsal and centrolateral thalamic nuclei, as well as the pedunculopontine nucleus displayed bilateral metabolic activations after intranigral substance P application [19].

Anatomical context of Thalamic Nuclei

• To test this hypothesis, bilateral electrolytic or excitotoxic ibotenic acid MG nuclear lesions were induced, and multiunit recording electrodes were chronically implanted into the anterior and posterior cingulate cortex, the anterior-ventral and medial-dorsal thalamic nuclei, and the basolateral nucleus of the amygdala before training [20].
• In each case of status type I, II, or III, the same anatomical structures that displayed high levels of 14C-2-deoxyglucose uptake also contained many cells that were immunoreactive for Fos, with the exception of the parataenial and mediodorsal thalamic nuclei and the substantia nigra pars reticularis [21].
• NCKX3 transcripts were most abundant in brain, with highest levels found in selected thalamic nuclei, in hippocampal CA1 neurons, and in layer IV of the cerebral cortex [22].
• In situ hybridization revealed high level, focal expression of 4.1B mRNA in select neuronal populations within the mouse brain, including Purkinje cells of the cerebellum, pyramidal cells in hippocampal regions CA1-3, thalamic nuclei, and olfactory bulb [23].
• In contrast, reactive astrocytes in the thalamic nuclei never expressed vimentin, and displayed an enlarged cell body with thick shortened processes [24].

Associations of Thalamic Nuclei with chemical compounds

• Although muscimol alone did not significantly affect LCGU in the external plexiform layer of the olfactory bulb or the anterior, periventricular, and parafascicular thalamic nuclei, rats treated with 0.4 mg/kg of scopolamine before 4.0 mg/kg of muscimol had LCGU decrements in those brain regions [25].
• The slow rhythm survived extensive ipsilateral thalamic destruction by means of electrolytic lesions or kainate-induced loss of perikarya in thalamic nuclei that were input sources to the recorded cortical neurons [26].
• Ionotropic glutamate receptor binding and subunit mRNA expression in thalamic nuclei in schizophrenia [27].
• Alterations in local cerebral glucose utilisation in specific thalamic nuclei following apomorphine [28].
• We investigated both alphaBGT and nicotine binding autoradiographically in different thalamic nuclei in autopsy brain tissue from patients with schizophrenia and DLB [29].

Gene context of Thalamic Nuclei

• Stimulation of mAChRs induced CYR61 expression in primary neurons and rat brain where CYR61 mRNA was detected in cortical layers V and VI and in thalamic nuclei [30].
• METHOD: N-Methyl-D-aspartate (NMDA), AMPA, and kainate receptor expression was determined in six thalamic nuclei from 12 subjects with DSM-III-R diagnoses of schizophrenia and eight psychiatrically normal individuals [27].
• In contrast, CB immunoreactivity is prevalent in medial thalamic nuclei (intralaminar and midline), the posterior complex, ventral posterior inferior nucleus, the ventral lateral anterior nucleus, ventral anterior, and ventral medial nuclei [31].
• Furthermore, BuChE activity, like AChE activity, is found in certain thalamic nuclei related to cognitive and behavioral functions [6].
• By comparison, the striatum and reticular and ventral posterolateral thalamic nuclei, which all showed synaptogyrin 1 labeling, contained significantly less synaptogyrin 3 [32].

Analytical, diagnostic and therapeutic context of Thalamic Nuclei

• It was shown that PDC microinjection into PPTg produced clear and consistent changes in Fos immunoreactivity in several thalamic nuclei, but most markedly in the centrolateral, ventrolateral and reticular nuclei [33].
• The SP innervation of somatosensory thalamic nuclei may be supplied, at least in part, by spinothalamic afferent as suggested by the depletion of SP after anterolateral chordotomy but not after ablation of the dorsal column nuclei [34].
• Bicuculline perfusion induced Fos-like immunoreactivity in the thalamic projection areas, including the PFC, and in the thalamic nuclei surrounding the dialysis probe [35].
• Atropine (Atr) or mecamylamine (MeC) were administered locally into the periaqueductal gray (PAG) of rabbits with chronically implanted electrodes into the motor-sensory cortex (MSC) ventro-posterolateral thalamic nuclei (NVPL), PAG and midbrain reticular formation (MRF) [36].

References