Disease relevance of Thalamus

• Here we show that DAP12-deficient (DAP12(-/-)) mice develop an increased bone mass (osteopetrosis) and a reduction of myelin (hypomyelinosis) accentuated in the thalamus [1].
• These findings implicate the thalamus as a novel site for disease specific alterations in dopamine neurotransmission, such as exist with nigral degeneration attending Parkinson's disease [2].
• Because long-standing hemispherectomy entails massive retrograde degeneration of thalamocortical neurons, the preserved P14 and N18 responses must reflect neural activities generated below the thalamus that are volume conducted to the scalp bilaterally [3].
• Whilst many reports mention neurofibrillary tangle pathology in the thalamus in progressive supranuclear palsy, there has been little detailed regional analysis of the distribution and density of thalamic pathology in this disease or in other parkinsonian syndromes [4].
• Although no subject felt chest pain during dipyridamole stress, neural activation in the thalamus and prefrontal cortex indicates that stimulation of A(1) adenosine receptors during dipyridamole stress may produce input from the heart to the thalamus through the vagal fiber [5].

Psychiatry related information on Thalamus

• Gamma-aminobutyric acid (G.A.B.A.) was measured in the nucleus accumbens and thalamus of brains from patients who had died with schizophrenia or Huntington's chorea (H.C.) and from control subjects [6].
• Relative to the controls, MS patients with memory deficits showed a significant bilateral reduction of rCMRglc in the hippocampus, cingulate gyrus, thalamus, associative occipital cortex, and cerebellum [7].
• Lower relative glucose metabolism in the total thalamus, mediodorsal nucleus, and pulvinar was associated with greater overall clinical symptoms as measured by the Brief Psychiatric Rating Scale [8].
• Nicotine also enhanced activation of a network of regions, including anterior cingulate cortex and bilateral thalamus, and modulated thalamocortical functional connectivity to a greater degree in schizophrenic than in control subjects during dichotic 2-back task performance [9].
• Selective down-regulation of the astrocyte glutamate transporters GLT-1 and GLAST within the medial thalamus in experimental Wernicke's encephalopathy [10].

High impact information on Thalamus

• Burst firing is thought to play an important role in the synchronized activity of the thalamus observed in absence epilepsy, but may also underlie a wider range of thalamocortical dysrhythmias [11].
• I have compared the numbers of neurons in the visual thalamus (lateral geniculate nucleus; LGN) and area V1 across primate species [12].
• T2 relaxation time measures in thalamus did not differ significantly between groups, and were not affected by methylphenidate [13].
• Immunohistochemical staining showed that this nucleus is defined by a dense calbindin-positive fibre plexus in the macaque, so we applied the same staining method to sections of human thalamus [14].
• Exclusively inhibitory action of iontophoretic acetylcholine on single neurones of feline thalamus [15].

Chemical compound and disease context of Thalamus

• Acute hypoxia (PaO2 = 20 +/- 1 mm Hg) increased the interstitial fluid adenosine concentrations significantly from 0.68 +/- 0.29 (SEM) to 1.60 +/- 0.35 microM in the frontal cortex and from 1.03 +/- 0.32 to 2.60 +/- 0.86 microM in the thalamus (n = 8) [16].
• RESULTS: Methylphenidate improved ADHD task performance, reduced rCBF in the prefrontal cortex (PFC), and increased rCBF in the right thalamus and precentral gyrus [17].
• Since increased brain histamine appears to have an antiepileptic effect through the H(1) receptor activity, kainic acid (KA)-induced status epilepticus in rat was used to study modulation of H(1) and H(3) receptors in the thalamus following seizures [18].
• Based on recordings from auditory thalamus neurons (n = 302) collected during anesthesia (pentobarbital, urethan, or ketamine/xylazine), waking (W), and slow-wave sleep (SWS), we investigated how bursts participate to frequency tuning, intensity-function, response latency (and latency variability), and stimulus detectability [19].
• PURPOSE: Physiological evidence has shown that the anterior thalamus (AN) and its associated efferents/afferents constitute an important propagation pathway for pentylenetetrazol (PTZ)-mediated generalized seizures in rodents [20].

Biological context of Thalamus

• The expression of CFTR mRNA and protein in discrete areas of brain, including the hypothalamus, thalamus, and amygdaloid nuclei, which are involved in regulation of appetite and resting energy expenditure, is identical [21].
• After birth, all mutant mice develop a progressive neurodegeneration in the frontal cortex, olfactory bulb and thalamus, characterized by massive apoptosis and upregulation of c-fos [22].
• Displaceable relaxin binding sites are distributed in discrete regions of the olfactory system, neocortex, hypothalamus, hippocampus, thalamus, amygdala, midbrain, and medulla of the male and female rat brain [23].
• We conclude that NPAS2 plays a role in sleep homeostasis, most likely at the level of the thalamus and cortex, where NPAS2 is abundantly expressed [24].
• This coherent theta activity, the result of a resonant interaction between thalamus and cortex, is due to the generation of low-threshold calcium spike bursts by thalamic cells [25].

Anatomical context of Thalamus

• The additional observation that thalamus/neocortex follows the same evolutionary scaling law as LGN/V1 may suggest that neocortex generally conforms to the same organizational principle as V1 [12].
• After systemic administration to immature rodents, L-cysteine destroys neurons in the cerebral cortex, hippocampus, thalamus, and striatum, but the underlying mechanism has never been clarified [26].
• They then cross the midline and enter the ipsilateral hypothalamus, turn posteriorly, and continue into the ipsilateral thalamus [27].
• The patterns of transport also indicate the existence of neuronal populations that selectively transport NT-3 and/or BDNF, but not NGF, such as spinal cord motor neurons, neurons in the entorhinal cortex, thalamus, and neurons within the hippocampus itself [28].
• Moreover, immature oligodendrocytes were arrested in the vicinity of the thalamus, suggesting that the primary defects in DAP12(-/-) mice are the developmental arrest of osteoclasts and oligodendrocytes [1].

Associations of Thalamus with chemical compounds

• In contrast, addicts showed an increased response to methylphenidate in the thalamus (a region that conveys sensory input to the cortex) [29].
• Inhibition and synchrony in slices from mice devoid of the gamma-aminobutyric acid type-A (GABAA) receptor beta3 subunit were examined, because in rodent thalamus, beta3 is largely restricted to reticular nucleus [30].
• In infants 5 weeks of age and younger, glucose utilization was highest in the sensorimotor cortex, thalamus, midbrain-brainstem, and cerebellar vermis [31].
• Lateralization of norepinephrine in human thalamus [32].
• Purinergic inhibition of GABA and glutamate release in the thalamus: implications for thalamic network activity [33].

Gene context of Thalamus

• Cortical size, lamination, thalamus, and thalamocortical pathfinding are normal in homozygous nestin-Emx2 mice [34].
• Our results suggest that normal thalamocortical development requires the actions of Pax6 within the dorsal thalamus itself [35].
• Furthermore, Dlx1 and Dlx2 are not expressed in the dorsal thalamus or in cortical projections neurons [36].
• Reciprocal patterns of expression are found within the dorsal thalamus for the Gbx-2 and Wnt-3 genes [37].
• Consequently, development of the dorsal and ventral thalamus and anterior pretectum requires cooperation between Emx2 and Otx2, whereas Emx2 expression is incompatible with development of the commissural region of the pretectum [38].

Analytical, diagnostic and therapeutic context of Thalamus

• Northern blot and in situ hybridization analyses revealed that MGL mRNA is heterogeneously expressed in the rat brain, with highest levels in regions where CB(1) cannabinoid receptors are also present (hippocampus, cortex, anterior thalamus, and cerebellum) [39].
• Here, we addressed this issue by simultaneously recording the extracellular activity of up to 135 neurons in the primary somatosensory cortex, ventral posterior medial nucleus of the thalamus, and trigeminal brainstem complex of adult rats, before and after a reversible sensory deactivation was produced by subcutaneous injections of lidocaine [40].
• Ligand autoradiography confirmed the lack of high-affinity binding to radiolabeled nicotine, cytisine, and epibatidine in the thalamus, cortex, and caudate putamen, although binding to a number of discrete nuclei remained [41].
• In 23 patients with moderate to severe Huntington's disease (HD) and 21 normal volunteers, the regional cerebral metabolic rate of glucose consumption (rCMRGlc) was measured in the cerebellum, thalamus, striatum, and cortex using positron emission tomography and the 18F-deoxyglucose method [42].
• Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains [43].

References