Disease relevance of Pou3f3

• Rats were exposed to a physiological stimulus, i.e., running, or a brain insult, i.e., status epilepticus, which gave rise to neuronal death, inflammation, and chronic seizures [1].
• A model for medulloblastoma-like primitive neuroectodermal tumors was established in rat using retrovirally transduced SV40 large T antigen (LT) as an inducing agent (O. D. Wiestler et al., Brain Pathol., 2: 47-59, 1992) [2].
• CONCLUSIONS: Brain death causes progressive liver dysfunction, which is made worse by the coexistence of hemodynamic instability [3].
• BACKGROUND AND PURPOSE: Brain acidosis from cerebral ischemia is characterized by average intracellular pH levels of approximately 5.8-6.2, which appear in turn to worsen cellular injury [4].
• BACKGROUND AND PURPOSE: Brain temperature during ischemia is known to strongly influence the extent of cellular injury [5].

Psychiatry related information on Pou3f3

• However, the beta adrenergic receptor antagonist propranolol impairs consolidation of declarative memory in humans [Science 287 (2000) 248]; [Nature 371 (1994) 702] and consolidation and reconsolidation of inhibitory avoidance learning in rats [Brain Res 368 (1986) 125]; [J Neurosci 19 (1999) 6623] [6].
• In a previous study, we found that electrolytic lesions of the PRh produced retrograde amnesia, without a temporal gradient, for water-maze problems acquired 4 weeks and 2 days before surgery [Behav. Brain. Res. 114 (2000) 119] [7].
• We recently showed that over 70% of these c-Fos immunoreactive neurons are GABAergic [M. Morales, J.R. Criado, P.P. Sanna, S.J. Henriksen, F.E. Bloom, Acute ethanol induces c-fos immunoreactivity in GABAergic neurons of the central nucleus of the amygdala, Brain Res, 798 (1998) 333-336] [8].
• Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 microg/100 g, i.p.) precipitates an acute neuropathy, a model of Wernicke's encephalopathy in man (Zimitat and Nixon, Metab. Brain Dis. 1999;14:1-20) [9].
• To reveal brain regions most significantly related to individual differences in exploratory behaviour, oxidative metabolism was measured by cytochrome c oxidase histochemistry in 2 months old Wistar rats with persistently high (HE) or low (LE) exploratory activity in a novel environment [10].

High impact information on Pou3f3

• The deduced amino acid sequence of pCSC-1 displayed a striking degree of homology with the eel, rat brain-1, and rat brain-2 Na+ channel, thereby identifying pCSC-1 as a related member of the family of Na+ channel genes [11].
• BACKGROUND/AIMS: Brain stem premotor neurons control swallowing through contacts with both afferent neurons and motoneurons [12].
• We used a tissue culture system in which fetal rat dorsal root ganglia, treated to eliminate contaminating fibroblasts (Wood, P., 1976, Brain Res. 115:361--375), appear to recapitulate many aspects of the developing peripheral nervous system [13].
• The amount of prostaglandin D2 increased significantly in the preoptic/hypothalamic region of rat brain 1 hr after the intraperitoneal administration of the lipopolysaccharide, whereas such increase was not observed in rats pretreated with indomethacin [14].
• As deduced previously (LeVay, S., D. H. Hubel, and T. N. Wiesel (1975) J. Comp. Neurol. 159: 559-576; Hubel, D. H., and D. C., Freeman (1977) Brain Res. 122: 336-343), there were portions of the map in which the stripes followed curves approximating isoeccentricity lines, but this relationship was not very exact or consistent [15].

Chemical compound and disease context of Pou3f3

• Evaluated 24 h later, MC stabilization had resulted in highly significantly better neurologic scores (P<0.001), decrease mortality (P=0.002), less brain swelling (P<0.001), and smaller hematoma volume growth (P<0.001) compared with saline and compound 48/80 [16].
• CONCLUSION: Brain angiotensin II could play a role in the pressor mechanism of DOCA-salt hypertension by increasing release of vasopressin via type 1 receptors [17].
• Male Wistar rats with unilateral carotid ligation were exposed to arterial hypoxia (PaO2 20-23 torr for 20 min) while body temperature was controlled at 37 degrees C, 36 degrees C, or 34 degrees C. Brain cortical concentrations of ATP, phosphocreatine (PCr) and lactate were measured microfluorometrically [18].
• Intracerebroventricular (ICV) injection of streptozotocin (STZ) has been reported to impair cerebral glucose utilization and energy metabolism (Nitsch and Hoyer: Neurosci Lett, 128:199-202, 1991) and also to prejudice passive avoidance learning in adult rats (Mayer et al.: Brain Res 532:95-100, 1990) [19].
• 4. Brain slices from microsphere-embolized rats contained areas, which were not stained with triphenyltetrazolium chloride (TTC), to a similar degree on the 3rd, 7th and 28th days, indicating the genesis of cerebral infarction [20].

Biological context of Pou3f3

• In agreement with this, we found the transactivation domain of Brn-1, which we mapped between amino acids 119 and 237, significantly weaker than the transactivation domain of Tst-1/Oct6/SCIP [21].
• When promoters consisting of a single POU protein-binding site adjacent to a TATA box were used as reporters in transient transfections, Brn-1 proved to be a weaker transcriptional activator than Tst-1/Oct6/SCIP [21].
• Effect of chronic administration of duloxetine on serotonin and norepinephrine transporter binding sites in rat brain [22].
• BACKGROUND AND PURPOSE: Brain mitochondria have a substantial capacity to generate reactive oxygen species after ischemia when the components of the respiratory chain are reduced and molecular oxygen is present [23].
• RESULTS: Brain DHA content of postpartum dams fed the deficient diet was decreased by 21% compared with age-matched virgin control animals, with a reciprocal increase in docosapentaenoic acid (22:5n6) to 243% [24].

Anatomical context of Pou3f3

• Using RNase protection and Northern blot hybridization with specific rat brain Na+ channel gene probes, expression of the rat brain-1 Na+ channel was observed in rat myocardium, but no detectable expression of the rat brain-2 gene was found [11].
• No significant pathomorphological changes were observed in liver, kidney, brain and gonads of F(2B) pups [25].
• In previous study (Lewis, E.R., and C. W. Cotman (1980) Brain Res. 96: 307--330; E. R. Lewis and C. W. Cotman, submitted for publication), we have shown that septal tissues grafted to the brain of a neonatal rat will extend fibers into special terminal laminae within the hippocampal formation of the recipient [26].
• (Verhofstad, A. A. J., H. W. M. Steinbusch, B. Penke J. Varga, and H. W. J. Joosten (1981) Brain Res. 212: 39-49) have reported that serotonin of the rat superior cervical ganglion is contained in a distinct and separate population of small intensely fluorescent (SIF) cells [27].
• In contrast, ascending inputs to the lateral septum appear to define at least 20 vertically oriented bands or subdivisions arranged orthogonal to the hippocampal input (Risold, P.Y. and Swanson, L.W., Chemoarchitecture of the rat lateral septal nucleus, Brain Res. Rev., 24 (1997) 91-113) [28].

Associations of Pou3f3 with chemical compounds

• Individual nuclei were removed from 300-micrometers frozen sections according to the punch-out method of Palkovits (Palkovits, M. (1973) Brain Res. 59: 449-450), and the content of E2 receptor was measured with a sensitive radioligand binding method [29].
• The sequence of the cDNA was compared to that recently published for kidney (brain)-type glutaminase (Banner, C., Hwang, J.-J., Shapiro, R.A., Wenthold, R.J., Nakatani, Y., Lampel, K.A., Thomas, J.W., Huie, D., and Curthoys, N.P. (1988) Mol. Brain Res. 3, 247-254) [30].
• BACKGROUND AND PURPOSE: Brain dopamine has been implicated as a mediator of brain neuronal damage resulting from ischemic injury [31].
• BACKGROUND: Chronic treatment of rats with certain selective serotonin or norepinephrine reuptake inhibitors produces significant decreases, respectively, in serotonin and norepinephrine transporter binding sites in brain [22].
• The efflux transport of the substrates of system A, such as L-proline (L-Pro), glycine (Gly), and alpha-methylaminoisobutyric acid (MeAIB), across the BBB was investigated using the in vivo Brain Efflux Index method [32].

Regulatory relationships of Pou3f3

• Microtubule-associated protein 1B (MAP1B) is expressed mainly in the brain during early development and plays important roles in the regulation of microtubule dynamics which is essential to neurite outgrowth and elongation [33].
• Assessment by c-Fos Immunostaining of Changes in Brain Neural Activity Induced by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Leptin in Rats* [34].

Other interactions of Pou3f3

• Using a HO-1 cDNA probe, we examined the level of HO-1 mRNA in normal rat brain and in brain 1 and 6 h following heat shock [35].
• The "paracrine core" of the nervous system and its adjunct (1985, Nieuwenhuys, Chemoarchitecture of the Brain. Springer, Berlin) is very rich in calbindin D-28k [36].
• Age-dependent changes in NMDAR subunit gene expression were observed in hippocampi of rats chronically exposed to Pb2+ during development [T.R. Guilarte, J.L. McGlothan, Hippocampal NMDA receptor mRNA undergoes subunit specific changes during developmental lead exposure, Brain Res. 790 (1998) 98-107] [37].
• PURPOSE: To establish a method for isolating highly purified brain capillary endothelial cells (BCECs) from rat brain by using magnetic cell sorting, and clarify the expression levels of multidrug resistance-associated protein (Mrp) subtypes in these highly purified BCECs [38].
• It has been identified that insulin was present in the central nervous system (CNS) with some types of action there, and it exerted important actions within the brain and functions as neuropeptide [39].

Analytical, diagnostic and therapeutic context of Pou3f3

• SUMMARY BACKGROUND DATA: Brain death, regarded as a given condition in organ transplantation, could have significant effects on the donor organ quality [3].
• RESULTS: Brain sucrose uptake increased after 3 and 48 hours of reperfusion, with maximal opening at 48 hours and return to normal by 14 days [40].
• RESULTS: Brain myo-inositol increased by 17% after acute myo-inositol administration and by 5% after chronic administration, as compared with the control groups [41].
• METHODS: Brain infarct was created in rats by ligation of a branch of the left middle cerebral artery followed by permanent occlusion of the left common carotid artery and temporary occlusion of the right common carotid artery [42].
• BACKGROUND: Brain death has been identified as an independent risk factor for chronic allograft dysfunction [43].

References