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At least 865 records · Page 48Linked to original sources
PubMed1990

Opioid receptor-mediated inhibition of dopamine and acetylcholine release from slices of rat nucleus accumbens, olfactory tubercle and frontal cortex.

The modulation of the electrically evoked release of [3H]dopamine (DA) and [14C]acetylcholine (ACh) by opioid receptor activation was examined in superfused slices from rat nucleus accumbens, olfactory tubercle, and frontal cortex. In all brain areas examined, [3H]DA release was inhibited by the kappa agonist, U 50,488 (1-100 nM), and this inhibition was fully antagonized by the selective kappa antagonist, norbinaltorphimine (nor-BNI). In the frontal cortex, the mu agonist, [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAGO, 0.01-1 microM), also inhibited the evoked release of tritium. However, further experiments (including the use of the D2-receptor agonist, LY 171555, and the alpha 2-adrenoceptor agonist, oxymetazoline) suggest strongly that in the frontal cortex DAGO only inhibits the release of [3H]catecholamine from noradrenergic nerve terminals, despite the use of desimipramine to prevent the uptake of [3H]DA into these terminals. [14C]ACh release from both the nucleus accumbens and olfactory tubercle, but not from the frontal cortex, was inhibited by DAGO (0.01-1 microM) and the delta agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE, 0.01-1 microM). These inhibitory effects were antagonized by 0.1 microM naloxone but not by 3 nM nor-BNI. The irreversible delta ligand, fentanyl isothiocyanate (FIT, 1 microM), only antagonized the inhibition caused by DPDPE. The results indicate that the inhibitory effects of opioids on the in vitro release of DA from dopaminergic nerve fibres arising from the substantia nigra and the ventral tegmental area are mediated by presynaptic kappa receptors only. In those regions where ACh release is modulated by opioids, the type of opioid receptor involved may depend on the type of neuron, i.e. interneuron or afferent neuron.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1980

An experimental study of the ventral striatum of the golden hamster. I. Neuronal connections of the nucleus accumbens.

As part of an experimental study of the ventral striatum, the horseradish peroxidase (HRP) method was used to examine the afferent and efferent neuronal connections of the nucleus accumbens. Following iontophoretic applications or hydraulic injections of HRP in nucleus accumbens, cells labeled by retrograde transport of HRP were observed in the ipsilateral telencephalon in the posterior agranular insular, perirhinal, entorhinal, and primary olfactory cortices, in the subiculum and hippocampal field CA1, and in the anterior and posterior divisions of the basolateral amygdaloid nucleus. In the diencephalon, labeled neurons were present ipsilaterally in the central medial, paracentral and parafascicular intralaminar nuclei, and in the midline nuclei parataenialis, paraventricularis, and reuniens. Retrograde labeling was observed in the ipsilateral brainstem in cells of the ventral tegmental area and dorsal raphe. Many of these projections to nucleus accumbens were found to be topographically organized. Anterograde transport of HRP from nucleus accumbens demonstrated ipsilateral terminal fields in the ventral pallidum and substantia nigra, pars reticulata. The afferent projections to nucleus accumbens from the posterior insular and perirhinal neocortices, intralaminar thalamus, and the dopamine-containing ventral tegmental area are analogous to the connections of the caudatoputamen, as are the efferents from nucleus accumbens to the substantia nigra and ventral globus pallidus. These connections substantiate the classification of nucleus accumbens as a striatal structure and provide support for the recently proposed concept of the ventral striatum. Furthermore, the demonstration that a number of limbic system structures, including the amygdala, hippocampal formation, entorhinal cortex, and olfactory cortex are important sources of afferents to the nucleus accumbens, suggests that the ventral striatum may serve to integrate limbic information into the striatal system.

Amygdala↗
PubMed2003

Chronic hypoxia in development selectively alters the activities of key enzymes of glucose oxidative metabolism in brain regions.

The immature brain is more resistant to hypoxia/ischemia than the mature brain. Although chronic hypoxia can induce adaptive-changes on the developing brain, the mechanisms underlying such adaptive changes are poorly understood. To further elucidate some of the adaptive changes during postnatal hypoxia, we determined the activities of four enzymes of glucose oxidative metabolism in eight brain regions of hypoxic and normoxic rats. Litters of Sprague-Dawley rats were put into the hypoxic chamber (oxygen level maintained at 9.5%) with their dams starting on day 3 postnatal (P3). Age-matched normoxic rats were use as control animals. In P10 hypoxic rats, lactate dehydrogenase (LDH) activity in cerebral cortex, striatum, olfactory bulb, hippocampus, hypothalamus, pons and medulla, and cerebellum was significantly increased (by 100%-370%) compared to those in P10 normoxic rats. In P10 hypoxic rats, hexokinase (HK) activity in hypothalamus, hippocampus, olfactory bulb, midbrain, and cerebral cortex was significantly decreased (by 15%-30%). Neither alpha-ketoglutarate dehydrogenase complex (KGDHC, which is believed to have an important role in the regulation of the tricarboxylic acid [TCA] cycle flux) nor citrate synthase (CS) activity was significantly decreased in the eight regions of P10 hypoxic rats compared to those in P10 normoxic rats. In P30 hypoxic rats, LDH activity was only increased in striatum (by 19%), whereas HK activity was only significantly decreased (by 30%) in this region. However, KGDHC activity was significantly decreased in olfactory bulb, hippocampus, hypothalamus, cerebral cortex, and cerebellum (by 20%-40%) in P30 hypoxic rats compared to those in P30 normoxic rats. Similarly, CS activity was decreased, but only in olfactory bulb, hypothalamus, and midbrain (by 9%-21%) in P30 hypoxic rats. Our results suggest that at least some of the mechanisms underlying the hypoxia-induced changes in activities of glycolytic enzymes implicate the upregulation of HIF-1. Moreover, our observation that chronic postnatal hypoxia induces differential effects on brain glycolytic and TCA cycle enzymes may have pathophysiological implications (e.g., decreased in energy metabolism) in childhood diseases (e.g., sudden infant death syndrome) in which hypoxia plays a role.

Aging↗
PubMed1983

Regional differences in the development of cholecystokinin-like activity in rat brain.

The postnatal development of cholecystokinin (CCK) in rat brain was studied by radioimmunoassay and bioassay of tissue extracts. Marked differences were found in the patterns of development in different regions of the brain. In the cerebellum and brainstem of newborn rats the concentrations of CCK8-like immunoreactivity were 40-100% those in adults, whereas in more rostral regions the concentrations were 1-10% of those in adults. Between 0 and 14 days in concentrations of CCK-like activity measured by radioimmunoassay increased up to 30-fold in hypothalamus, cortex and olfactory bulb; in the cortex there were further increases up to 42 days. Cortical CCK was also measured by bioassay on rabbit gall bladder in vitro; bioactivity was identified in foetuses, and after birth showed a similar pattern of increase to that measured by radioimmunoassay. Immunoreactive material in extracts of neonatal cerebellum, brainstem and cortex was identified as CCK8 on the basis of cross-reactivity with different antisera, and chromatographic properties on gel filtration. The results raise the possibility of different rates of maturation of central CCKergic systems.

Animals↗
PubMed1996

Differential activation of microglia and astrocytes following trimethyl tin-induced neurodegeneration.

We have investigated the response of astrocytes and microglia to trimethyl tin intoxication in the septum, hippocampus, olfactory bulb, and pyriform cortex of the rat. Microglia were studied qualitatively using lectin histochemistry, and astrocytes were examined both qualitatively with immunohistochemistry, and quantitatively using an immunoassay for glial fibrillary acidic protein. Our results show that activated microglia first appeared 2 days after trimethyl tin intoxication in the lateral septum and hippocampus. Four days after trimethyl tin intoxication, the same regions revealed a most intense microglial reaction characterized by microglial hypertrophy and the formation of phagocytic clusters. By day 7, microglial activation in the septum and hippocampus had lessened, suggesting that the cells were reverting to the resting phenotype. The microglial response in the pyriform cortex and olfactory bulb, while being later in onset than in the septum and hippocampus, showed a similar progression of microglial changes reaching maximal intensity 7 days after trimethyl tin intoxication. Significant increases in the expression of glial fibrillary acidic protein were observed in all regions examined and typically occurred after microglial activation was already underway. We conclude that microglial and astroglial reactions which occur in response to trimethyl tin-induced neuronal necrosis are separated in time, with microglial activation preceding astrogliosis. In addition, our study stresses the importance of microglia as an endogenous source of CNS macrophages, and illustrates the merit of histochemical analysis with microglial markers for the early delineation of neurotoxicant-induced brain damage.

Animals↗
PubMed1998

Cloning and characterization of glial cell line-derived neurotrophic factor receptor-B: a novel receptor for members of glial cell line-derived neurotrophic factor family of neurotrophic factors.

Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor with diverse biological functions. Signal transduction of GDNF is mediated by binding to a glycosyl-phosphatidylinositol (GPI)-linked receptor GDNFR-alpha and activation of c-RET tyrosine kinase. The recent discovery of a new GDNF homolog neurturin raises the possibility that multiple receptors exist for the members in the GDNF family. Here we report isolation of the gene encoding a new receptor called GDNFR-beta. Sequence analysis indicated that GDNFR-beta is also a GPI-linked protein, with 47% identity to GDNFR-alpha. The GDNFR-beta transcript was preferentially expressed in the brain, spleen and lung, but moderate levels of GDNFR-beta mRNA were also found in kidney and the entire gastrointestinal track. In situ hybridization revealed high expression levels in the entorhinal cortex and olfactory bulb, followed by cortex, septum, inferior and superior colliculus, and zona inserta. A laminar pattern of expression was detected in layer III of the cortex. Treatment with GDNF of PC12 cells transfected with the GDNFR-beta gene activated mitogen-activated protein kinase (MAPK) and elicited neurite outgrowth. GDNFR-alpha and GDNFR-beta together form a new family of GPI-linked receptors for GDNF-like molecules.

Amino Acid Sequence↗
PubMed2003

Role of interferon-gamma and nitric oxide in the neuropathogenesis of avirulent Semliki Forest virus infection.

Semliki Forest virus (SFV) infection of mice provides a useful model for the analysis of viral neuropathogenesis. In this study, the roles of interferon (IFN)-gamma and nitric oxide (NO) in the pathogenesis of SFV infection were assessed using mice deficient in inducible nitric oxide synthase (iNOS-/-), an enzyme important in the production of NO, and mice deficient in IFN-gamma receptor (IFN-gammaR-/-). Gene-knockout and wildtype mice were infected intranasally with the avirulent A7 strain of SFV and neuropathological lesions were correlated with levels of IFN-gamma, tumour necrosis factor (TNF)-alpha and interleukin (IL)-10 in the olfactory bulbs and frontal cortex. Lesions in IFN-gammaR-/- mice were characterized by higher levels of neuronal necrosis than in wildtype mice. The higher levels of neuronal necrosis were associated with increased levels of SFV antigen in neurones and increased numbers of macrophages and B cells. Relative differences in the severity of demyelination between IFN-gammaR-/- and wildtype mice were not detected. Similar levels of neuronal necrosis and SFV antigen labelling occurred in iNOS-/- mice and wildtype mice and levels of demyelination and macrophage infiltration in the iNOS-/- mice were lower than those in the wildtype strain. A rapid, but transient increase in the concentration of IFN-gamma was demonstrated in the frontal cortex of all infected mice samples. IL-10 levels in the frontal cortex and olfactory bulbs of SFV-infected iNOS-/- mice exceeded those present in the wildtype mice. This study, taken with our previous reports, provides further evidence that type 1 T cell responses are important in the control of brain viral clearance and the prevention of neuronal necrosis, but not in the development of demyelination.

Alphavirus Infections↗
PubMed1992

Cloning of a novel somatostatin receptor, SSTR3, coupled to adenylylcyclase.

The gene encoding a novel mouse somatostatin receptor termed mSSTR3 was isolated and characterized. The sequence of mSSTR3 shows 46 and 47% identity with mSSTR1 and mSSTR2, respectively. mSSTR3 binds somatostatin-14 and somatostatin-28 with high affinity, but shows very low affinity for the somatostatin analogs MK-678 and SMS-201-995. In addition, mSSTR3 is coupled to pertussis toxin-sensitive G proteins and mediates somatostatin inhibition of forskolin-stimulated and dopamine D1 receptor-stimulated cAMP formation, indicating that it is coupled to adenylylcyclase. The pharmacological properties of mSSTR3 and its ability to couple with adenylylcyclase distinguish SSTR3 from the other cloned somatostatin receptors and indicates that it mediates biological functions different from SSTR1 or SSTR2. In situ hybridization indicates that SSTR3 mRNA is widely distributed in the mouse brain, and its expression in the nucleus of the lateral olfactory tract and in the piriform cortex, the primary olfactory cortex in the rodent brain, suggests that SSTR3 may participate in the processing and modulation of primary sensory information.

Adenylyl Cyclases↗
PubMed1992

Olfactory pathways and the sense of smell.

Rats were trained using operant conditioning to detect isoamyl acetate vapor generated by an olfactometer. They received lesions of olfactory pathways and were tested for retention of the odor detection task and trained on two-odor tasks. Deficits in odor detection and two-odor discrimination were related to the extent to which lesions disconnected the olfactory bulb from the forebrain. Transection of only the lateral olfactory tract, only the anterior limb of the anterior commissure, or lesions of the olfactory tubercle had little effect but combined lesions of these structures produced severe deficits in both odor detection and discrimination. Only rats with almost complete transection of the olfactory peduncle or cortex were anosmic; those with transections that spared a small segment of tissue between the olfactory bulb and olfactory cortex had detectable olfactory function. The results are discussed with regard to efferent connections of the olfactory bulb.

Animals↗
PubMed1999

Castration differentially alters [3H]nisoxetine binding to norepinephrine uptake sites in olfactory bulb and frontal cortex of male rats.

In the present study, [3H]nisoxetine binding to norepinephrine (NE) uptake sites and [3H]norepinephrine uptake were investigated within olfactory bulb (OB) and frontal cortex homogenates from intact and castrated male rats. Statistically significant reductions in the number of [3H]nisoxetine binding sites (Bmax) were found in OB from the castrates, while significantly increased Bmax values were obtained in the frontal cortex. Castration also significantly altered the affinity (Kd) of [3H]nisoxetine binding in the frontal cortex, but not in the OB. Assessment of [3H]norepinephrine uptake showed that in neither brain regions were there any statistically significant differences in Km nor Vmax between the castrated and intact male rats, indicating that the basal uptake process is not changed following castration in either of these brain areas. These results demonstrate the differential effects of castration upon [3H]nisoxetine binding sites between the OB and frontal cortex. Such findings provide new evidence for one of the mechanisms by which androgens may modulate central noradrenergic activity.

Animals↗
PubMed2005

Differential in vivo inhibition of [3H]nemonapride binding by atypical antipsychotics in rat striatum, olfactory lobes, and frontal cortex.

Dopamine D2 receptor blockade is thought to be mandatory for antipsychotic action because most of the currently used antipsychotics have high affinity at these receptors. Here, we examined the in vivo binding characteristics of the D2-like receptor antagonist [3H]nemonapride in rat brain areas including the striatum, olfactory lobes and frontal cortex and its inhibition by a series of D2 antagonist antipsychotics. In vivo affinity of [3H]nemonapride was similar (apparent Kd value: 0.05 micromol/kg) in all brain regions examined. The estimated number of binding sites was higher in the striatum (66 fmol/mg wet weight) than in the olfactory lobes (28 fmol/mg wet weight) and the frontal cortex (21 fmol/mg wet weight). In the striatum, [3H]nemonapride binding was inhibited in a dose-dependent manner with the following order of potency (ED50, mg/kg): nemonapride (0.04), raclopride (0.13), spiperone and risperidone (0.14), haloperidol (0.21), clozapine (7.2) and thioridazine (9.4); in the olfactory lobes: nemonapride (0.03), raclopride and spiperone (0.09), haloperidol (0.10), risperidone (0.15), thioridazine and clozapine (11); in the frontal cortex, only the high affinity dopamine D2 antagonist compounds nemonapride (0.05), haloperidol (0.09), and raclopride (0.12) significantly decreased the binding of [3H]nemonapride. The present data suggest that conventional and atypical antipsychotics may be distinguished by their differential occupancy of striatal versus frontocortical D2-like receptors in vivo.

Animals↗
PubMed1999

Regional distribution of metallothionein, zinc, and copper in the brain of different strains of rats.

The regional brain distribution of metallothionein (MT), zinc, and copper in the brain was determined in nine anatomical regions (olfactory bulb, cortex, corpus striatum, hippocampus, thalamus plus hypothalamus, pons plus medulla oblongata, cerebellum, midbrain, and white matter) and was compared between two different strains of rat (Sprague-Dawley [SD] and Lewis). No significant difference was observed in the whole-brain MT level between the two strains (17.8 +/- 3.4 microg/g in SD rats and 20.3 +/- 2.3 microg/g in Lewis rats). In SD rats, however, MT was more highly expressed in the white matter than in the other regions studied. In contrast, MT concentration was highest in the cortex and lowest in the olfactory bulb in Lewis rats. The MT levels in the cortex, corpus striatum, hippocampus, and thalamus plus hypothalamus were significantly lower in SD rats than in Lewis rats. In both strains, the olfactory bulb contained markedly higher levels of both zinc and copper than the other regions (27.9 +/- 6.8 microg/g zinc in SD rats and 27.6 +/- 6.9 microg/g zinc in Lewis rats, and 5.2 +/- 1.5 microg/g copper in SD rats and 11.1 +/- 4.8 microg/g copper in Lewis rats). The next highest zinc levels were seen in the hippocampus, whereas the next highest copper levels were in the corpus striatum in both SD and Lewis rats. The high levels of zinc and copper in the olfactory bulb were not accompanied by concomitant high MT concentrations. These results indicate that the strain of rat as well as the anatomical brain region should be taken into account in MT and metal distribution studies. However, the highest concentrations of zinc and copper in olfactory bulb were common to both SD and Lewis rats. The discrepancy between MT and the metal levels in olfactory bulb suggests a role for other proteins in addition to MT in the homeostatic control of zinc and copper.

Animals↗