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PubMed1995

Taurine allosterically inhibits binding of [35S]-t-butylbicyclophosphorothionate (TBPS) to rat brain synaptic membranes.

The modulatory effects of taurine on [35S]-t-butylbicyclophosphorothionate (TBPS) binding to rat brain synaptic membranes were evaluated and compared with that of GABA. Taurine allosterically inhibited TBPS binding by interacting with a bicuculline-sensitive site, similar to GABA. Taurine was as effective as GABA but less potent. The potency of taurine inhibition of TBPS binding varied among brain regions with cerebellum > olfactory bulb > cortex, similar to that of GABA. Inhibition of TBPS binding to cortical membranes measured under nonequilibrium conditions yielded a dynamic biphasic inhibition curve that was similarly shaped for GABA and taurine. The effect of taurine on TBPS binding was pharmacologically specific in that beta-alanine and guanadinoethanesulfonate were as effective as taurine, while hypotaurine and alpha-aminoethylhydrogen sulfate were only partially effective at high concentrations, and isethionic acid was without effect. Taurine, similar to GABA, enhanced the effects of pentobarbital on TBPS binding when present at concentrations that were otherwise ineffective on their own. The results of these studies support the notion that taurine interacts with the GABA recognition site of the GABAA receptor complex.

Allosteric Regulation↗
PubMed1992

Region-specific expression of GABAA receptor alpha 3 and alpha 4 subunits mRNAs in the rat brain.

The expression of mRNAs encoding the alpha 3 and alpha 4 subunits of the gamma-aminobutyric acid A (GABAA) receptor in the rat brain was investigated by in situ hybridization histochemistry. Both subunits showed a wide but uneven distribution, which did not coincide with the distribution of any other subunit so far reported. The cerebral cortex, anterior olfactory nucleus, lateral septum, subiculum, lateral and medial nuclei of the amygdaloid complex, anterior nuclei of the thalamus, pars compacta of the substantia nigra, trigeminal sensory nuclei, and cochlear nucleus were some of the areas where strong expression of mRNA for both the alpha 3 and alpha 4 subunits was detected. In the mitral cell layer of the olfactory bulb, the preoptic area and locus coeruleus, strong expression of only the alpha 3 subunit was detected. In the granular cell layer of the olfactory bulb, caudate-putamen, tenia tecta, pyramidal cell layer of the CA region and granular cell layer of the dentate gyrus in the hippocampal formation, dorsomedial and ventrolateral nuclei of the thalamus, dorsal part of the lateral geniculate body, preolivary nuclei and pontine nuclei, only the alpha 4 subunit showed strong expression. The diverse distribution of these two subunits is considered to indicate that each has a different role in the central nervous system.

Animals↗
PubMedDate not supplied

Cholecystokinin receptor binding levels in the genetically obese rat brain.

Cholecystokinin (CCK) receptor binding levels were compared between groups of genetically obese (fa/fa) and non-obese (Fa/-) Zucker rats of both sexes. The radioligand used was the iodinated octapeptide (CCK-8). Binding was measured in eight brain regions. The relative distribution among different brain regions of specifically bound CCK per mg protein was similar in all groups of animals. High binding levels were present in the olfactory bulb, cortex and caudate nucleus. Moderate levels were seen in hippocampus and hypothalamus, and low levels were observed in hindbrain, midbrain and thalamus. Obese animals of both sexes had significantly higher CCK receptor binding levels in the hippocampus and in the midbrain in comparison to lean controls. The male obese animals also had significantly elevated binding levels in the thalamic sample. These results demonstrate a correlation between genetic obesity and elevated CCK receptor binding levels in specific brain regions.

Animals↗
PubMedDate not supplied

Distinct binding sites for substance P and neurokinin A (substance K): co-transmitters in rat brain.

The distribution of binding sites in rat brain for iodinated neurokinin A and iodinated substance P were compared using autoradiography. Distinct patterns of binding for the two iodinated tachykinins were noted. Binding sites for iodinated neurokinin A were noted in the olfactory bulb, cortex, supraoptic n., paraventricular n., certain amygdaloid n., hippocampus, medial habenula, interpeduncular n., n. of the tractus solitarius, and dorsal horn of the spinal cord. This pattern was in contrast to low levels of binding of iodinated substance P to the cortex, supraoptic n., paraventricular n., and the interpeduncular n., but substantial density of binding sites in numerous other regions.

Animals↗
PubMed1994

Gastric inhibitory polypeptide (GIP) binding sites in rat brain.

Synthetic porcine gastric inhibitory polypeptide (GIP) was iodinated and purified by reverse-phase HPLC and used to localize saturable [125I]GIP binding sites by radioligand binding to frozen sections of rat brain followed by autoradiography. Saturable [125I]GIP binding sites were expressed in several brain regions including cerebral cortex, anterior olfactory nucleus, lateral septal nucleus, subiculum, inferior colliculus, and inferior olive. Saturable [125I]GIP binding was time dependent, reversible, high affinity, and specific for GIP. Scatchard analysis of equilibrium binding resulted in an estimated dissociation constant (Kd) of 16-62 pM for the rat brain [125I]GIP binding sites. Peptides with amino acid sequences similar to GIP such as secretin, vasoactive intestinal polypeptide (VIP), glucagon, and peptide histidine isoleucine (PHI) only partially inhibited saturable [125I]GIP binding at concentrations approximately 10,000-100,000-fold higher than GIP. Saturable [125I]GIP binding was not observed in other rat organs surveyed such as spinal cord, pituitary, stomach, small intestine, colon, pancreas, liver, heart, or skeletal muscle. We conclude that a saturable [125I]GIP binding site with the pharmacological properties of an authentic GIP receptor is expressed in certain regions of the rat brain.

Animals↗
PubMed1988

Regional localization of the mRNA coding for the neuropeptide cholecystokinin in the rat brain studied by in situ hybridization.

The regional localization of mRNA coding for the neuropeptide cholecystokinin (CCK) has been studied in the rat brain by in situ hybridization using a 32P-labelled synthetic 32 mer oligonucleotide. Autoradiograms were quantified using computer-assisted microdensitometry. High levels of hybridization were observed in the neocortex, claustrum, endopiriform nucleus, cingular cortex, amygdala, olfactory bulb, hippocampus, ventral tegmental area, geniculate nucleus, several thalamic nuclei and substantia nigra compacta. Very weak signal was detected in the striatum, the cerebellum and the brainstem. The topographic distribution of CCK neurons observed overlaps in part with that previously described by immunohistochemical techniques. However, some discrepancies were also found, particularly in the thalamus. These results show that in situ hybridization with oligonucleotide probes together with a semiquantitative method described can be used to map the expression of the CCK mRNA in rat brain sections as well as its modification after pharmacological or physiological manipulations.

Animals↗
PubMed1990

Autoradiographic localization of mas proto-oncogene mRNA in adult rat brain using in situ hybridization.

The cellular localization and the distribution of the mas proto-oncogene/angiotensin receptor mRNA have been studied in the male rat brain using in situ hybridization with radiolabelled mas cRNA probes. Neuronal cell populations in the forebrain were selectively labelled. A strong specific labelling was demonstrated in the dentate gyrus, the CA3 and CA4 areas of the hippocampus, the olfactory tubercle (medical part), the piriform cortex and the olfactory bulb, while a weak to moderate labelling was present all over the neocortex and especially in the frontal lobe.

Animals↗
PubMed1994

Time course of cholinergic and monoaminergic changes in rat brain after immunolesioning with 192 IgG-saporin.

192 IgG-saporin, an immunotoxin targeted at the low affinity NGF receptor, was infused into the lateral ventricle of rat brain. Three days and one week post lesion, choline acetyltransferase activity was markedly decreased in cortex, hippocampus, olfactory bulbs, and septum (brain regions innervated by the cholinergic neurons of the basal forebrain) with no change in cerebellum, striatum or pons. Measurement of monoamine levels revealed increases in HVA, DOPAC and dopamine, primarily in the olfactory bulbs at the 28-day time point only, suggesting a compensation for cholinergic inactivity. High levels of basal forebrain cholinergic lesioning can be obtained with this immunotoxin with minimal or no effects on monoaminergic or other cholinergic systems.

Animals↗
PubMed1995

Sleep deprivation increases brain serotonin turnover in the Djungarian hamster.

Djungarian hamsters well adapted to a short photoperiod were subjected to 4 h of total sleep deprivation (SD) by gentle handling. Tissue concentrations of monoamines and of their metabolites were measured from several brain areas using HPLC with electrochemical detection. The 5-hydroxyindoleacetic acid/5-hydroxytryptamine (5-HIAA/5-HT) ratio was significantly increased after SD in the hippocampus, hypothalamus and brain stem, indicating increased serotonin (5-HT) turnover in those areas, while no changes were found in the frontal cortex and olfactory bulb. Dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) concentrations were elevated in the hypothalamus, while the noradrenaline concentrations did not change in any of the measured areas. We conclude that a short SD, which has been shown to elevate EEG slow-wave activity during recovery sleep, specifically increases 5-HT turnover in the brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Region-specific expression of messenger RNAs encoding GABAA receptor subunits in the developing rat brain.

The distribution and levels of messenger RNAs encoding the alpha 1, beta 1, beta 2, beta 3, and gamma 2 subunits of the GABAA receptor in the developing and adult rat brain were investigated using quantitative in situ hybridization histochemistry and subunit-specific probes. Regional localization of the subunit messenger RNAs was determined with film autoradiography and expression in identified neuronal cell populations was examined using higher resolution techniques. Each of the GABAA receptor subunit messenger RNAs exhibits a distinct pattern of localization in the developing and adult brain. Of the subunits examined, the alpha 1, beta 2, and gamma 2 are the most abundant and are found in many brain regions, including the olfactory bulb, cortex, hippocampus, thalamic nuclei, and inferior colliculus. In addition, these subunit messenger RNAs are prominent in the cerebellum where virtually all cells of the deep cerebellar nuclei and Purkinje cell layer are labeled. The levels of most of the subunit messenger RNAs, with the exception of that encoding the beta 1 subunit, increase during postnatal development. While the alpha 1, beta 2, and gamma 2 subunit messenger RNAs rise in parallel in many regions and identified cell populations, different subsets of receptor subunit messenger RNAs are co-ordinately expressed at other sites. The greatest increases in subunit messenger RNA levels occur in the cerebellar cortex during the second postnatal week, a period coincident with cerebellar maturation. The co-distribution of different GABAA receptor subunit messenger RNAs in various regions of the developing and adult nervous systems supports the hypothesis that multiple receptor compositions exist. Moreover, that different subunit messenger RNAs exhibit coordinate changes in expression in different regions and cell populations suggests that receptor gene expression is modulated by cell type-specific signals. The temporal changes in subunit messenger RNA levels in the cerebellum raise the possibility that synaptogenesis may play a role in receptor gene regulation in this brain region.

Animals↗
PubMed1992

Effects of stress on opioid receptor binding in the rat central nervous system.

The endogenous opioid peptides are known to play a significant role in the modulation and/or mediation of numerous environmental or experimental stressors. However, the specific opioid peptide(s) and receptor type(s) involved, under what physiologic conditions they are engaged and within which regions of the CNS is not well understood. We therefore examined the effects of both a chronic and an acute stressor-90-h water deprivation and a single 20-min foot shock on opioid receptor binding in 17 specific rat brain nuclei. [3H]DSTLE (Tyr-D-Ser-Gly-Phe-Leu-Thr) and [3H]DAGO(Tyr-D-Gly-Phe-NMe-Phe-Gly-ol) were used to label delta and mu receptors, respectively. Foot shock induced profound antinociception as measured by tail-flick latency which outlasted the stressor by several minutes. However, only the septum responded with a decrease in [3H]DAGO binding to this type of stress-induced analgesia. No other alterations in either [3H]DAGO or [3H]DSTLE binding were seen in response to foot shock. In contrast, water deprivation induced increases in [3H-DAGO] binding in the septum as well as increases in [3H]DSTLE binding in the caudate and accumbens nuclei. Moreover, the presumptive mild stress of handling in the foot shock control group was sufficient to decrease mu or delta receptor binding in seven out of 17 brain regions investigated (including the frontal cortex and olfactory tubercle where both mu and delta binding were increased) when compared to unhandled deprivation control animals. These changes in opioid receptor binding may have been the result of alterations in treatment-induced peptide release, receptor regulation, or interactions with other released neurotransmitter ligand/receptor complexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1992

Calretinin and calbindin-D28k in rat brain: patterns of partial co-localization.

Calretinin and calbindin-D28k are homologous calcium-binding proteins, each present in a variety of neurons in the brain. Their distributions in the rat brain have been compared at the cellular level to determine whether they tend to occur in the same or in different cells, and to determine whether calbindin-positive cells show any common features once crossreaction with calretinin has been eliminated. The results show great heterogeneity. Most cells which contain one of the proteins do not contain the other, but many cells do contain both; even in the ventral cochlear nucleus, where there is abundant calretinin and most calbindin-like immunoreactivity is due to crossreaction, a few cells contain both proteins. In the substantia nigra and ventral tegmental area, many cells are double-positive but some only contain one or the other protein. Only the triangular septal nucleus is uniformly positive for both proteins. Cells which look like local-circuit neurons in many forebrain areas (cortex, hippocampus, olfactory bulb, anterior olfactory nucleus) are exclusively positive for either calretinin or calbindin, in spite of their similar morphology. In the more heterogeneous parts of the brain (including hypothalamus central gray and substantia gelatinosa), there are mixtures of calretinin-positive, calbindin-positive, and double-positive cells. In comparison with previous data on the chick, some aspects of the distributions are conserved, but double-positive cells are more frequent in the rat. The degree of heterogeneity observed, even within comparatively well-defined neuronal populations, makes it difficult to infer in what neuronal properties these proteins could be involved.

Animals↗
PubMed2004

Dietary restriction differentially protects from neurodegeneration in animal models of excitotoxicity.

Reduced caloric intake obtained through long-term dietary restriction has been found beneficial in some animal models of neurodegeneration. We report here that rats maintained under dietary restriction from the second to the eighth month of age are fully protected towards degeneration of GABAergic neurons in the hippocampus and the olfactory-entorhinal cortex caused by systemic administration of the convulsant toxin, kainic acid. However, in a different model of excitotoxic neurodegeneration, injection of ibotenic acid in the forebrain magnocellular basal nucleus, the decrease of a cholinergic marker in the target areas of the cortex was only partially protected by dietary restriction. Thus, in different experimental models neurodegeneration can be differentially rescued by dietary restriction. Analysis of alterations in the expression of relevant genes in different experimental conditions, could help in better understanding these differences.

Animals↗
PubMed2005

Time course of response to estradiol replacement in ovariectomized mice: brain apolipoprotein E and synaptophysin transiently increase and glial fibrillary acidic protein is suppressed.

The current study examined the effect of long-term estradiol replacement in ovariectomized mice. Estradiol-17beta (E2) pellets or vehicle pellets were implanted at the time of ovariectomy (OVX) in young adult female mice. Five mice from each group were sacrificed at 5, 14, 28 and 49 days after OVX and pellet replacement. Western blotting of homogenates from somatosensory cortex, hippocampus, olfactory bulb and cerebellum was performed to obtain concentrations of glial fibrillary acidic protein (GFAP), apolipoprotein E (apoE) and synaptophysin (SYN). At 5 days after OVX, GFAP levels were not affected by E2 replacement. In contrast to GFAP, synaptophysin and apoE concentrations were significantly elevated by 15% and 25%, respectively, in the E2-replaced group compared to the vehicle-replaced group at 5 days but by 14 days concentrations were equivalent. Late in the time course of this study, at 49 days, GFAP concentrations were higher in the E2-deprived mice but did not increase in the E2-replaced group. Immunocytochemistry for GFAP confirmed this observation. Of note was that these effects occurred in all four brain regions measured. These observations suggest that estradiol is able to suppress reactive gliosis. In addition, E2 replacement in OVX mice is associated with transiently higher levels of apoE and synaptophysin.

Animals↗
PubMed2005

Presence of splice variant forms of cytochrome P4502D1 in rat brain but not in liver.

Cytochromes P450 (P450), a family of heme-containing proteins, is involved in the oxidative metabolism of both foreign and endogenous compounds. Although liver is quantitatively the major organ involved in the metabolism of most xenobiotics, there is increasing evidence that these enzymes are present in extrahepatic tissues, such as lung, kidney, brain, etc and they may contribute to the in situ metabolism of xenobiotics in these organs. The possible relationship between genetic polymorphism seen in P4502D6 and incidence of neurodegenerative diseases, such as Parkinson's disease, has prompted the characterization of P4502D enzymes in rat brain. In the present study, we demonstrate that P4502D1 (the rat homologue of human P4502D6) is constitutively expressed in rat brain and the mRNA and protein are localized predominantly in neuronal cell population in the olfactory bulb, cortex, cerebellum, and hippocampus. An alternate spliced transcript of CYP2D1 having exon 3 deletion was detected in rat brain but not in liver. Deletion of exon 3 causes frame shift and generates a stop codon at 391 bp relative to the start codon ATG leading to premature termination of translation. Thus, Northern blotting and in situ hybridization represent contributions from functional transcripts and alternate spliced variants that do not translate into functional protein. Further, the splice variant having partial inclusion of intron 6 detected in human brain was not detected in rat brain indicating that alternate spliced gene products of P450 enzymes are generated in species-specific and tissue-specific manner.

Alternative Splicing↗
PubMed2005

In vivo and ex vivo MRI detection of localized and disseminated neural stem cell grafts in the mouse brain.

The application of stem cells as delivery vehicles opens up the opportunity for targeting therapeutic proteins to the damaged or degenerating central nervous system. Neural stem cell (NSC) lines have been shown to engraft, differentiate and correct certain central nervous system diseases. The present study was performed to test the ability of magnetic resonance imaging (MRI) in detecting transplanted NSCs under conditions of limited migration in the normal adult mouse brain versus widespread migration when the cells are transplanted neonatally. The C17.2 NSC line was labeled in vitro with superparamagnetic iron oxide (SPIO) particles and the labeled cells were implanted intracranially. Serial in vivo gradient echo MR imaging was performed using a 4.7 T horizontal bore magnet. High resolution ex vivo images of the isolated brains were performed at 9.4 T, and the presence of iron was correlated with Prussian blue staining in histological sections. Adult animals injected with SPIO-labeled stem cells exhibited hypointense regions near the injection site that were observed up to 32 days after injection. In neonatally transplanted animals, MR signal intensity from transplanted NSCs was not apparent in in vivo imaging but ex vivo MR images revealed small hypointense regions throughout the brain including the olfactory bulbs, cortex and the cerebellum, reflecting the wide distribution of the engrafted cells. These regions were correlated with Prussian blue staining, which confirmed the presence of SPIO particles inside the engrafted cells. We have shown that MRI is capable of differentiating localized and widespread engraftment of C17.2 stem cells in the central nervous system.

Animals↗
PubMed2004

Response to kainic acid injections: changes in staining for zinc, FOS, cell death and glial response in the rat forebrain.

A pool of zinc is present in synaptic vesicles in a population of glutamatergic neurones. Zinc appears to modulate synaptic transmission and cause neuronal death. The status of vesicular zinc, neuronal death and glial reaction in the rat forebrain was analysed after a systemic injection of kainic acid in order to establish a model for future studies on zinc function. Rats received a systemic injection of kainic acid (10 mg/kg) and were killed 3, 6, 12, 24 and 48 h post-treatment. Timm's method and zinquin staining were used to detect zinc. Immunostaining for Fos-like proteins and staining with Fluoro-Jade B were used to detect cell reaction and degeneration, respectively. Glial fibrillary acidic protein and tomato lectin were used as glial markers. Zinquin staining for zinc rose transitorily in neuronal somata 6 h after injection (not observed at 24-48 h) in the piriform and entorhinal cortices, amygdala and hippocampus. In contrast sulphide/silver staining for zinc showed virtually no rise in cytoplasmic zinc (except in cornus ammonis field 1 of the hippocampus) 6 h after injection, and a decrease (bleaching) in some terminal fields starting 12 h after injection and increasing at 24-48 h. The areas most affected by the zinc bleaching were the olfactory bulb, piriform and entorhinal cortices, endopiriform and amygdaloid nuclei. Transitory Fos immunostaining (within neuronal nuclei) was observed between 3 and 12 h after kainate treatment in many telencephalic areas: olfactory bulb, cortex (piriform, hippocampal and neocortex) and amygdaloid nuclei. This was accompanied by changes in glial markers starting 3 h after injection. Fluoro-Jade B staining in neurones (degeneration) appeared 6 h after treatment and increased later. Degenerating areas generally coincided with those showing Fos immunoreactivity. Zinquin and sulphide/silver methods revealed various pools of zinc after kainate injection: a cytoplasmic pool and a terminal field (or vesicular) pool. Cytoplasmic zinc (zinquin) was coincident, in time and location, with cell degeneration, thus implicating zinc in cell death. This zinc may not have come from presynaptic stores, since no bleaching (sulphide/silver method) was observed 6 h after injection. Future experiments altering zinc pools (e.g. by chelating agents) may elucidate the function of zinc.

Animals↗
PubMed2006

Anatomical localization of leucine-rich repeat kinase 2 in mouse brain.

Mutations in leucine-rich repeat kinase 2 (LRRK2) have recently been identified in autosomal dominant late-onset Parkinson's disease. Expression of LRRK2 has previously been reported in brain; however, no precise anatomical information is yet available. We have performed in situ hybridization and quantitative reverse transcription polymerase chain reaction to map LRRK2 mRNA expression in mouse brain. We find LRRK2 is highly expressed in the striatum, cortex and olfactory tubercle; however, little or no expression is found in the substantia nigra, where dopaminergic neurons preferentially degenerate in Parkinson's disease. These findings suggest that LRRK2 mRNA is expressed in dopamine-receptive areas rather than in the dopamine-synthesizing neurons. Consistent with a role LRRK2 in Parkinson's disease, dysfunction of leucine-rich repeat kinase 2 protein in dopamine-innervated areas may to lead to altered dopaminergic neurotransmission and degeneration of the nigro-striatal pathway.

Animals↗