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PubMed2004

The dual response of protein kinase Fyn to neural trauma: early induction in neurons and delayed induction in reactive astrocytes.

In the developing central nervous system, a src-related protein-tyrosine kinase fyn participates in the myelination process, neuronal growth, and cytoskeletal organization. In adults, fyn has been implicated in learning and memory formation. To test if fyn expression is modulated by neuronal activity, we performed quantitative in situ hybridization (ISH) using brain sections of the adult rats that had undergone either kainic acid (KA)-induced seizures or neuronal deafferentation (entorhinal cortex lesion, ECL). In the KA model, a few hours after seizure activities, fyn mRNA was elevated in the dentate gyrus (DG) (+45%), cerebral cortex layer III (+35%), and piriform cortex (+25%). Conversely, fyn mRNA consistently decreased in the hippocampal neurons after transection of the major axonal inputs from the entorhinal cortex. Although fyn expression in the brain has been allegedly limited to neurons and oligodendrocytes, we provide in this study the first evidence that fyn mRNA is highly expressed in the astrocytes involved in reactive gliosis. In the KA model, the occurrence of fyn-overexpressing astrocytes increased with the progress of neuronal damage in the CA1 and CA3 regions of the hippocampus. In contrast, fyn-overexpressing astrocytes were not observed in the granular cell layer of dentate gyrus (DG), where neurons were not damaged. Likewise, in the ECL model, the most drastic change in fyn mRNA expression took place at the reactive astrocytes near the stab wound sites, where fyn mRNA levels were doubled 4-10 d after the lesion. Collectively, our data suggest that (i) an early induction of fyn mRNA in neurons is linked to neuronal activity, and (ii) the delayed induction of fyn mRNA in reactive astrocytes near the damaged cells may play novel signaling roles during glial response.

Animals↗
PubMed1997

Opposite effects of GABAB receptor antagonists on absences and convulsive seizures.

In Wistar rats with spontaneous non-convulsive absence epilepsy, absence seizures were dose dependently suppressed by intraperitoneal administration of the GABAB receptor antagonists CGP 36742, 50-400 mg/kg, and CGP 56999, 0.25-0.75 mg/kg, and by bilateral microinjections of the same compounds into the lateral nuclei of the thalamus. In rats susceptible to audiogenic seizures, intraperitoneal administration of both GABAB receptor antagonists, at doses which suppressed absence seizures, facilitated the elicitation of sound-induced tonic seizures. In non-epileptic control rats, intraperitoneal injections of higher doses of CGP 36742 (800-2400 mg/kg) and CGP 56999 (3-6 mg/kg) induced delayed clonic convulsions, which were suppressed by pretreatment with baclofen. c-Fos protein was expressed after GABAB receptor antagonist-induced seizures in the cortex, hippocampus, amygdala, perirhinal and piriform cortex. Intra-cortical and hippocampal microinfusion of both GABAB receptor antagonists produced focal seizures. In conclusion, GABAB receptor antagonists suppress non-convulsive absence seizures by blocking thalamic GABAB receptors, while they induce convulsions in cortical and limbic structures.

Animals↗
PubMed2000

Regional expression and role of cyclooxygenase-2 following experimental traumatic brain injury.

Prostaglandins, potent mediators of inflammation, are generated from arachidonic acid (AA) via the action of cyclooxygenase-1 and -2 (COX-1 and COX-2). In this study, we report that lateral cortical impact injury in rats significantly increases COX-2 protein levels both in the cortex surrounding the injury site and the ipsilateral hippocampus. COX-2 protein level was elevated as early as 3 h postinjury and persisted for up to 3 days. Increases in immunoreactivity were detected not only in the adjacent cortex and hippocampus, but were also observed in the contralateral cortex and hippocampus, the ipsilateral piriform cortex and the ipsilateral amygdaloid complex. COX-2 immunoreactive cells appear morphologically normal and do not present any of the characteristic features of apoptosis. Double immunostaining experiments using either a neuron-specific or an astroglial-specific marker show that the expression of COX-2 is localized almost exclusively in neuronal cells. Administration of the COX-2 inhibitor 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzenesulfona mide (celecoxib, marketed as Celebrex) worsens motor, but not cognitive, performance, suggesting that COX-2 induction following traumatic brain injury may play a protective role.

Amygdala↗
PubMed2001

c-Fos expression in rat brain after repetitive transcranial magnetic stimulation.

We investigated neuronal response to repetitive transcranial magnetic stimulation (rTMS) and electroconvulsive shock (ECS) in terms of c-Fos expression. In rats at postnatal day 49, six rTMS sessions induced widespread nuclear c-Fos-like immunoreactivity in frontal cortex, lateral orbital cortex, striatum, lateral septal nucleus, piriform cortex, dentate gyrus, Ammon's horn, cingulate cortex, parietal cortex, thalamus, occipital cortex, and amygdala; this reactivity was greater than with two sessions of rTMS or sham rTMS. ECS produced even stronger c-Fos expression than six sessions of rTMS in all regions except thalamus (no difference) and striatum (stronger with rTMS). Thus, functional modification of neuroanatomic substrates as demonstrated by c-Fos expression may partially differ between rTMS and ECS.

Animals↗
PubMed1993

Fos immunoreactivity after stimulation or inhibition of muscarinic receptors indicates anatomical specificity for cholinergic control of striatal efferent neurons and cortical neurons in the rat.

Cholinergic neurons play a major role in the control of striatal activity via muscarinic receptors. The action of acetylcholine also appears to be dependent on the striosome-matrix compartmentalization of the striatum. This study was designed to find out whether modification of acetylcholine tone activates neurons in the striatum and forebrain of the rat. We looked for the appearance of immunoreactivity to Fos, a regulatory protein that is thought to convert synaptic signals into changes in gene expression. Pharmacological manipulation of muscarinic receptors was found to induce specific patterns of Fos immunoreactivity in distinct neuronal populations of the forebrain, including the striatum. Oxotremorine, a non-selective muscarinic agonist, induced Fos immunoreactivity in the striatum with a large predominance in striosomes (mostly in enkephalinergic neurons), in layers 4 and 6 of the cortex, and also in the piriform cortex and septum. The muscarinic agonist pilocarpine had an identical effect in the cortex, but the striosomal prevalence was less clear-cut than that observed after oxotremorine. Treatment with dopamine-depleting agents (6-hydroxydopamine or reserpine) and inhibitors of glutamate and opiate receptor (MK-801 and naloxone respectively) had no effect on the action of oxotremorine. This suggests that the induction of Fos provoked by oxotremorine does not involve dopamine, glutamate or opiates. Atropine, a non-specific muscarinic antagonist, also induced Fos immunoreactivity in the striatum but with matrix predominance (mostly in substance P neurons), as well as in the cingulate cortex, and the olfactory tubercle. Scopolamine, a muscarinic antagonist, induced Fos in both striosomal and matrix compartments in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1999

FAST and SLOW amygdala kindling rat strains: comparison of amygdala, hippocampal, piriform and perirhinal cortex kindling.

In our companion paper, we selectively bred offspring of a Long Evans Hooded and Wistar rat cross for either fast or slow rates of amygdala kindling (Racine et al., 1999. Development of kindling-prone and kindling resistant rats: Selective breeding and electrophysiological studies, Epilepsy Res. 35, 183-195). Within 10 generations, there was no overlap in the distribution of kindling rates between these newly developed FAST and SLOW kindling strains. In the present report, we compared the local excitability, kindling rates, and convulsion profiles of kindling sites in either the amygdala, dorsal hippocampus, piriform cortex or perirhinal cortex in the two strains. Local excitability, measured as the local afterdischarge (AD) threshold and its duration, showed varied effects between structures and strains. Before kindling, the AD threshold was lower in the FAST than the SLOW rats in the hippocampus, piriform and perirhinal cortices, but not the amygdala (the selection structure). Also, the duration of the AD threshold duration was significantly longer in the FAST than in the SLOW rats in all structures, except the CA1 hippocampus. Most of these differences were maintained after kindling. Kindling itself was significantly faster in the FAST compared with the SLOW rats in all structures; however, the different structural kindling rates showed proportional differences between strains that were about five times different in the amygdala compared with only about two times different in the hippocampus. This suggested a selection bias for the amygdala and its networks. As in other rat strains, the fastest kindling rates were seen in the perirhinal cortex followed by the piriform cortex, amygdala and hippocampus in both FAST and SLOW rats. Other important differences between strains and structures occurred in the stage-5 convulsion profiles, including latency to forelimb clonus, clonus duration and duration of associated local afterdischarges. The differences in kindling profiles between strains and structures were discussed with respect to possible underlying mechanisms, significance for epileptogenesis, and impact on other normal behaviours.

Amygdala↗
PubMed1998

Behavioral changes and expression of heat shock protein hsp-70 mRNA, brain-derived neurotrophic factor mRNA, and cyclooxygenase-2 mRNA in rat brain following seizures induced by systemic administration of kainic acid.

Kainic acid-induced seizures in rats represent an established animal model for human temporal lobe epilepsy. However, it is well-known that behavioral responses to the systemic administration of kainic acid are inconsistent between animals. In this study, we examined the relationship between expression of genes, neuropathological damage, and behavioral changes (seizure intensity and body temperature) in rats after systemic administration of kainic acid. The considerable differences in the response to kainic acid-induced seizures were observed in rats after a single administration of kainic acid (12 mg/kg i.p.). There was no detection of the expression of heat shock protein hsp-70 mRNA and HSP-70 protein in brain of vehicle-treated controls and in animals exhibiting weak behavioral changes (stage 1-2). A moderate expression of hsp-70 mRNA was detected throughout all regions (the pyramidal cell layers of CA1-3 and dentate gyrus) of the hippocampus, the basolateral, lateral, central and medial amygdala, the piriform cortex, and the central medial thalamic nucleus of rats that developed moderate seizures (stage 3-4). Marked expression of hsp-70 mRNA was detected in the all regions (cingulate, parietal, somatosensory, insular, entorhinal, piriform cortices) of cerebral cortex and all regions of hippocampus, and the central medial thalamic nucleus of the rats that developed severe seizures (stage 4-5). In addition, marked HSP-70 immunoreactivity was detected in the pyramidal cell layers of CA1 and CA3 regions of hippocampus, all regions (cingulate, parietal, somatosensory, insular, piriform cortices) of cerebral cortex, and the striatum of rats that developed severe seizures (stage 4-5). Furthermore, a marked expression of cyclooxygenase-2 (COX-2) mRNA and brain-derived neurotrophic factor (BDNF) mRNA levels by kainic acid-induced behavioral seizures (stage 3-4 or stage 4-5) was detected in all hippocampal pyramidal cell layers, granule layers of dentate gyrus, piriform cortex, neocortex, and amygdala. The present study suggest that the behavioral changes (seizure intensity and body temperature) and neuropathological damage after systemic administration of kainic acid are inconsistent between animals, and that these behavioral changes (severity of kainic acid-induced limbic seizures) might be correlated with gene expression of hsp-70 mRNA, COX-2 mRNA, and BDNF mRNA in rat brain.

Animals↗
PubMed1992

Cytoarchitecture and neural afferents of orbitofrontal cortex in the brain of the monkey.

The orbitofrontal cortex of the monkey can be subdivided into a caudal agranular sector, a transitional dysgranular sector, and an anterior granular sector. The neural input into these sectors was investigated with the help of large horseradish peroxidase injections that covered the different sectors of orbitofrontal cortex. The distribution of retrograde labeling showed that the majority of the cortical projections to orbitofrontal cortex arises from a restricted set of telencephalic sources, which include prefrontal cortex, lateral, and inferomedial temporal cortex, the temporal pole, cingulate gyrus, insula, entorhinal cortex, hippocampus, amygdala, and claustrum. The posterior portion of the orbitofrontal cortex receives additional input from the piriform cortex and the anterolateral portion from gustatory, somatosensory, and premotor areas. Thalamic projections to the orbitofrontal cortex arise from midline and intralaminar nuclei, from the anteromedial nucleus, the medial dorsal nucleus, and the pulvinar nucleus. Orbitofrontal cortex also receives projections from the hypothalamus, nucleus basalis, ventral tegmental area, the raphe nuclei, the nucleus locus coeruleus, and scattered neurons of the pontomesencephalic tegmentum. The non-isocortical (agranular-dysgranular) sectors of orbitofrontal cortex receive more intense projections from the non-isocortical sectors of paralimbic areas, the hippocampus, amygdala, and midline thalamic nuclei, whereas the isocortical (granular) sector receives more intense projections from the dorsolateral prefrontal area, the granular insula, granular temporopolar cortex, posterolateral temporal cortex, and from the medial dorsal and pulvinar thalamic nuclei. Retrograde labeling within cingulate, entorhinal, and hippocampal cortices was most pronounced when the injection site extended medially into the dysgranular paraolfactory cortex of the gyrus rectus, an area that can be conceptualized as an orbitofrontal extension of the cingulate complex. These observations demonstrate that the orbitofrontal cortex has cytoarchitectonically organized projections and that it provides a convergence zone for afferents from heteromodal association and limbic areas. The diverse connections of orbitofrontal cortex are in keeping with the participation of this region in visceral, gustatory, and olfactory functions and with its importance in memory, motivation, and epileptogenesis.

Afferent Pathways↗
PubMed2002

The mouse Laf4 gene: exon/intron organization, cDNA sequence, alternative splicing, and expression during central nervous system development.

The cerebral cortex is a tissue with a high degree of neuronal diversity. It consists of six cell layers with a unique set of neuronal subtypes. A crucial step in the process of cortical differentiation is the transition from a mitotically active neuroblast to a postmitotic young neuron. To identify genes involved in the control of this transition, we applied a novel method of cDNA subtraction based on mirror-orientation selection. One of the genes we have identified in our screening proved to be a mouse homolog of the human putative transcription factor LAF4. We identified alternatively spliced forms of mouse Laf4 that encode several forms of putative protein with potentially different transactivation functions. Two forms are expressed mainly during embryogenesis, whereas the other forms are expressed mainly in adults. We have found that Laf4 transcription becomes very quickly upregulated as soon as young cortical neurons leave the ventricular zone (VZ), the cortical-proliferative compartment. This coincides with the initial steps of cortical differentiation. Laf4 becomes downregulated in postnatal cortex, indicating its involvement in the transcriptional regulation of the early steps of cortical differentiation. We have also examined Laf4 expression in the brains of Sey and reeler mutants. Laf4 was downregulated in the lateroventral part of the cerebral cortex and completely lost in the piriform cortex of the Sey mutant embryos. We also compared its expression during central nervous system development with that of its closest homolog, Fmr2, a gene implicated in mental retardation in humans.

Alternative Splicing↗
PubMed1983

Afferent fibers to the cingular vocalization region in the squirrel monkey.

Three squirrel monkeys (Saimiri sciureus) received horseradish peroxidase injections in the anterior cingulate cortex at the level of the genu of the corpus callosum, a region yielding vocalization when electrically stimulated. Retrogradely labeled neurons were found at the cortical level within the dorsomedial and lateral prefrontal cortex (areas 9 and 10), orbital cortex (area 11), premotor cortex (areas 44, 6b, and 8), frontoparietal operculum, insula, cortex of the superior temporal sulcus, piriform cortex, subiculum, posterior cingulate, and retrosplenial cortex. Subcortical telencephalic projections came from the the claustrum, diagonal band of Broca, nucleus basalis Meynert, nuclei basalis lateralis and accessorius amygdalae, and cells at the periphery of globus pallidus. Diencephalic structures projecting to the anterior cingulate cortex were the thalamic nuclei anterior medialis, anterior ventralis, ventralis anterior, ventralis lateralis pars medialis, medialis dorsalis, pulvinaris medialis, centralis superior lateralis and limitans; the intralaminar nuclei paracentralis, centralis lateralis and parafascicularis; and the midline nuclei periventricularis, parataenialis, centralis superior, centralis inferior, centralis medialis, and reuniens. In the hypothalamus, projections came from the periventricular, lateral and posterior part, as well as the supramamillary nucleus. Midbrain afferent fibers came from the ventral tegmental area of Tsai, medial substantia nigra, reticular formation, area praerubralis, nucleus peripeduncularis, and periaqueductal gray. The most posterior labeled neurons were found in the locus ceruleus, dorsal tegmental nucleus of Gudden, nucleus annularis, nucleus centralis superior Bechterew, nucleus dorsalis raphae and the most dorsomedial part of the nucleus reticularis tegmenti pontis. Some of those projections have functional significance in the light of the hypothesis that the cingular cortex is involved in the volitional control of emotional reactions on the one hand and the influence of primary emotional reactions on intentional behavior on the other.

Afferent Pathways↗
PubMed2005

Molecular characterization and immunohistochemical localization of palmdelphin, a cytosolic isoform of the paralemmin protein family implicated in membrane dynamics.

Palmdelphin is a newly identified cytosolic isoform of paralemmin-1, a lipid raft-associated protein implicated in cell shape control. Like paralemmin-1, palmdelphin is phosphorylated, giving rise to electrophoretic band heterogeneity that is most pronounced in the brain. In ultracentrifugation and gel filtration palmdelphin behaves as a non-globular monomer. Its C-terminal region binds glutamine synthetase. Immunohistochemical analysis of the rat brain shows a prominent localization of palmdelphin in the cerebral cortex, hippocampus, amygdala, septum, indusium griseum, piriform cortex, nucleus supraopticus, and nucleus of the lateral olfactory tract. Many of the circumscript palmdelphin-positive areas are related to the olfactory system. Immunoperoxidase electron microscopy reveals a discontinuous distribution of palmdelphin immunoreactivity, in the form of spots scattered throughout the cytoplasm of selected neuronal perikarya and dendrites, including dendritic spines, often in association with endomembranes, and in a pattern which is similar to that of the cytoplasmic fraction of paralemmin-1. In subcellular fractionation experiments palmdelphin behaves as a cytosolic protein which, however, can be partially recruited from cytosol to the detergent-resistant fraction of a membrane/cytoskeletal cell ghost preparation. These observations suggest that palmdelphin may peripherally associate with endomembranes or cytoskeleton-linked structures.

Amino Acid Sequence↗
PubMed2005

Neuronal intranuclear inclusions and neuropil aggregates in HdhCAG(150) knockin mice.

We studied the development of neuronal intranuclear inclusions (NIIs), neuropil aggregates (NAs), and expression of expanded repeat polyglutamine protein in the HdhCAG(150) knockin mouse model of Huntington's disease (HD). Diffuse nuclear localization of huntingtin protein (htt) was noted initially within striatal neurons at approximately 28 weeks, followed by the development of striatal htt immunoreactive NIIs by approximately 40 weeks. Striatal NIIs were observed initially in clusters within the matrix compartment but subsequently became diffusely distributed throughout the striatum. In the oldest animals (107 weeks), NIIs were enlarged and diffuse nuclear htt immunoreactivity reduced. Expression of ubiquitin immunoreactive NIIs paralleled but lagged behind the expression of htt immunoreactive NIIs. Abundant NIIs were found by approximately 75 weeks in layers 3 and 4 of somatosensory cortex and in layer 2 of piriform cortex. In the oldest animals, greater than 100 weeks, some NIIs were found in many brain regions. NAs were found mainly within the globus pallidus and substantia nigra, perhaps reflecting expression in striatal terminals. Cyclic AMP response element binding protein (CBP) was not localized to NIIs, arguing against gross sequestration of this transcriptionally active protein. Comparison of the relative levels of a common polyglutamine epitope in HdhCAG(150) knockin and hprtCAG(146) knockin mice shows greater expression of the polyglutamine epitope in the phenotypically less aggressive HdhCAG(150) knockin line. HdhCAG(150) knockin mice may be a model of early pathologic changes in HD.

Aging↗
PubMed1997

Thyrotropin-releasing hormone (TRH) is markedly increased in the rat brain following soman-induced convulsions.

Soman is an organophosphorus (OP) compound which irreversibly inhibits acetylcholinesterase (AChE), the primary synaptic inactivator of acetylcholine. Resultant excessive cholinergic activity elicits generalized convulsions and brain lesions. Recent evidence suggests that other neurotransmitter/neuromodulator systems may be affected by the OP compounds as well. Since we have shown that both electrically and chemically induced seizures cause significant and prolonged increases in the neuropeptide thyrotropin-releasing hormone (TRH) in epileptogenic sites, we examined soman-induced convulsion effects on CNS TRH. Rats were injected with either soman (100 microg/kg SC; equivalent to 0.9 LD50) or saline and observed for convulsive activity. Forty-eight hours post injection, dramatic increases of TRH over control levels were seen in frontal cortex (30-fold), pooled cortex (24-fold), hippocampus (16-fold), piriform cortex (14-fold), entorhinal cortex (11-fold), and amygdala (2-fold). No change was observed in either hypothalamus or pituitary. Our results demonstrate, for the first time, a substantial effect of an OP on a specific neuropeptide system in vivo. The neurochemical and behavioral consequences of the soman-induced increases in TRH, especially in the frontal cortex, are presently unknown. Clearly, much more work is required to discern the exact role TRH has following soman exposure.

Animals↗
PubMed1999

Gas6, a ligand for the receptor protein-tyrosine kinase Tyro-3, is widely expressed in the central nervous system.

Gas6 (growth arrest specific gene-6) is a ligand for members of the Axl subfamily of receptor protein-tyrosine kinases. One of these receptors, Tyro-3, is widely expressed in the central nervous system. We have used biochemical and histological techniques, including in situ hybridization, to determine the expression patterns of Gas6 mRNA and protein during development. Gas6 is widely expressed in the rat central nervous system (CNS) beginning at late embryonic stages and its levels remain high in the adult. Gas6 is detected as a single 85 kDa protein, which is encoded by a single 2.5 kb mRNA species. At embryonic day 14 it is detected in the heart, blood vessels, testes, choroid plexus, and in the ventral spinal cord. In the adult, Gas6 is expressed in the cerebral cortex, (predominantly in layer V), the piriform cortex, and the hippocampus (areas CA1, CA3 and the dentate gyrus). It is also expressed in thalamic and hypothalamic structures, the midbrain, and in a subset of motor and trigeminal nuclei. In the cerebellum, it is expressed in Purkinje neurons and deep cerebellar nuclei. Protein S, a protein related to Gas6, is only detected at low levels in the CNS. The spatial and temporal profiles of Gas6 expression suggest that it could potentially serve as the physiologically relevant ligand for Tyro-3 in the postnatal rat nervous system.

Animals↗
PubMed1997

Amphetamine sensitization enhances regional c-fos expression produced by conditioned fear.

Chronically administered amphetamine can result in a paranoid psychosis that can be re-induced in former amphetamine abusers by psychological stressors. In an attempt to investigate the neurobiological correlates of this phenomenon, the present study examined the effects of prior D-amphetamine sensitization on regional c-fos expression induced by a psychological stressor. Rats received intermittent footshock in a distinctive environment for 30 min/day for three days. Three days after the last fear conditioning session, the animals received injections of saline or D-amphetamine (4 mg/kg, i.p.) once every second day for 16 days (eight injections in total). After a 14-day drug abstinent period, the animals were placed in the fear conditioning apparatus but without footshock. The amphetamine sensitization procedure significantly enhanced the effects of conditioned fear on c-fos expression in several brain regions. These included the cingulate cortex area 3, agranular insular cortex (layers 2 and 3), claustrum, piriform cortex, the shell region of the nucleus accumbens, medial striatum, ventral lateral septum, and CA3 and polymorphic layer of the hippocampal formation. These results indicate that D-amphetamine sensitization can have long-lasting effects on the neural circuitries activated by conditioned stressors.

Animals↗
PubMed2000

Chronic ethanol administration alters immunoreactivity for GABA(A) receptor subunits in rat cortex in a region-specific manner.

BACKGROUND: Chronic ethanol administration has a plethora of physiological effects. Among the most consistently observed findings is a change in the expression pattern of gamma-aminobutyric acid type A (GABA(A)) receptor subunits in the rat brain cortex. These findings led to the hypothesis of "subunit substitution" to account for changes in receptor function without changes in receptor number. METHODS: We used subunit (alpha1 and alpha4) specific antibodies and a combination of immunohistochemistry and immunoblotting to examine subregions of cortex (prefrontal, cingulate, motor, parietal, and piriform) for their response to 2 weeks of forced ethanol administration. RESULTS: Overall, cortical immunoreactivity for the alpha1 subunit was decreased and for the alpha4 subunit increased whether measured immunohistochemically or by immunoblotting. Piriform cortex exhibited a bidirectional change in GABA(A) receptor alpha1 and alpha4 immunoreactivity, similar to that previously observed in preparations of whole cortex. However, in parietal cortex, declines in alpha1 immunoreactivity (55 +/- 12% control value [CV] and 88.3 +/- 4.3% CV; immunohistochemistry and immunoblotting, respectively) were not accompanied by concomitant increases in alpha4 immunoreactivity (104 +/- 8% CV and 116 +/- 9.3% CV; immunohistochemistry and immunoblotting, respectively). Conversely, alpha4 immunoreactivity increased in cingulate cortex (210 +/- 30% CV and 134 +/- 9.5% CV; immunohistochemistry and immunoblotting, respectively) without a decline in alpha1 immunoreactivity (90 +/- 4% CV and 91.3 +/- 3.9% CV; immunohistochemistry and immunoblotting, respectively). Prefrontal and motor cortex exhibited GABA(A) receptor subunit peptide alterations, but these changes varied with the method of analysis. CONCLUSIONS: These findings demonstrate that ethanol dependence results in nonuniform changes in GABA(A) receptor subunit peptide levels across the rat brain cortex and suggest that mechanisms which subserve functional changes in receptor activity may vary in accordance with anatomic or cellular differences within the cortex.

Cerebral Cortex↗
PubMed2002

The decreased cellular expression of neuropeptide Y protein in rat brain structures during ethanol withdrawal after chronic ethanol exposure.

BACKGROUND: Neuropeptide Y (NPY) has been implicated in the alcohol-drinking behaviors of rodents. This study investigated the possible involvement of NPY in the neuroadaptational mechanisms to chronic ethanol exposure and its withdrawal. METHODS: Male Sprague-Dawley rats were treated either with Lieber-DeCarli ethanol diet or control diet for 15 days, and ethanol-fed rats were withdrawn for 0 and 24 hr. The protein expression of NPY was determined in cortical, hippocampal, amygdaloid, striatal, and hypothalamic structures by using the gold-immunolabeling histochemical procedure. RESULTS: It was found that ethanol withdrawal, but not ethanol treatment, produced significant reductions in NPY protein levels in (1) layers IV and V of the frontal and parietal cortex, (2) layer II of the piriform cortex, (3) the central and medial nuclei of the amygdala, and (4) the paraventricular nucleus of the hypothalamus in rat brain. Chronic ethanol exposure and its withdrawal had no effect on the NPY protein levels in layers II, III, and VI of the frontal and parietal cortex or cingulate gyrus, in hippocampal (CA1, CA2, CA3, and dentate gyrus) and striatal (caudate putamen and globus pallidus) structures, or in the ventro-medial hypothalamus and basolateral amygdala. However, chronic ethanol exposure and its withdrawal produced significant reductions in NPY protein levels in the arcuate nucleus of the hypothalamus and in layers IV and V of the cingulate gyrus. CONCLUSIONS: These results suggest that the decreased protein levels of NPY in the central and medial nuclei of the amygdala, as well as in the cortical and hypothalamic structures, during ethanol withdrawal may play an important role in the neuromechanisms of some ethanol withdrawal symptoms.

Alcohol Drinking↗
PubMed1992

Glucose transporter expression in brain. cDNA sequence of mouse GLUT3, the brain facilitative glucose transporter isoform, and identification of sites of expression by in situ hybridization.

Complementary DNAs encoding the mouse GLUT3/brain facilitative glucose transporter have been isolated and sequenced. The predicted amino acid sequence indicates that mouse GLUT3 is composed of 493 amino acids and has 83 and 89% identity and similarity, respectively, to the sequence of human GLUT3. In contrast to human GLUT3 mRNA, which can be readily detected by RNA blotting in all human tissues that have been examined, mouse GLUT3 mRNA was only present at significant levels in brain. In situ hybridization showed differential expression of GLUT3 mRNA in several regions of adult mouse brain. Specific expression was observed in the hippocampus, with GLUT3 mRNA levels being higher in areas CA1 to CA3 than in the dentate gyrus. It was also detected in the Purkinje cell layer of the cerebellum and in the cerebral cortex, with higher expression in the piriform cortex than in other regions of the cortex. Antisera to mouse GLUT3 immunoblotted a series of proteins of 45-50 kDa in mouse brain plasma membranes. These results are consistent with GLUT3 being a neuronal glucose transporter.

Amino Acid Sequence↗