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PubMed1995

Constitutive expression of metallothionein genes in mouse brain.

Metallothioneins (MTs) are ubiquitous low-molecular-weight proteins that are induced by a variety of inducers, including metals, lipopolysaccharides (LPS), cytokines, oxidative stress, etc., and are thought to play a protective role against various toxic insults. The constitutive level of metallothionein is an important determinant of a tissue's susceptibility to toxic insults. In the present study, we report the constitutive expression of MT mRNAs in adult mouse brain. Analysis of total RNA from whole brain by Northern blot and solution hybridization showed that mRNAs for all three MT isoforms (I, II, III) were constitutively expressed in mouse brain, and there was no remarkable difference in their expression. However, in quantitative terms the order of expression was MT-I > MT-III > MT-II. The expression of MT-III and MT-II was about 70 and 50% of that of MT-I, respectively. Examination of their constitutive expression in different brain regions revealed that the three isoforms were expressed in all seven brain regions studied (olfactory bulb, cortex, caudate, hippocampus, thalamus, cerebellum, and brain stem), and there was only about a twofold difference in MT mRNA expression from one region of the brain to another. However, olfactory bulb had the highest mRNA expression for all three isoforms, as revealed by slot blot analysis. Constitutive expression of MT-I and -II mRNA, but not MT-III mRNA, was high in cerebellum. In order to study the cellular localization of MT mRNA, in situ hybridization of MT-I and MT-III mRNA was performed. For comparison, LPS was used to enhance MT-I mRNA signal because LPS is a good inducer of MT-I mRNA expression in mouse brain. In situ hybridization revealed that certain brain regions had distinctly localized high levels of expression of MT mRNAs. In brains of untreated mice, the constitutive expression of MT-I mRNA was high in the ependymal cell layer lining the lateral ventricles and in the Purkinje cell layer of cerebellum. The signal in the Purkinje cell layer was not on the Purkinje cells themselves, but was on locations consistent with that of glial cells. In LPS-treated mice, the signal in cerebellum was higher, and distinct signal appeared in the choroid plexus. However, signal in ependyma was similar to that in untreated mice. Pia mater in LPS-treated, but not in untreated, mouse brain showed enhanced signal for MT-I mRNA.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Transneuronal transport of peroxidase-conjugated wheat germ agglutinin (WGA-HRP) from the olfactory epithelium to the brain of the adult rat.

The sensory neurons of the olfactory epithelium, as a consequence of their odor detection function, contact both the external environment and the central nervous system. The possibility that substances applied to the epithelium might reach the central nervous system was investigated by the intranasal application of peroxidase-conjugated wheat germ agglutinin (WGA-HRP). WGA-HRP was transported through olfactory receptor axons to the glomerulus of the olfactory bulb. Reaction product was localized electron microscopically to tubulovesicular profiles and dense bodies in sensory axons. Evidence of transneuronal transport was indicated by reaction product localized in dense bodies in dendrites postsynaptic to receptor cell axons. Periglomerular, tufted and mitral cells in the olfactory bulb also were transneuronally labeled. Anterograde transneuronal labeling occurred in the olfactory tubercle, piriform cortex and surrounding the lateral olfactory tract. Retrograde transneuronal label was found in neurons of the basal forebrain with the largest number of perikarya in the lateral nucleus of the horizontal limb of the diagonal band, a major source of cholinergic afferents to the olfactory bulb. These data suggest that substances, specifically those which bind to receptors, are transported from the olfactory receptor neurons in the nasal epithelium to the brain. Thus, the olfactory system may provide a route of entry for exogenous substances to the basal forebrain.

Animals↗
PubMed2006

Localization of the scaffolding protein RACK1 in the developing and adult mouse brain.

RACK1 is a multifunctional scaffolding protein known to be involved in the regulation of various signaling cascades in the central nervous system (CNS). In order to gain insight into the neurological functions of RACK1, we examined the expression of RACK1 mRNA and protein during gestation and in the adult mouse brain. Several expression patterns were observed. At embryonic day 11.5 (E11.5), RACK1 is expressed in a high-dorsal to low-ventral gradient throughout the brain. At E13.5, RACK1 is most abundant in the telencephalon. In the developing cortical primordium, RACK1 protein is expressed in a high-rostromidline to low-caudolateral gradient that appears to be regulated post-transcriptionally. At E18.5, RACK1 is expressed most abundantly in layers 1-4 of the cortex, striatum, hippocampus, dentate gyrus and specific thalamic nuclei. In the adult mouse, RACK1 is ubiquitously expressed in neuronal perikarya in most brain regions, with relatively higher levels in hippocampus, olfactory bulb, cortex and cerebellum. Subcellular staining was detected mainly in the cell bodies and extending into dendrites, whereas RACK1 was not present significantly in axonal fibers or nuclei. We also determined brain regions in which RACK1 interacts with one of its binding partners, the betaII isoform of protein kinase C (betaIIPKC). We found that betaIIPKC had a much more restricted expression pattern than RACK1 and overlapped with the scaffolding protein only in certain regions, including the CA1 area of the hippocampus, cerebellum and striatum. Our results suggest an important role for RACK1 during CNS development and support multiple functions of the protein in the adult brain.

Animals↗
PubMedDate not supplied

NGF-mediated alteration of NF-kappaB binding activity after partial immunolesions to rat cholinergic basal forebrain neurons.

There are age-associated cognitive and cholinergic deficits in the neurotrophin-dependent cholinergic basal forebrain neurons (CBFNs). There are also increases in the activity of the transcription factor NF-kappaB in the aged rodent brain that may reflect chronic enhancement of stress response signaling. We used partial immunolesions (PIL) to CBFN to examine the role of endogenous NGF on choline acetyltransferase (ChAT) activity and NGF-mediated NF-kappaB alteration after cholinergic deafferentation. We injected 192 IgG-saporin, an immunotoxin selectively taken up by neurotrophin receptor p75(NTR)-bearing neurons, into lateral ventricles, followed by infusions of anti-NGF to assess NF-kappaB, ChAT and NGF responses to PIL after anti-NGF infusion. Treatment with anti-NGF decreased ChAT activity by 17-34% in the cortex, hippocampus, and olfactory bulb and PIL decreased ChAT activity by 47-73%. Changes in AChE activity levels paralleled those observed for ChAT after PIL. NGF protein levels in the olfactory bulb, but not the cortex or hippocampus, increased significantly after PIL treatment. Infusion of anti-NGF abolished the PIL-induced eight-fold NGF increase in CNS. NF-kappaB binding activity to the IgG-kappaB and ChAT specific NF-kappaB consensus sequences, increased in the cortex but not hippocampus after PIL followed by anti-NGF infusion. It is likely that immunolesion-induced changes in ambient NGF levels may perturb NF-kappaB activity.

Acetylcholinesterase↗
PubMed1999

Afferents to the rostral olfactory bulb in sheep with special emphasis on the cholinergic, noradrenergic and serotonergic connections.

The olfactory bulb (OB) is involved in the processing of olfactory information particularly through the activation of its afferents. To localize their cell origin in sheep, a specific retrograde fluorescent tracer, Fluoro-Gold, was injected into the olfactory bulb of seven ewes. By using immunocytochemical techniques, retrogradely labeled neurons were colocalized with choline acetyltransferase, tyrosine hydroxylase, dopamine-beta-hydroxylase and serotonin to characterize cholinergic, noradrenergic and serotonergic Fluoro-Gold-labeled neurons. Most afferents originated from the ipsilateral side of the injection site. The OB received major inputs from the anterior olfactory nucleus (AON), the piriform cortex (PC), the olfactory tubercle, the diagonal band of Broca (DBB) and the amygdala. Other retrogradely labeled neurons were observed in the taenia tecta, the septum, the nucleus of the lateral olfactory tract, the preoptic area, the lateral hypothalamic area, the mediobasal hypothalamus, the lateral part of the premammillary nucleus, the paraventricular nucleus of the hypothalamus, the paraventricular thalamic nucleus, the central grey, the substantia nigra (SN), the ventral tegmental area (VTA), the lateral nucleus to the interpeduncular nucleus (IIP), the raphe and the locus coeruleus (LC). Contralateral labeling was also found in the AON, the PC, the SN compacta, the VTA, the IIP and the LC. Cholinergic Fluoro-Gold-labeled neurons belonged to the horizontal and vertical branch of the DBB. Noradrenergic afferents came from the LC and serotoninergic afferents came from the medial raphe nuclei and the 1IP. These data are discussed in relation with olfactory learning in the context of maternal behavior in sheep.

Animals↗
PubMed2000

Characterization of [(3)H]Quisqualate binding to recombinant rat metabotropic glutamate 1a and 5a receptors and to rat and human brain sections.

We have investigated the binding properties of [(3)H]quisqualate to rat metabotropic glutamate (mGlu) 1a and 5a receptors and to rat and human brain sections. Saturation isotherms gave K:(D) values of 27 +/- 4 and 81 +/- 22 nM: for mGlu1a and mGlu5a receptors, respectively. Several compounds inhibited the binding to mGlu1a and mGlu5a receptors concentration-dependently. (S:)-4-Carboxyphenylglycine, (S:)-4-carboxy-3-hydroxyphenylglycine, and (R,S)-1-aminoindan-1,5-dicarboxylic acid, which completely inhibited [(3)H]quisqualate binding to the mGlu5a receptor, were inactive in a functional assay using this receptor. The distribution and abundance of binding sites in rat and human brain sections were studied by quantitative receptor radioautography and image analysis. Using 10 nM: [(3)H]quisqualate, a high density of binding was detected in various brain regions with the following rank order of increasing levels: medulla, thalamus, olfactory bulb, cerebral cortex, spinal cord dorsal horn, olfactory tubercle, dentate gyrus molecular layer, CA1-3 oriens layer of hippocampus, striatum, and cerebellar molecular layer. The ionotropic component of this binding could be inhibited by 30 microM: kainate, revealing the distribution of mGlu1+5 receptors. The latter were almost completely inhibited by the group I agonist (S:)-3,5-dihydroxyphenylglycine. The binding profile correlated well with the cellular sites of synthesis and regional expression of the respective group I receptor proteins revealed by in situ hybridization histochemistry and immunohistochemistry, respectively.

Animals↗
PubMed2005

Cyto- and chemoarchitecture of the monotreme olfactory tubercle.

This study was undertaken to determine whether the olfactory tubercles of two monotremes (platypus and echidna) showed cyto- or chemoarchitectural differences from the tubercles of therian mammals. Nissl staining was applied in conjunction with enzyme reactivity for NADPH diaphorase and acetylcholinesterase, and immunoreactivity for calcium binding proteins (parvalbumin, calbindin and calretinin) and tyrosine hydroxylase (echidna only). Golgi impregnations of the tubercle were also available for the echidna. The olfactory tubercle is a poorly laminated structure in the echidna, despite the pronounced development of other components of the echidna olfactory system, and the dense cell layer of the olfactory tubercle was found to be discontinuous and irregular. Granule cell clusters (islands of Calleja) were present, but were small, poorly defined and did not show the intense NADPH diaphorase activity seen in marsupial and placental mammals. A putative small island of Calleja magna was seen in only one echidna out of four. In Golgi impregnations of the echidna olfactory tubercle, the most abundant neuron type was a medium-sized densely spined neuron similar to that seen in the olfactory tubercle of some therians. Large spine-poor neurons were also seen in the polymorphic layer. In the platypus, the olfactory tubercle was very small but showed more pronounced lamination than the echidna, although no granule cell clusters were seen. In both monotremes, the development of the olfactory tubercle was poor relative to other components of the olfactory system (bulb and piriform cortex). The small olfactory tubercle region in the platypus is consistent with poor olfaction in that aquatic mammal, but the tubercle in the echidna is more like that of a microsmatic mammal than other placentals occupying a similar niche (e.g., insectivores).

Animals↗
PubMed2003

Time course of early motor and neuropathological anomalies in a knock-in mouse model of Huntington's disease with 140 CAG repeats.

Huntington's disease (HD) is caused by an abnormal expansion of CAG repeats in the gene encoding huntingtin. The development of therapies for HD requires preclinical testing of drugs in animal models that reproduce the dysfunction and regionally specific pathology observed in HD. We have developed a new knock-in mouse model of HD with a chimeric mouse/human exon 1 containing 140 CAG repeats inserted in the murine huntingtin gene. These mice displayed an increased locomotor activity and rearing at 1 month of age, followed by hypoactivity at 4 months and gait anomalies at 1 year. Behavioral symptoms preceded neuropathological anomalies, which became intense and widespread only at 4 months of age. These consisted of nuclear staining for huntingtin and huntingtin-containing nuclear and neuropil aggregates that first appeared in the striatum, nucleus accumbens, and olfactory tubercle. Interestingly, regions with early pathology all receive dense dopaminergic inputs, supporting accumulating evidence for a role of dopamine in HD pathology. Nuclear staining and aggregates predominated in striatum and layer II/III and deep layer V of the cerebral cortex, whereas neuropil aggregates were found in the globus pallidus and layer IV/superficial layer V of the cerebral cortex. The olfactory system displayed early and marked aggregate accumulation, which may be relevant to the early deficit in odor discrimination observed in patients with HD. Because of their early behavioral anomalies and regionally specific pathology, these mice provide a powerful tool with which to evaluate the effectiveness of new therapies and to study the mechanisms involved in the neuropathology of HD.

Animals↗
PubMed1984

Origin and plastic properties of late components evoked in the rat's but not in the armadillo's prepyriform cortex.

Following ipsilateral olfactory bulb (IOB) stimulation long-latency (62-89 ms) gross and unit responses were evoked in the prepyriform cortex of rats prepared under urethane or pentobarbital, but were absent in 23 armadillos explored under the same anesthetics. Depth profile and current source density analysis revealed that generators of early and late components (LC) lie within cortical layers Ia-Ib, suggesting that LC may represent a compound depolarizing excitatory postsynaptic potential, generated by recurrent excitation of pyramidal cells. LC satisfied, in addition, several parametric requirements for habituation, favoring the hypothesis that late response waning following a period of predictable, repetitive and invariant stimulation, might be related to behavioral habituation to odors.

Animals↗
PubMed1992

Two vertebrate homeobox genes related to the Drosophila empty spiracles gene are expressed in the embryonic cerebral cortex.

We cloned two homeobox genes, Emx1 and Emx2, related to empty spiracles, a gene expressed in very anterior body regions during early Drosophila embryogenesis, and studied their expression in mouse embryos. Emx1 expression is detectable from day 9.5 of gestation whereas Emx2 appears to be already expressed in 8.5 day embryos. Both genes are expressed in the presumptive cerebral cortex and olfactory bulbs. Emx1 is expressed exclusively there, whereas Emx2 is also expressed in some neuroectodermal areas in embryonic head including olfactory placodes in earlier stages and olfactory epithelia later in development.

Amino Acid Sequence↗
PubMed2006

Increased olfactory sensitivity in euthymic patients with bipolar disorder with event-related episodes compared with patients with bipolar disorder without such episodes.

OBJECTIVE: Some patients with bipolar disorder experience mood episodes following emotional life events, whereas others do not. There is evidence that orbitofrontal hypoactivity may be related to this, because the orbitofrontal cortex is involved in the regulation of emotional and behavioural responses to external events. The close anatomical and functional connection between the orbitofrontal cortex and olfactory processing suggests that patients with bipolar disorder and heightened emotional reactivity may exhibit altered olfactory function compared with patients with bipolar disorder who do not exhibit this sensitivity. METHODS: In this pilot study, olfactory function was assessed in patients with bipolar disorder and a history of event-triggered episodes (n = 7) and in patients with bipolar disorder without such a history (n = 9) at the Department of Psychiatry and the Taste and Smell Clinic of the University of Dresden, Germany. Each patient's bipolar disorder was in remission at study entry, and they were on monotherapy with mood stabilizers. Assessment included olfactory event-related potentials (ERP) and psychophysical tests for odour threshold, odour identification and olfactory quality discrimination. RESULTS: Odour thresholds were lower in patients with bipolar disorder and event-triggered episodes compared with the other patient group. In addition, patients with event-triggered episodes exhibited shorter N1 peak latencies of the olfactory ERP. CONCLUSIONS: Our findings indicate disinhibition of orbitofrontal areas involved in the processing of emotional events in a subset of patients with bipolar illness.

Adult↗
PubMed1993

Muscarinic receptor-mediated induction of Fos protein in rat brain.

Recent studies have shown that the centrally active muscarinic agonist pilocarpine induces c-fos mRNA in rat cortex. Here we describe the localization of muscarinic receptor-induced FOS protein, within the rat central nervous system (CNS), following administration of pilocarpine (25 mg/kg). High levels of FOS induction were apparent in many forebrain structures including the primary olfactory (piriform) cortex, nucleus accumbens, amygdala, hippocampus, neocortex and supra-optic nucleus of the hypothalamus. Within the neocortex FOS induction followed a laminar distribution being highest in layers 4 and 6 with lower induction seen in layers 2 and 5. Other areas showing FOS induction included the striatum, septum, inferior colliculus, thalamus, hypothalamus and several brainstem nuclei. Both atropine (10 mg/kg) and pirenzepine (100 mg/kg) reduced FOS induction suggesting that a pirenzepine-sensitive muscarinic receptor was involved. The possible significance of muscarinic-mediated FOS induction, to cholinergic kindling and the cholinergic hypothesis of learning and memory, is discussed.

Animals↗
PubMed2004

Odors detected by mice deficient in cyclic nucleotide-gated channel subunit A2 stimulate the main olfactory system.

It is believed that odor transduction in the mammalian main olfactory system only involves the cAMP-signaling pathway. Here, we report on odor responsiveness in mice with a disrupted cyclic nucleotide-gated (CNG) channel subunit A2. Several odorants, including putative pheromones, can be detected and discriminated by these mice behaviorally. These odors elicit responses in the olfactory epithelium, main olfactory bulb, and olfactory (piriform) cortex of CNGA2 knock-out mice. In addition, responses to odors detected by CNGA2 knock-out mice are relatively insensitive to inhibitors of the cAMP pathway. These results provide strong evidence that cAMP-independent pathways in the main olfactory system of mammals participate in detecting a subset of odors.

Animals↗
PubMed2004

Members of the Wnt, Fz, and Frp gene families expressed in postnatal mouse cerebral cortex.

The functions of Wingless-Int (Wnt) signaling, studied intensely in embryonic brain development, have been comparatively little investigated in the postnatal brain. We report remarkably patterned gene expression of Wnt signaling components in postnatal mouse cerebral cortex, lasting into young adulthood. Wnt genes are expressed in gene-specific regional and lamina patterns in each of the major subdivisions of the cerebral cortex: the olfactory bulb (OB), the hippocampal formation, and the neocortex. Genes encoding Frizzled (Fz) Wnt receptors, or secreted Frizzled-related proteins (sFrps), are also expressed in regional and lamina patterns. These findings suggest that Wnt signaling is active and regulated in the postnatal cortex and that different cortical cell populations have varying requirements for a Wnt signal. The OB, in particular, shows gene expression of a large variety of Wnt signaling components, making it a prime target for future functional studies. The penultimate components of the canonical Wnt pathway are the Tcf/Lef1 transcription factors, which regulate transcription of Wnt signaling target genes. Surprisingly, we found little Tcf/Lef1 expression in the postnatal neocortex. These observations suggest that noncanonical Wnt pathways predominate, which will require functional testing. However, Lef1 is widely expressed in the dorsal thalamus, and Wnt ligands and receptors are expressed, respectively, in cortical areas and thalamic nuclei that are interconnected. Thus, canonical Wnt signaling could be utilized in a major cortical input by Fz- and Lef1-expressing thalamic cells that innervate the Wnt-expressing cortex.

Animals↗
PubMed1994

Regional and temporal pattern of expression of nerve growth factor and basic fibroblast growth factor mRNA in rat brain following electroconvulsive shock.

We have previously reported that focally evoked limbic motor seizures rapidly increase levels of mRNA encoding nerve growth factor (NGF) and basic fibroblast growth factor (bFGF) in specific limbic system areas of the adult rat brain. The present studies examined the effect of both minimal and maximal electroconvulsive shock, applied via corneal electrodes, on NGF and bFGF mRNA levels in several limbic (entorhinal cortex, hippocampus, olfactory bulb) and extralimbic (striatum and cerebellum) brain regions. By 5 h following limbic motor seizures induced by low-intensity (minimal) electroshock (LES) (0.2 s, 50-70 mA; three times over a 1-h period), bFGF mRNA was significantly increased in entorhinal cortex and hippocampus, but not in the other regions examined. In contrast, tonic extensor seizures evoked by maximal electroshock (MES) (0.2 s, 150 mA; three times over a 1-h period) were associated with a significant increase in bFGF mRNA in all limbic and extralimbic regions examined. In the same animals, increases in NGF mRNA were limited to entorhinal cortex and hippocampus. Adrenal steroids were not required for the seizure-induced increase in NGF or bFGF mRNAs, based on the finding that adrenalectomized rats exhibited electroshock-induced increases in both NGF and bFGF mRNAs equivalent to the increase observed in sham-operated rats. It is suggested that the increase in mRNA levels for the neurotrophic factors occurs selectively in those regions which are especially activated by the specific seizure model, and represents an adaptive response to repeated noninjurious neuronal stimulation.

Adrenalectomy↗
PubMed2002

Time-dependent increase in basic fibroblast growth factor protein in limbic regions following electroshock seizures.

Brief experimentally induced seizures have been shown to increase the expression of mRNA encoding basic fibroblast growth factor (FGF-2) in specific brain regions. However, the extent to which this change in mRNA affects the expression of FGF-2 protein in these brain regions has not been examined. In the present study, we exposed rats to brief non-injurious seizures to determine whether this treatment would lead to an increase in FGF-2 protein expression in selected brain regions. Because initial results indicated that the elevation of FGF-2 protein was not significant following acute seizure exposure, we examined both acute and chronic seizure treatment to determine whether FGF-2 protein expression could be increased under conditions of repeated seizures. Brief limbic seizures were induced by minimal electroconvulsive shock (ECS) given as daily treatments for 1 (acute) or 7 (chronic) days. FGF-2 protein was measured in hippocampus, rhinal cortex, frontal cortex, and olfactory bulb at 20, 48, and 72 h following the last seizure. No significant increases in FGF-2 protein were observed in any region following acute ECS. In the chronic ECS-treated groups, significantly elevated FGF-2-like immunoreactivity was found in the frontal and rhinal cortex as compared with the same regions from both control and acute ECS animals. Increases after chronic ECS were maximal at 20 h, and remained significantly elevated as long as 72 h. These increases were predominantly observed for the 24-kDa and 22/22.5-kDa FGF-2 isoforms. Because chronic ECS, which has been shown to be protective against neuronal cell death, induced significantly more FGF-2 immunoreactivity than did acute ECS, we suggest that FGF-2 expression may be an important substrate for the neuroprotective action of non-injurious seizures. A prolonged induction of the high molecular weight isoforms of FGF-2, as occurs after chronic ECS, may selectively reduce the vulnerability of certain brain regions to a variety of neurodegenerative insults.

Animals↗
PubMed1994

Distribution and characteristics of a 90 kDa protein, KG-CAM, in the rat CNS.

The distribution of a 90 kDa protein, termed KG-CAM, was examined in the developing and adult rat central nervous system (CNS) using the monoclonal antibody 11-59. The amino acid sequence of this protein revealed a sequence homology with a group of chick cell adhesion molecules from the immunoglobulin superfamily: DM-GRASP; SC1; and BEN. Immunolabeling of cells cultured from the embryonic and neonatal rat brain demonstrates that the protein recognized by 11-59 is on the external surface of a subpopulation of neurons and a limited population of glial cells. When the 11-59 antibody was used to stain sections of the adult brain and spinal cord, a number of different structures were labeled. The most intense immunoreactivity was found in the somatosensory system, the basal ganglia, the cortex, the olfactory system, and the circumventricular organs. One of the more interesting aspects of KG-CAM is the spatially and temporally regulated patterns of expression observed during the development of the CNS. For example, the dendrites of layer II pyramidal cells in the granular retrosplenial cortex are immunopositive for 11-59 while the dendrites are in the process of bundling in layer I, but not before bundling begins or after the process is completed. These findings reveal the varied roles of this adhesion molecule in the developing brain and spinal cord, as well as its potential role in the maintenance of the structural integrity of the adult CNS.

Activated-Leukocyte Cell Adhesion Molecule↗