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PubMed1989

Ontogeny of substance P-containing neurons in relation to serotonin-containing neurons in the central nervous system of the mouse.

In order to begin to investigate the developmental factors influencing co-localized neurotransmitters in the central nervous system, we have studied the ontogenesis of coexisting transmitters, substance P and serotonin, in cells of the medullary raphe of the fetal mouse using double-label immunocytochemistry. The results indicate that initial detection of these neurotransmitters occurs at embryonic day 12 in non-overlapping cell populations. Substance P-like immunoreactivity is first co-localized with serotonin in cells of the caudal medullary raphe (raphe pallidus and raphe obscurus) at embryonic day 13. The percentage of serotonin cells containing substance P was estimated at embryonic day 13 and subsequent gestational ages both by double-label immunofluorescence using fluorescein- and rhodamine-conjugated secondary antibodies and also by the elution technique. Double-label immunofluorescence routinely and reliably yielded the highest proportion of co-localized cells. At embryonic day 13, 89% of serotonin cells contained substance P-like immunoreactivity. A consistently high degree of co-localization occurred throughout embryonic development (87% at postnatal day 3) and into adulthood (87%). Colchicine treatment was required at older ages to elicit these data. Unexpectedly, we found that neurons containing substance P-like immunoreactivity in the piriform cortex and in the hypothalamus transiently expressed serotonin immunoreactivity during normal ontogenesis.

Aging↗
PubMed1990

Regional distribution of ethanol-inducible cytochrome P450 IIE1 in the rat central nervous system.

A specific form of cytochrome P450, P450 IIE1, active in ethanol oxidation, is known to be induced about 10-fold in rat liver following ethanol treatment. This isozyme of P450 participates effectively in the metabolic activation of precarcinogens, such as N-dimethylnitrosamines, and of solvents such as carbon tetrachloride and benzene. In the present investigation, two different polyclonal antisera against P450 IIE1 were used in order to map the regional distribution of this P450 form in the rat central nervous system. The presence of P450 IIE1 in various brain regions was confirmed by Western blot analysis. The P450 IIE1-immunoreactivity was heterogeneously distributed between brain areas. Neuronal cell bodies and glial cells of presumed astroglial as well as oligodendroglial identity contained immunoreactivity. All fiber tracts harbored P450 IIE1-immunoreactive glial cells as did the ependymal lining of the ventricular wall as well as small and large vessels throughout the brain. P450 IIE1-immunoreactive glial cells were present in all areas of the neocortex, in the olfactory bulb, in the piriform cortex and in several different thalamic nuclei. In the cerebellum, P450 IIE-immunoreactivity was found in all cell layers and was exclusively localized to glial cells and their processes. Staining of blood vessels was prominent in the white matter where P450 IIE1-immunoreactive glial cells were seen to have end-feet on the vessels. A subgroup of pyramidal cells of the frontal cortex showed strong P450 IIE1-immunoreactivity, as did a component of the olfactory nerve which innervates the accessory bulb. In the hippocampal region, the pyramidal cells of all subfields were P450 IIE1-immunoreactive. Some polymorphic cells of the hilus and subfield CA stained intensely with the P450 IIE1 antibodies. A high density of P450 IIE1-immunoreactivity was detected throughout the striatal complex. The immunoreactivity was localized to neuronal cell bodies as well as the neurophil. Fibers of the nigrostriatal system were strongly P450 IIE1-immunoreactive. Mechanical lesions of this pathway showed an accumulation of P450 IIE1-immunoreactivity proximal to the lesion relative to the striatum and a depletion in the reticular part of the substantia nigra, suggesting that the antigen may be transported from the striatum to the substantia nigra. In the brain stem a high density of P450 IIE-immunoreactive neurons was detected in the substantia nigra, the pontine nucleus, lateral superior olive and the nucleus of the trigeminal nerve and facial nucleus. A great number of large- to medium-sized immunoreactive neurons were situated in the central gray and in the reticular formation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Distribution of nerve growth factor receptor-like immunoreactivity in the adult rat central nervous system. Effect of colchicine and correlation with the cholinergic system--I. Forebrain.

Nerve growth factor receptor, as recognized by the monoclonal antibody 192-IgG, was localized to multiple regions of the adult rat forebrain. Immunoreactive cell bodies and fibers were seen in both sensory and motor regions which are known to contain cholinergic and non-cholinergic neurons. Specifically, nerve growth factor receptor immunoreactivity was present in cells lining the olfactory ventricle, rostral portion of the lateral ventricle, in basal forebrain nuclei, caudate putamen, globus pallidus, zona incerta and hypothalamus. Immunoreactive cells which were situated subpially along the olfactory ventricle and anterior portions of the lateral ventricle, and in the arcuate nucleus resembled neuroglia but could not definitively identified at the light microscopic level. Animals pretreated with intracerebroventricular colchicine displayed significantly increased nerve growth factor receptor immunoreactivity in all previously positive neurons and particularly in the medial preoptic area and ventral premammillary nucleus of the hypothalamus. In such animals, receptor immunoreactivity also appeared in previously non-immunoreactive cells of the hippocampal CA3 region and polymorph layer of the dentate gyrus as well as in the mitral cell layer of the olfactory bulb. Nerve growth factor receptor-immunoreactive fibers and varicosities were seen in the olfactory bulb, piriform cortex, neocortex, amygdala, hippocampus, thalamus, olivary pretectal nucleus and hypothalamus. In most regions, such fiber-like immunoreactive structures likely represented axon terminals, although in some areas, neuroglial or extracellular localizations could not be excluded. In this context, diffuse, non-fibrillar receptor immunoreactivity occurred in the lateral habenular nucleus and medial terminal nucleus of the accessory optic tract. Furthermore, intense nerve growth factor receptor immunoreactivity occurred along certain regions of the pial surface on the ventral surface of the brain. The distribution of nerve growth factor receptor-immunoreactive cell bodies and fibers in multiple sensory and motor nuclei suggests wide-spread influences of nerve growth factor throughout the adult rat forebrain. There is a high degree of overlap with regions containing choline acetyltransferase immunoreactivity. However, significant disparities exist suggesting that certain nerve growth factor receptor-containing non-cholinergic neurons of the rat forebrain may also be affected by nerve growth factor.

Animals↗
PubMed1991

Autoradiographic localization of subtypes of angiotensin II antagonist binding in the rat brain.

The non-peptide angiotensin II receptor compounds DuP 753 and WL 19 were utilized to detect subtypes of [125I]Sar1-Ile8-angiotensin II binding to angiotensin II receptors in the rat brain. In rat forebrain homogenates, DuP 753 and WL 19 produced a partial displacement of [125I]Sar1-Ile8-angiotensin II binding with DuP 753 displacing approximately 65% of the binding and WL 19 displacing approximately 35% of the binding. Using the techniques of quantitative receptor autoradiography, a distinct regional distribution of the subtypes of angiotensin II antagonist bind was detected. The angiotensin II-1 binding site (the receptor subtype preferentially displaced by DuP 753) appeared to predominate in the dipsogenic, cardiovascular and endocrine areas, including the subfornical organ, paraventricular and periventricular nuclei of the hypothalamus, anterior pituitary, dorsal motor nucleus of the vagus, nucleus of the solitary tract and the area postrema. Additional areas that contained predominantly the angiotensin II-1 receptor subtype were the ventral hippocampus, substantia gelatinosa of the trigeminal nucleus, nucleus of the lateral olfactory tract, piriform cortex and median preoptic nucleus. The angiotensin II-2 binding site (displaced by WL 19) was the predominant subtype in the thalamus, inferior olive, lateral septum, subthalamic nucleus, locus coeruleus, medial geniculate and medial amygdala. Several areas of the brain appeared to contain both receptor subtypes, including the superior and inferior colliculi, and the olfactory bulb. The angiotensin II-1 binding site was concentrated in areas of the brain involved in mediating angiotensin II effects on drinking, endocrine status and blood pressure. Localization of angiotensin II-2 sites in the thalamus and areas of the brain which process sensory information suggests a novel modulatory role for angiotensin II at this receptor subtype. These results indicate that DuP 753 and WL 19 are highly selective for angiotensin II binding site subtypes in the brain and that, in general these subtypes are compartmentalized in distinct brain regions. The non-peptide compounds used in these studies should provide excellent tools to discern the functional role of angiotensin II receptor subtypes in the brain.

Angiotensin II↗
PubMed1992

Mapping of the distribution of polysialylated neural cell adhesion molecule throughout the central nervous system of the adult rat: an immunohistochemical study.

In the nervous system, the neural cell adhesion molecule changes at the cell surface during development, from a form highly enriched in polysialic residues to several isoforms containing much less sialic acid, and is thought to participate in the structuring of neuronal groups and in the establishment of neuronal connections. Recent observations have indicated, however, that it may not be restricted to developing tissues since it is still present in certain adult neuronal centres which can undergo morphological reorganization. In this study, therefore, we examined systematically the distribution of polysialylated neural cell adhesion molecule immunoreactivity throughout the central nervous system of adult male and female rats, using light microscopic immunocytochemistry and immunoblot analysis with an antibody that specifically recognizes the polysialic residues of the molecule. Concomitantly, we compared this immunoreactivity to that due to all isoforms of the neural cell adhesion molecule, detected with a polyclonal serum raised against the NH2-terminal of the protein. Immunoreactivity due to the polysialylated isoform was consistently visualized in several discrete areas of the adult brain and spinal cord. An intercellular punctate immunolabelling characterized the staining in certain hypothalamic and thalamic nuclei, superficial laminae of the dorsal horn of the spinal cord, ventral portion of the dentate gyrus of the hippocampus, lateral geniculate, parabrachial and habenular nuclei, bed nucleus of the stria terminalis, mesencephalic central gray and olfactory bulb. In other areas, such as the piriform cortex, dorsal aspect of the dentate gyrus and fimbria and lamina X of the spinal cord, isolated neuronal-like cells were either completely filled with immunolabel or showed a surface reaction on their cell bodies and processes. Highly immunoreactive isolated glial-like cells were also noted within the ependymal layer of the central canal and lateral ventricles and at times in the peripheral white matter of the spinal cord. In contrast to this discrete localization, staining due to all isoforms of the neural cell adhesion molecule was widespread and diffuse throughout the brain and spinal cord. The expression of the polysialylated isoform in the supraoptic nucleus and hippocampus was confirmed by immunoblot analysis; it occurred together with weakly sialylated isoforms. No obvious differences were detected in the amount or distribution of immunoreactivity due to the polysialylated isoform in relation to the sex or age of the animals (between three and 12 months of age). Our study thus demonstrates that well-defined areas of the central nervous system of the adult rat continue to express the polysialylated isoform of the neural cell adhesion molecule.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Immunohistochemical distribution of neurons containing the G-proteins Gq alpha/G11 alpha in the adult rat brain.

A new class of G-proteins, the Gq family, has been recently identified and found to be involved in phospholipase C activation. The alpha subunits of the Gq and G11 members of this family are separate polypeptides but appear to have the same function. In this study, the cellular distribution in the adult rat brain of these G-proteins, Gq alpha/G11 alpha, was determined by immunohistochemistry using an antipeptide antiserum directed against the predicted C-terminal decapeptide which is conserved between these polypeptides. The specificity of the antiserum was verified by Western blot analysis using rat brain homogenates. Immunoreactivity was detected in neurons, where it was localized in the dendrites and at the periphery of the cell bodies. The staining was abundant in the dendrites of cerebellar Purkinje cells and hippocampal CA1 pyramidal cells. Staining was also found in neurons in the olfactory bulb, minor and major islets of Calleja, anterior olfactory nuclei and piriform cortex; the different cortical areas especially in their superficial layers; caudate-putamen, accumbens and olfactory tubercle; lateral septum and amygdala; hippocampal CA2-4 sectors of Ammon's horn, dentate gyrus and hilus; hypothalamic supraoptic nucleus; cerebellar granular layer; colliculi and superficial layers of the dorsal horn of the spinal cord. In conclusion, the brain neuronal localizations of Gq alpha/G11 alpha match that of phospholipase C, 1,4,5-triphosphate receptor and, to a lesser extent 1,4,5-triphosphate-3-kinase.

Animals↗
PubMed1992

Regional stimulatory and inhibitory effects of guanine nucleotides on [125I]galanin binding in rat brain: relationship with the rate of occupancy of galanin receptors by endogenous galanin.

Galanin has been shown to stimulate feeding or modulate neuroendocrine secretions when administered centrally. In the present work, using quantitative autoradiography, we documented the existence of [125I]galanin specific binding sites in several hypothalamic nuclei expected to mediate these effects. In standard binding conditions, [125I]galanin specific binding can be visualized in the hypothalamic ventromedial nucleus, stria terminalis, piriform cortex, central amygdaloid nucleus and medial amygdaloid nucleus, while it is almost undetectable in most neuroendocrine or autonomic hypothalamic areas. We hypothesized that high endogenous galanin levels in these regions might mask galanin receptors. We first showed that a high ionic strength/acid wash of brain slices is effective in removing more than 80% of specifically prebound [125I]galanin in all tested regions. After such treatments, specific binding sites could be revealed in the hypothalamus namely in the parvocellular paraventricular nucleus, periventricular nucleus, arcuate nucleus and median eminence. In contrast, regions already labeled in standard conditions exhibited a slight decrease in [125I]galanin binding. Thus, regions were ranked from low to high rate of occupancy of galanin receptors by endogenous galanin, the rate of occupancy of galanin receptors being maximal in median eminence (greater than 90%). We thus studied the regional effect of guanine nucleotides on [125I]galanin specific binding. A high concentration (100 microM) of guanyl 5'-yl imidodiphosphate, a nonhydrolyzable analog of GTP directly added to the incubation medium, inhibited [125I]galanin binding in all telencephalic regions. On the same sections and only in regions of high index of galanin receptor occupancy (arcuate nucleus, median eminence, dorsomedial nucleus, paraventricular nucleus, and periventricular hypothalamic nucleus), guanyl 5'-yl imidodiphosphate paradoxically enhanced [125I]galanin binding. The effects of acid preincubation and guanyl 5'-yl imidodiphosphate incubation on [125I]galanin binding were strongly correlated in these hypothalamic areas (r = 0.97). In all regions, guanyl 5'-yl imidodiphosphate increased the rate of dissociation of [125I]galanin. In competition studies, guanyl 5'-yl imidodiphosphate decreased the IC50 s of unlabeled galanin which were homogenized around 4 nM in most telencephalic and hypothalamic regions. Thus, the guanyl 5'-yl imidodiphosphate-induced stimulation of [125I]galanin specific binding measured in the neuroendocrine and autonomic hypothalamus is linked to an increase in receptor capacity and not to a rise in receptor affinity. Both inhibitory and stimulatory guanyl 5'-yl imidodiphosphate effects observed in [125I]galanin equilibrium binding studies were dose-dependent and guanine nucleotide-specific with guanyl 5'-yl imidodiphosphate more potent than GTP or GDP.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Regulation of neurotrophin and trkA, trkB and trkC tyrosine kinase receptor messenger RNA expression in kindling.

Levels of messenger RNA for nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, and the tyrosine kinase receptors trkA, trkB and trkC have been studied using in situ hybridization in the rat brain 2 h and four weeks after kindling-induced seizures. Epileptiform activity evoked by hippocampal stimulation and exceeding 70 s lead to a concomitant and transient increase of brain- derived neurotrophic factor, nerve growth factor, trkB and trkC messenger RNA expression in dentate granule cells after both focal and generalized seizures. Brain-derived neurotrophic factor messenger RNA levels were also increased bilaterally in the CA1-CA3 regions, amygdala and the piriform, entorhinal, perirhinal, retrosplenial and temporal cortices after generalized seizures. The magnitude of the increases was similar throughout the development of kindling and in the fully kindled brain. No changes of trkA messenger RNA were observed. In amygdalar kindling, elevated brain-derived neurotrophic factor messenger RNA levels developed more rapidly in the amygdala-piriform cortex than after stimulation in the hippocampus but changes in the hippocampal formation were only seen in few animals. Intraventricular 6-hydroxydopamine or a bilateral fimbria-fornix lesion did not alter basal expression or seizure-evoked changes in messenger RNA levels for neurotrophins or trk receptors but increased the number of animals exhibiting elevated levels after the first stimulation, probably due to a prolongation of seizure activity. Both in sham-operated and fimbria-fornix-lesioned rats seizure activity caused a marked reduction of neurotrophin-3 messenger RNA levels in dentate granule cells. The results indicate that activation of the brain-derived neurotrophic factor gene, at least in dentate granule cells, is an "all-or-none" type of response and dependent on the duration but not the severity of seizures or the stage of kindling epileptogenesis. Changes in brain-derived neurotrophic factor, nerve growth factor, neurotrophin-3 and trkB and trkC were observed concomitantly in the dentate gyrus, which suggests that seizure activity sets in motion a cascade of genomic events possibly mediated via a common mechanism. Since altered messenger RNA levels outside hippocampus were detected only for brain-derived neurotrophic factor, neurotrophin and trk gene expression in these regions seems to be regulated differently.

Amygdala↗
PubMed1993

Serotonin2/1C receptor activation causes a localized expression of the immediate-early gene c-fos in rat brain: evidence for involvement of dorsal raphe nucleus projection fibres.

Immunocytochemistry has been used to monitor the expression of the immediate-early gene c-fos in rat brain following administration of the serotonin2/1C receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane. At parenteral doses of 2 or 8 mg/kg the drug caused a highly localized expression of the Fos protein in frontal, parietal, cingulate and piriform cortex as well as in claustrum, mamillary bodies, globus pallidus, amygdala, nucleus accumbens and dorsomedial striatum. In particular, the location of heavy Fos immunoreactivity in the primary somatosensory cortex corresponds precisely to that region (layer Va) shown in other reports to receive a dense input of fine, non-varicose fibres which may arise from the dorsal raphe nucleus. All of the Fos-positive brain regions in the present study have been previously demonstrated to contain serotonin2 receptor ligand binding sites. Interestingly, no Fos-positive cells were found in the hippocampus, another brain region known to contain serotonin2 receptors. Pretreatment of animals with the serotonin2/1C receptor antagonist ritanserin (0.4 mg/kg) markedly attenuated Fos expression in all reactive areas of the brain. Counts of reactive cells indicated that this antagonism of the Fos response was statistically significant in these brain regions. Spiperone (1 mg/kg), a mixed serotonin2 and dopamine D2 antagonist, also attenuated the Fos response in the same regions, but had the effect of inducing Fos expression on its own in other extrapyramidal brain regions. Double labelling of reactive cells with different antisera recognizing Fos and neuron-specific enolase, and lack of double labelling with a glial fibrillary acidic protein antiserum, indicated that the Fos expression was in neurons within the brain nuclei examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamines↗
PubMed1995

Expression patterns of a glutamate-binding protein in the rat central nervous system: comparison with N-methyl-D-aspartate receptor subunit 1 in rat.

Using radioactive in situ hybridization histochemistry, we examined the topographical patterns of expression of the messenger RNA encoding a glutamate-binding protein (N-methyl-D-aspartate receptor glutamate-binding protein in rat; NMDARgbs) in the central nervous system of the rat. Expression patterns of N-methyl-D-aspartate receptor glutamate-binding protein were compared with those of N-methyl-D-aspartate receptor subunit 1 (NMDAR1) of the N-methyl-D-aspartate receptor on adjacent sections. N-methyl-D-aspartate receptor glutamate-binding protein is not expressed in glial cells. The expression of both N-methyl-D-aspartate receptor glutamate-binding protein and N-methyl-D-aspartate receptor subunit 1 was observed in virtually all neurons throughout the central nervous system. The mean level of N-methyl-D-aspartate receptor subunit 1 expression was higher than that of N-methyl-D-aspartate receptor glutamate-binding protein. Similar topographical patterns of expression of N-methyl-D-aspartate receptor glutamate-binding protein and N-methyl-D-aspartate receptor were observed in most regions, except in discrete thalamic, hypothalamic and brainstem nuclei. Concomitantly for N-methyl-D-aspartate receptor glutamate-binding protein and N-methyl-D-aspartate receptor subunit 1, the highest expression levels were distributed in the mitral layer of main and accessory olfactory bulbs, granule cell layer of the dentate gyrus, polymorphic and pyramidal layers of CA1-3 fields of Ammon's horn. A slightly less prominent expression was observed in the glomerular and granule cell layers of main and accessory olfactory bulbs, anterior olfactory nucleus, layer 2 of piriform cortex, olfactory tubercle and taenia tecta. In the cerebellum, the prominent level of N-methyl-D-aspartate receptor glutamate-binding protein expression was slightly higher in the Purkinje cell layer than in the granule cell layer, an opposite pattern being observed for N-methyl-D-aspartate receptor subunit 1. A moderately high expression level of both messenger RNAs was observed in the medial septal nucleus, nucleus of the diagonal band of Broca, dorsal part of the endopiriform nucleus, and in the anteroventral and anterolateral parts of the bed nucleus of the stria terminalis. In the neocortex, the mean expression level of N-methyl-D-aspartate receptor glutamate-binding protein is moderate, while the mean level of N-methyl-D-aspartate receptor subunit 1 expression is high. With both probes, layer IV is slightly less labeled than the other layers.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Mapping of perineuronal nets in the rat brain stained by colloidal iron hydroxide histochemistry and lectin cytochemistry.

Net-like structures, visualized with the Golgi technique and several histochemical and immunocytochemical methods, have been described to ensheath somata, parts of dendrites and axon initial segments of various types of neurons. The origin and function of these perineuronal nets have been controversially discussed. Recently, it was confirmed that they are glia-associated. In the present study such perineuronal nets were demonstrated by using colloidal iron hydroxide staining for detection of polyanionic components and the plant lectins Vicia villosa agglutinin and Wisteria floribunda agglutinin with affinity for N-acetylgalactosamine. This paper shows their distribution patterns and the occurrence of regional specialization of these nets which might provide a basis to suggest functional implications of these structures. Perineuronal nets were found in more than 100 brain regions, such as neocortex, hippocampus, piriform cortex, basal forebrain complex, dorsal lateral septal nucleus, lateral hypothalamic area, reticular thalamic nucleus, zona incerta, deep parts of superior and inferior colliculus, red nucleus, substantia nigra, some tegmental nuclei, cerebellar nuclei, dorsal raphe and cuneiform nuclei, central gray, trochlear nucleus, pontine and medullar reticular nuclei, superior olivary nucleus and vestibular nuclei. Neurons enwrapped by perineuronal nets not only differ in morphology but also in transmitter content. In neocortical and hippocampal regions there occurs a much higher number of perineuronal nets ensheathing non-pyramidal cells than in paleocortical structures. Most subcortical regions containing perineuronal nets were found to be integrated in motor functions. The findings are discussed with respect to known electrophysiological data of cell types described in our investigation as net-associated. There are some indications that such cells may represent fast firing types.

Animals↗
PubMed1994

Quantitative autoradiographic studies of the effects of bilateral olfactory bulbectomy in the rat brain: central- and peripheral-type benzodiazepine receptors.

We investigated the discrete regional effects of bilateral olfactory bulbectomy on central- and peripheral-type benzodiazepine receptors in rat brains at weekly intervals until one month after bulb ablation. Persistent increases in [3H]flunitrazepam binding to central benzodiazepine receptors were observed in the cingulum (27%) and in the frontal (15%) and parietal (14%) cortices. Progressive increases in central benzodiazepine receptors, reaching statistical significance four weeks after olfactory bulbectomy, were observed in the ventromedial thalamic nucleus (35%), the lateral hypothalamic region (22%), the basolateral amygdaloid nucleus (23%) and substantia nigra (25%). Persistent major increases (between four- and six-fold) in [3H]PK-11195 [eH]1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline carboxamide binding to peripheral-type benzodiazepine receptors were observed in all anterior olfactory nuclei. Similarly, throughout the time period studied, [3H]PK-11195 binding densities were increased two- to three-fold in the piriform cortex and lateral olfactory tract. These observations confirm the usefulness of [3H]PK-11195 binding as a marker of neuronal insult in the brain. Moreover, the persistent regional increases in [3H]flunitrazepam binding to central-type benzodiazepine receptors suggest that GABAergic transmission is altered following olfactory bulb ablation.

Animals↗
PubMed1994

Age-related deposition of glia-associated fibrillar material in brains of C57BL/6 mice.

With advancing age, clusters of unusual granules appear in the brains of C57BL/6 (B6) mice. At the light, confocal laser and electron microscopic levels, the granules represent aggregations of fibrillar material often associated with astrocytes. The fibrillar material is largely free of normal organelles and has been located within astrocytic somata and processes, although in many cases the material is found in the neuropil and is surrounded by a discontinuous membrane. The deposits occur predominantly in hippocampus, but also in piriform cortex, cerebellum and less frequently in some other brain regions. They become evident about six months of age and increase markedly in both number and size thereafter. Incidence of the deposits varies greatly among inbred mouse strains. At six to 12 months of age, granules are abundant in male and female B6, and are absent in BALB/c, CBA, DBA/2 and A mice. In hybrid strains with a B6 background the deposits are also present and thus appear to manifest dominant genetic heritability. Similar granular structures have been described in adult brains of the senescence accelerated mouse and have been noted, albeit very rarely, in aged mice from other strains. While immunostaining of the granules with several polyclonal antisera was found by preabsorption with antigens to be non-specific, immunolabeling with monoclonal antibodies to heparan sulfate proteoglycan core protein and to laminin suggest these or related molecules as components of the fibrillar material. The presence of glycosaminoglycans is supported by staining with periodic acid-Schiff and Gomori's methenamine silver methods. The functional significance of the murine deposits is not yet clear. The deposits do not represent senile plaques with beta-amyloid deposition, but they might mimic the deposition of extracellular matrix molecules that is hypothesized to be a precursor condition for plaque formation and cerebral amyloidosis. Furthermore, the genetic differences in the incidence of the fibrillar deposits has potential to model aspects of familial neurodegenerative diseases.

Aging↗
PubMed1996

Sequential patterns of inhibin subunit gene expression following hypoxic-ischemic injury in the rat brain.

Injury to the central nervous system initiates a series of signals that control cell survival and rearrangement, leading to some functional recovery. Using a unilateral model of hypoxic-ischemic brain injury, we report strong induction of inhibin beta A and alpha subunit messenger RNA in several regions of the brain and provide evidence for novel roles for the inhibin/activin family of peptides in modulating neural function. Expression was visualized by in situ hybridization and the beta A subunit was observed as early as 1 h after injury in the dentate gyrus of the non-ligated hemisphere. Strong induction was seen in the hippocampus, piriform cortex and amygdala on the non-ligated hemisphere 24 h after injury. The early induction of inhibin beta A was associated with seizure activity, since administration of the anticonvulsant carbamazepine (8 mg/kg) markedly attenuated the signal. Only background expression was observed for the alpha and beta B subunits at these early time points. A bilateral induction of both beta A and alpha subunit messenger RNA was demonstrated in the meningeal membrane from three to seven days after injury. This second wave was not blocked by carbamazepine. Thirdly, beta A and alpha subunit expression was observed in the infarct from days 5 to 7. However, expression was not co-localized with isolectin B4 staining for reactive microglia or astrocytes, but instead the pattern of distribution strongly suggested that inhibin/activin was induced around microvessels. These data demonstrated three distinct waves of beta A subunit expression following hypoxic-ischemic injury, two of which coincided with alpha subunit expression. The early induction of beta A subunit was seizure related, whereas subsequent co-induction of beta A and alpha subunit suggested involvement in vascular and meningeal reactions. These results suggest specific roles for both activin and inhibin in the central nervous system during recovery from injury.

Animals↗
PubMed1996

Evidence for aspartate-immunoreactive neurons in the neostriatum of the rat: modulation by the mesencephalic dopamine pathway via D1-subtype of receptor.

Aspartate-like immunoreactivity was visualized in the neostriatum of rats using indirect immunofluorescence techniques and antibodies raised against aspartate conjugated to keyhole limpet hemocyanine. In normal rats only a few aspartate-positive cell bodies with limited processes were observed. A moderate increase was seen after treatment with (+)methamphetamine and haloperidol. A dramatic increase in the number and fluorescence intensity was observed in the unilaterally 6-hydroxy-dopamine lesioned rats after multiple injections of the D1-dopamine receptor agonist SKF 38393. In these rats strongly fluorescent processes as well as extensive terminal varicose fibre networks were observed. This increase could partly be blocked by the D1-dopamine receptor antagonist SCH 23390. Using a modified technique the aspartate-positive cell bodies and processes were observed even when the antiserum was diluted 1:80,000. Positive cell bodies and fibres were also seen on the ipsilateral side outside the neostriatum, for example in the islet of Calleja and in the piriform cortex. The aspartate-positive cells were negative for dopamine- and cyclic AMP-regulated phosphoprotein-32, a marker for neurons bearing dopamine D1-receptor subtype. A proportion of the aspartate-positive neurons (20%) contained neuropeptide tyrosine-like immunoreactivity. On adjacent sections there was a marked up-regulation of preprodynorphin-like immunoreactivity. The up-regulation of dynorphin and aspartate was only observed when there was an almost complete denervation of the neostriatum as visualized with antiserum to tyrosine hydroxylase, a marker for dopamine fibres. The present results raise the possibility that aspartate may act as a neurotransmitter released from interneurons in the neostriatum.

Animals↗
PubMed1996

Seizure-induced differential expression of messenger RNAs for neurotrophins and their receptors in genetically fast and slow kindling rats.

Levels of messenger RNAs for brain-derived neurotrophic factor, nerve growth factor and neurotrophin-3, and their high-affinity receptors, TrkB and TrkC, were analysed in the brains of genetically fast and slow kindling rats using in situ hybridization. Basal expression of neurotrophins and Trk messenger RNAs in the hippocampal formation, amygdala, frontoparietal and piriform cortices did not differ between the two strains. At 2 h after the third generalized grade 5 seizure, induced by kindling stimulations in the amygdala, increased expression of brain-derived neurotrophic factor messenger RNA was detected in the dentate gyrus granule cell layer, amygdala, frontoparietal and piriform cortices of the fast kindlers. Similar seizure-evoked increases of brain-derived neurotrophic factor messenger RNA levels were also observed in the amygdala and piriform cortex of slow kindlers. However, in these animals, brain-derived neurotrophic factor messenger RNA expression was not significantly altered by the seizures in the dentate gyrus granule cell layer and frontoparietal cortex. Furthermore, the seizure-induced increase of nerve growth factor, TrkB and TrkC messenger RNAs and decrease of neurotrophin-3 messenger RNA levels in the dentate gyrus granule cell layer was only observed in fast, but not in slow, kindlers. The neurotrophins are believed to regulate synaptic plasticity and efficacy and to facilitate long-term potentiation and kindling epileptogenesis. The present data suggest that the slow and fast kindling rates in the two strains studied here might partly be due to differences in seizure-evoked neurotrophin and Trk synthesis.

Amygdala↗
PubMed1994

Neuroanatomical pathways linking vision and olfaction in mammals.

Retinal projections to several telencephalic structures have been demonstrated in a wide range of mammalian species following intraocular injections of tritiated amino acids and cholera toxin subunit-B conjugated to horseradish peroxidase. Since these regions are also innervated by olfactory fibers, we investigated the distribution of convergent projections using simultaneous injections of different anterograde tracers in the eye and olfactory bulbs. Convergent projections from the retina and from the olfactory bulbs were observed in the piriform cortex, olfactory tubercle, the cortical region of the medial amygdala, lateral hypothalamus, and the bed nucleus of the stria terminalis. A few retinal fibers also invade the nucleus of the lateral olfactory tract, the bed nucleus of the accessory olfactory bulb and the diagonal band of Broca. Injections of retrograde tracers in the medial amygdala, the bed nucleus or the lateral hypothalamus shows that the visuo-olfactory convergence mainly involves projections originating from the accessory olfactory bulb, and to a lesser extent from the ventromedial region of the main olfactory bulb. Fewer than 20 retinotelencephalic ganglion cells were identified in the retina, mainly located contralateral to the injection site. Ganglion cells were medium sized and possessed two long slender opposing dendrites. These retinal and olfactory projections could provide an anatomical substrate for the modulation of gonadotropin hormone levels and the olfactory influence on light mediated rhythms related to reproductive physiology.

Animals↗
PubMed1982

Differential projections from locus coeruleus to olfactory bulb and olfactory tubercle: an HRP study.

The microiontophoretic administration of horseradish peroxidase (HRP) to the olfactory bulb (OB) or olfactory tubercle (OT) in cats and rats yielded similar results in both species. After an OB HRP-injection ipsilateral and contralateral labelled neurons were seen in the piriform cortex, polymorphic layer of OT, magnocellular preoptic region, lateral hypothalamus, ventromedial hypothalamic nucleus and locus coeruleus (LC). In both species more labelled structures were found after an OT HRP-injection than after an OB HRP-injection. The substantia nigra in rats was more abundantly labelled after an OT injection than after an OB one. In cats the dorsal and the ventral raphe were also labelled. In either species, OT HRP-injections resulted in a higher frequency of LC labelled neurons than after OB injections. These results favor the hypothesis that the OT plays an important role as a relay station for efferent inflow from the brain stem en route to the OB.

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