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PubMed1990

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

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

Animals↗

PubMed1990

Effect of LiCl pretreatment on cholinomimetic-induced seizures and seizure-induced brain edema in rats.

Male Sprague-Dawley rats received LiCl (5 mEq/kg; sc) or saline 24 h prior to injection of cholinomimetics. Physostigmine (PHY, 0.54-0.80 mg/kg), diisopropylfluorophosphate (DFP, 1.3-2.5 mg/kg), pilocarpine (PIL, 23-30 mg/kg), or saline was injected subcutaneously at time 0. Rats were observed for seizure activity for 2 h, survivors were killed 24 h later and edema was measured in samples from parietal and piriform cortices, dorsal thalmus, and hippocampus. None of the rats pretreated with saline had seizures when given doses of cholinomimetics alone. However, rats pretreated with LiCl had the following incidence of seizures: PHY 68%, DFP 71% and PIL 100%. Rats given cholinomimetic agents alone did not have brain edema. In contrast, all LiCl-pretreated rats that seized had pronounced brain edema which was greatest in the piriform cortex. Thus, these studies demonstrate that LiCl pretreatment potentiates cholinomimetic-induced seizures. Further, cholinomimetic-induced seizures produce brain changes resulting in edema.

Animals↗

PubMed1991

The N-methyl-D-aspartate receptor antagonist MK-801 induces increases in dopamine and serotonin metabolism in several brain regions of rats.

MK-801 (dizocilpine maleate), a non-competitive, N-methyl-D-aspartate receptor antagonist which induces a characteristic phencyclidine-like motor syndrome in rodents, was administered to rats after handling habituation to examine the effects of this drug on concentrations of monoamines and their metabolites in 14 brain regions. MK-801 increased dopamine and serotonin metabolism in several regions, the most marked effects being determined in frontal and piriform cortex, nucleus accumbens and striatum. The data indicate that not only effects on dopaminergic transmission but also on serotonergic transmission may be involved in the pharmacological actions of MK-801.

Animals↗

PubMed1992

Localization of interleukin 6 mRNA and interleukin 6 receptor mRNA in rat brain.

The cytokine interleukin 6 (IL6) has several effects on the central nervous system in addition to the well established regulation of the acute phase inflammatory response. Therefore, the distribution of IL6- and IL6 receptor mRNA in the rat brain has been investigated by in situ hybridization using [35S]-labeled oligonucleotides. The messages of both genes were found in the CA1-CA4 regions as well as in the dentate gyrus of the hippocampus, in the habenulae, the dorsomedial and the ventromedial hypothalamus, in the internal capsule, the optic tract and in the piriform cortex. These data indicate both neuronal and glial localization of IL6 and IL6 receptor and their involvement in an autocrine or paracrine action of the cytokine in centrally regulated functions including neuroendocrine control.

Animals↗

PubMed1992

Activation of basal forebrain cholinergic neurons differentially regulates brain-derived neurotrophic factor mRNA expression in different projection areas.

Afferent cholinergic pathways from the basal forebrain were activated by injections of the glutamate analog quisqualate either into the nucleus basalis or into the medial septal nucleus. Nucleus basalis injections had no effect on the expression of brain-derived neurotrophic factor (BDNF) mRNA in its neocortical projection areas as measured by in situ hybridization. In contrast, 7 h after an injection into the septum the level of BDNF mRNA increased 3- to 5-fold in the dentate gyrus, throughout CA1 to CA3 in the hippocampus and in the piriform cortex.

Afferent Pathways↗

PubMed1992

Localization of mRNA for beta-adrenergic receptor kinase in the brain of adult rats.

A cDNA encoding rat beta-adrenergic receptor kinase (beta-ARK) was cloned and sequenced. By in situ hybridization histochemistry of adult brain, beta-ARK mRNA was expressed intensely in the cerebellar granule cell layer and moderately in the hippocampal pyramidal cells and dentate granule cells. The neocortex and piriform cortex expressed it moderately to weakly, whereas the thalamus and hypothalamus expressed it weakly to faintly. No significant expression of the mRNA was detected in the caudate-putamen. Weak expression of beta-ARK mRNA was detected in several nuclei of the brainstem and in the spinal gray matter.

Animals↗

PubMed1993

High-dose ketamine does not induce c-Fos protein expression in rat hippocampus.

The effects of high-dose ketamine on the c-fos protein (c-Fos) expression were investigated in rat by an immunohistochemical technique. The administration of 100 mg/kg ketamine i.p. induced seizure-like activity (limbic seizure). No c-Fos immunoreactivity was observed in hippocampus, piriform cortex and amygdala, while it was observed in neocortex and thalamus. These findings disagree with the reports that ketamine depresses the neuronal function of the neocortex and thalamus, while it stimulates the limbic system.

Amygdala↗

PubMed1993

Distribution and characterization of melatonin receptors in the brain of the Japanese quail, Coturnix japonica.

2-[125I]iodomelatonin was used to study the distribution and properties of the melatonin receptor in the Japanese quail brain. High receptor density was detected in the major targets of direct retinal input (optic tectum, nucleus of the optic basal rout, ventrolateral geniculate nucleus), as well as areas representing terminals in the visual pathways (nucleus rotundus, ectostriatum, thalamo-hyperstriatal pathway). Binding was also found in the piriform cortex, the hypophyseal pars tuberalis, the oculomotorius nucleus and the associated Edinger-Westphal nucleus, and in the nuclei of the third, fourth and sixth cranial nerves. A comparison of the receptor pharmacological profile to that of the mammalian brain demonstrated pharmacological identity of the two binding sites. In the saturation experiments, GPT gamma S decreased the binding affinity, numerical Kd values increasing from approximately 35 pM to approximately 150 pM.

Animals↗

PubMed1994

C-fos expression after single and kindled audiogenic seizures in Wistar rats.

In naive Wistar rats susceptible to sound, a single audiogenic seizure induced the expression of c-fos in the subcortical auditory nuclei whereas the forebrain was almost completely devoid of any labelling. After kindling of audiogenic seizures by 40 daily exposures to sound, the seizure induced a strong c-fos expression in the amygdala, the piriform cortex, the hippocampus and the neocortex. These results confirm: (1) that audiogenic seizures are brain-stem seizures related to dysfunction of auditory pathways, and (ii) that kindling of audiogenic seizures recruits forebrain and limbic structures into the seizure network.

Acoustic Stimulation↗

PubMed1995

The levels of neurotrophin-3 protein in the rat brain determined by enzyme immunoassay show a pattern distinct from nerve growth factor.

Using the monoclonal antibody 3W3 a two-site enzyme immunoassay (EIA) for neurotrophin-3 (NT-3) was established. The assay was sensitive to levels of NT-3 below 10 pg/ml and does not recognize nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF). In the adult rat brain, highest levels of NT-3 (1-1.5 ng/g tissue) were found in hippocampus and piriform cortex. Also the cerebellum contained detectable NT-3 protein. In the postnatal (P1 and P5) rat brain very high levels of NT-3 (7-9 ng/g) were found in the cingulate cortex consistent with previous observations of a local, transient NT-3 mRNA expression. NT-3 was also found prenatally in hippocampus, telencephalon and cerebellum. The EIA shows that the pattern of NT-3 protein in brain tissues is distinct from that of NGF.

Aging↗

PubMed1995

Ref-1 expression in adult mammalian neurons and astrocytes.

Ref-1 is a nuclear protein that possesses DNA repair activity and has a role in the redox activation of Fos and Jun transcription factors. Using an antibody to Ref-1 we investigated the expression and distribution of this protein in the adult rat brain. Ref-1 was located in the nucleus of neurons and glial fibrillary acidic protein-positive astrocytes throughout the brain. Levels were particularly high in granule cells of the dentate gyrus, piriform cortex neurons, and Purkinje cells of the cerebellum, and lower in CA1 pyramidal cells, striatal neurons, and the neurons of the neocortex. These results suggest that the action of inducible transcription factors such as c-Jun in mammalian neurons is likely to be regulated by constitutively expressed Ref-1, in particular in dentate granule cells. The high levels of Ref-1 in glial fibrillary acidic protein-positive astrocytes suggest that it may also modulate the action of inducible transcription factors in these cells, particularly after brain injury. The possibility also exists that Ref-1 may primarily function as a DNA repair enzyme in brain cells.

Animals↗

PubMed1996

Presynaptic localization of a metabotropic glutamate receptor, mGluR8, in the rhinencephalic areas: a light and electron microscope study in the rat.

The present study indicated presynaptic localization of a metabotropic glutamate receptor, mGluR8, in projection neurons of the main olfactory bulb of rat. An antibody was produced by using a peptide corresponding to C-terminal 23 amino acids of mouse mGluR8. It was confirmed that the C-terminal 23 amino acids of rat mGluR8 were the same as those of mouse mGluR8 except for one, and that the antibody specifically recognized mGluR8 in the rat rhinencephalon. In layer Ia of the piriform cortex (a target area of projection fibers from the main olfactory bulb), mGluR8-like immunoreactivity (mGluR8-LI) was reduced after transection of the lateral olfactory tract, and mGluR8-LI was observed in axon terminals which were filled with round synaptic vesicles and made asymmetric synapses with dendritic spines.

Animals↗

PubMed1984

Immunohistochemical distribution of somatostatin-like immunoreactivity in the central nervous system of the adult rat.

The localization and distribution of somatostatin (growth hormone release-inhibiting hormone; somatotropin release-inhibiting factor) have been studied with the indirect immunofluorescence technique of Coons and collaborators and the immunoperoxidase method of Sternberger and coworkers using specific and well-characterized antibodies to somatostatin, providing semiquantitative, detailed maps of somatostatin-immunoreactive cell profiles and fibers. Our results demonstrate a widespread occurrence of somatostatin-positive nerve cell bodies and fibers throughout the central nervous system of adult, normal or colchicine-treated, albino rats. The somatostatin cell bodies varied in size from below 10 micron up to 40 micron in diameter and could have only a few or multiple processes. Dense populations of cell somata were present in many major areas including neocortex, piriform cortex, hippocampus, amygdaloid complex, nucleus caudatus, nucleus accumbens, anterior periventricular hypothalamic area, ventromedial hypothalamic nucleus, nucleus arcuatus, medial to and within the lateral lemniscus, pontine reticular nuclei, nucleus cochlearis dorsalis and immediately dorsal to the nucleus tractus solitarii. Extensive networks of nerve fibers of varying densities were also found in most areas and nuclei of the central nervous system. Both varicose fibers as well as dot- or "dust-like" structures were seen. Areas with dense or very dense networks included nucleus accumbens, nucleus caudatus, nucleus amygdaloideus centralis, most parts of the hypothalamus, nucleus parabrachialis, nucleus tractus solitarii, nucleus ambiguus, nucleus tractus spinalis nervi trigemini and the dorsal horn of the spinal cord. One exception is the cerebellum which only contained few somatostatin-positive cell bodies and nerve fibers. It should be noted that somatostatin-positive cell bodies and fibers did not always conform to the boundaries of the classical neuroanatomical nuclei, but could often be found in areas between these well-established nuclei or occupying, in varying concentrations, only parts of such nuclei. It was difficult to identify with certainty somatostatin-immunoreactive axons in the animals studied. Some pathways could, however, be demonstrated, but further experimental studies are necessary to elucidate the exact projections of the somatostatin-immunoreactive neurons in the rat central nervous system.

Animals↗

PubMed1984

Maturation of kainic acid seizure-brain damage syndrome in the rat. II. Histopathological sequelae.

The histopathological sequelae of parenteral administration of kainic acid were investigated in immature rats (3-35 days of age). The brains were fixed 1-14 days after the administration of kainate and the damage evaluated by means of argyrophylic (Fink-Heimer, Gallyas or Nauta-Gygax) and Nissl stains. In animals of less than 18 days of age there was no sign of damage even after 1-2 h of severe tonico-clonic convulsions. Between 18 and 35 days after birth, there was a progressive increase in the severity of the damage, the adult pattern being reached at the latter age. As in adult animals, brain damage was most severe in structures which are part of the limbic system, i.e. the hippocampal formation, lateral septum, amygdaloid complex, claustrum, piriform cortex, etc. In addition to neuronal abnormalities, the following reactions were observed: hypertrophy and swelling of satellite oligodendroglia, proliferation of hypertrophic microglia, proliferation of astroglia and hypertrophy of endothelial cells in the capillary wall. The latter type of change, together with local coagulative necrosis, was almost exclusively restricted to the granular and molecular layers of the fascia dentata. In the hippocampal formation we found a temporal gradient of vulnerability. The earliest and most consistent neuronal alterations were largely restricted to interneurons of the hilar region and to a lesser extent to non-pyramidal neurons of strata oriens and radiatum. The severe necrotic destruction of the pyramidal layer of CA3 is conspicuous at a later age (postnatal day 30-35) and with longer survival times. Our results suggest that: (1) the neurotoxin only induces brain damage once it also causes limbic motor seizures and its associated metabolic activations, notably in the amygdala; (2) the earliest pathological sequelae occur in interneurons of the hilar region and (3) sclerosis of the vulnerable region of the Ammon's horn--the CA3 region--is only obtained once the dentate granules and their mossy fibres are fully operational, thereby reflecting the crucial role of this axonal connection in eliciting hippocampal damage.

Age Factors↗

PubMed1987

Neurotensin in the human brain.

The localization of neurotensin-immunoreactive sites in the adult human brain was investigated by the indirect immunoperoxidase method of Sternberger [Sternberger (1979) Immunocytochemistry. Wiley, New York]. Our results demonstrate a widespread, albeit uneven occurrence of neurotensin-immunoreactive cells and processes throughout the central nervous system. Immunoreactive cells are prominent in the medial hypothalamus and in various regions of the limbic system, including the amygdaloid body, septal area, bed nucleus of the stria terminalis and piriform cortex. A few cells were also found in the dorsal synencephalon, superior colliculus, periaqueductal grey and spinal trigeminal nucleus. The distribution of immunoreactive fibres corresponds well with that reported for rodents. Areas with the highest concentration of neurotensin-immunoreactive processes included all the areas where immunoreactive neurons were found and, in addition, periventricular thalamic nuclei, the sublenticular region, lateral parts of the brainstem reticular formation and the vagus-solitarius complex. Comparison mapping studies of melanin-containing neurons on sections treated with neurotensin antiserum revealed an anatomical relation between almost all the catecholaminergic cell clusters with peptide-containing fibres.

Brain↗

PubMed1988

Monoclonal antibody immunohistochemistry of adult rabbit olfactory structures.

Immunohistochemical staining patterns of two monoclonal antibodies produced against the rabbit olfactory bulb were studied in adult rabbit olfactory structures. One monoclonal antibody 112D5 (monoclonal antibody 2D5) stained all of the olfactory receptor cells, whereas the other 114G12 (monoclonal antibody 4G12) stained the upper two-thirds to three-fourths of the receptor cell layer. The negative region in the receptor cell layer was designated the deep compartment. Neither monoclonal antibody stained the supporting cells, basal cells, or Bowman's glands. Monoclonal antibody 2D5 stained the olfactory nerve layer and glomeruli in the olfactory bulb, whereas monoclonal antibody 4G12 stained the whole of the olfactory bulb, particularly the glomeruli and the mitral cells. The piriform cortex was unstained by monoclonal antibody 2D5 whereas the highest immunoreaction to monoclonal antibody 4G12 was in layer Ia. Immunoblot analysis revealed that the molecular weight values of monoclonal antibody 4G12 antigens in the olfactory epithelium were approx. 26,000. Thus, monoclonal antibody 4G12, specific to neurons, recognized an epitope different from the olfactory marker protein specific to the olfactory receptor neurons.

Animals↗

PubMed1989

Distribution of insulin receptor-like immunoreactivity in the rat forebrain.

Previous studies have suggested that insulin may play a role in the hormonal regulation of neurotransmitter metabolisms within the central nervous system. In order to provide additional information to support this hypothesis, we examined the distribution of insulin receptors within the forebrain of adult male rats. Insulin receptors were localized by immunocytochemistry, using an antibody directed against the carboxy-terminus of the beta-subunit of the insulin receptor. The antibody specificity was tested by immunoprecipitation of brain insulin receptors with antiserum and the purity of the receptor-antibody preparation was determined using hormone binding-assays with radiolabeled insulin and insulin-like growth factor-l. Insulin receptor-like immunoreactivity was found in a widespread, but selective, distribution on neurons throughout the rat forebrain. Double-labeling with glial fibrillary acidic protein did not demonstrate any detectable insulin receptor-like immunoreactivity on glial cells. Areas with the highest density of insulin receptor-like immunoreactivity were found in the olfactory bulbs, hypothalamus and median eminence, medial habenula, subthalamic nucleus, subfornical organ, CA 1/2 pyramidal cell layer of the hippocampus and piriform cortex. Double-staining of hypothalamic sections with somatostatin and vasopressin antisera revealed insulin receptor-like immunoreactivity on a subpopulation of somatostatin neurons in the periventricular region and on vasopressin neurons in the supraoptic nucleus. A moderately dense insulin receptor-like immunoreactivity was observed in layers II-IV of cerebral cortex, medial amygdala, reticular thalamic nucleus, zona incerta, and preoptic and septal regions, whereas a low density of insulin receptor-like immunoreactive neurons was found in basolateral amygdala and most thalamic regions. The basal ganglia and most parts of the thalamus were almost devoid of insulin receptor-like immunoreactivity. Our findings provide morphological support for a direct action of insulin on selected regions of the rat forebrain and suggest that the insulin receptor may modulate synaptic transmission or the release of neurotransmitters and peptide hormones in the CNS.

Animals↗

PubMed1989

Autoradiographic localization of particulate cyclic AMP-dependent protein kinase in mammalian brain using [3H]cyclic AMP: implications for organization of second messenger systems.

Cyclic AMP's regulatory role as an intracellular second messenger is well established. In brain and other tissues, specific proteins that bind cyclic AMP have been shown to be the regulatory subunits of cystolic and particulate cyclic AMP-dependent protein kinases. This study of the autoradiographic localization of specific [3H]cyclic AMP binding revealed the heterogeneous distribution of particulate cyclic AMP-dependent protein kinase in the mammalian central nervous system. Specific [3H]cyclic AMP binding to tissue sections was of high affinity (KD = 60 nM) and saturable (Bmax = 5 pmol/mg protein). Purine and pyrimidine nucleotide analogues demonstrated inhibition constants against [3H]cyclic AMP binding consistent with the specific labelling of cyclic AMP-dependent protein kinase (e.g. 8'-bromo-cyclic AMP: IC50 = 130 nM; inosine 3',5'-cyclic monophosphate: IC50 = 1 microM; uridine 3',5'-cyclic monophosphate: IC50 = 60 microM). Variations in the levels of [3H]cyclic AMP binding presumably reflect the presence of differing amounts of particulate cyclic AMP-dependent protein kinase in different neuronal populations. Highest densities were associated with neuronal cell layers such as the pyramidal cells of the piriform cortex and hippocampus, and granule cells of the dentate gyrus and cerebellum. High levels of binding were also found in other cortical and limbic structures, while moderate levels were found in hypothalamic, thalamic and midbrain areas. Excitotoxic lesions confirmed the localization of the enzyme in hippocampal pyramidal cells and cerebellar granule cells. Localizations reported in this study are largely consistent with results obtained using immunohistochemical methods to label cyclic AMP-dependent protein kinases. Recently, [3H]forskolin, a potent and selective activator of adenylate cyclase, the enzyme responsible for the formation of cyclic AMP from adenosine 5'-triphosphate, has been used to localize the activated catalytic component of this enzyme in rat brain. Regions described as being intensely labelled with [3H]forskolin (e.g. basal ganglia, hilus of the dentate gyrus and molecular layer of the cerebellum) were found to be associated with relatively low [3H]cyclic AMP binding levels. These findings suggest a marked difference between the localization of the two related enzyme entities. However, the distribution of the enzymes is indirectly correlated as high levels of particulate cyclic AMP-dependent protein kinase are present in the soma of neurons with high concentrations of adenylate cyclase in their terminals. Alternatively, it is possible that [3H]forskolin localizes only a subpopulation of adenylate cyclase.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗