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PubMed1987

Ontogenesis of adenosine deaminase activity in rat brain.

The activity of adenosine deaminase (ADA) was determined in whole brain of rats at the embryonic age of 15 days through to adulthood and in nine brain regions in rats 1 day old through to adulthood. In 1-day-old rats, the highest activity was seen in olfactory bulbs (550 +/- 15 nmol/mg protein/30 min) and this was 4.5-fold higher than that in the pons, which was the lowest. In adult animals, olfactory bulb still contained the greatest activity, which was about eightfold higher than hippocampus, which had the lowest. Except for hypothalamus, where ADA activity increased nearly twofold in rats between the ages of 1 and 50 days, significant decreases of as much as fivefold were found in whole brain, superior colliculus, cortex, hippocampus, cerebellum, olfactory bulbs, and olfactory nucleus. In contrast, ADA activity in pons and subcortex remained relatively constant throughout the developmental period. The Km values for ADA in whole brain at 18 days gestation (48 +/- 5 microM) were not significantly different from that observed in adult rats (38 +/- 7 microM), whereas the Vmax values decreased significantly from 339 +/- 9 to 108 +/- 8 nmol/mg protein/30 min. Taken together, the developmental patterns observed in the various brain regions appear not to correspond to any one particular process such as periods of rapid cell proliferation, cell death, synaptogenesis, or myelination. Nor do they correspond to known developmental profiles of transmitters, their receptors, or their metabolic enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Deaminase↗
PubMed1986

Circadian rhythms in neurotransmitter receptors in discrete rat brain regions.

Circadian rhythms were measured in alpha 1-, alpha 2- and beta-adrenergic, acetylcholine muscarinic (ACh), and benzodiazepine (BDZ) receptor binding in small regions of rat brain. Rhythms in alpha 1-receptor binding were measured in olfactory bulb, frontal, cingulate, piriform, parietal, temporal and occipital cortex, hypothalamus, hippocampus, pons-medulla, caudate-putamen and thalamus-septum. No rhythm was found in cerebellum. Rhythms in alpha 2-receptor binding were measured in frontal, parietal and temporal cortex, and pons-medulla. No rhythm was found in cingulate, piriform or occipital cortex, or hypothalamus. Rhythms in binding to beta-receptors were measured in olfactory bulb, piriform, insular, parietal and temporal cortex, hypothalamus and cerebellum. No rhythms were found in frontal, entorhinal, cingulate, or occipital cortex, hippocampus, caudate-putamen, or pons-medulla. Rhythms in ACh receptor binding were measured in olfactory bulb, parietal cortex and caudate-putamen. No rhythms were found in frontal or occipital cortex, nucleus accumbens, hippocampus, thalamus-septum, pons-medulla or cerebellum. Rhythms in BDZ receptor binding were measured in olfactory bulb, olfactory and occipital cortex, olfactory tubercle, nucleus accumbens, amygdala, caudate-putamen, hippocampus and cerebellum. No rhythms were found in parietal cortex, pons-medulla or thalamus-septum. The 24-hr mean binding to receptors varied between 3- and 10-fold, the highest in cortex and the lowest, usually, in cerebellum. The piriform cortex was particularly high in alpha 1- and alpha 2-adrenergic receptors; the nucleus accumbens and caudate, in ACh receptors; and the amygdala, in BDZ receptors. Most adrenergic and ACh receptor rhythms peaked in subjective night (the period when lights were off under L:D conditions), whereas most BDZ receptor rhythms peaked in subjective day (the time lights were on in L:D). Perhaps in the rat, a nocturnal animal, the adrenergic and ACh receptors mediate activity and the functions that accompany it, and the BDZ receptors mediate rest, and with it, sleep.

Animals↗
PubMed1993

Distribution of the neurons containing inositol 1,4,5-trisphosphate 3-kinase and its messenger RNA in the developing rat brain.

As a result of its interaction with a specific receptor, inositol 1,4,5-trisphosphate (InsP3) mobilizes intracellular calcium. The metabolism of InsP3 is rather complex: InsP3 3-kinase produces Inositol 1,3,4,5-tetrakisphosphate (InsP4), a putative second messenger also involved in the intraneuronal calcium homeostasis. The distribution of the messenger RNA coding for the recently cloned InsP3 3-kinase was studied in the developing rat brain by using oligonucleotides derived from the rat cDNA sequence and in situ hybridization combined with Northern blot analysis. In addition, the locations of the enzyme were determined by immunohistochemistry in combination with Western blot analysis. By Northern blot and Western blot analyses on rat brain, the kinase was not detected in the embryo, was first found slightly at birth, and reached adult levels around 2-3 postnatal weeks. These findings were confirmed in the different positive regions by in situ hybridization conducted at the macroscopic level. At the cellular level, the mRNA was found exclusively in the neuronal populations previously demonstrated in the adult. The levels of transcripts per neuron were however higher in the adult than in the neonate brain. The enzyme mRNA could be detected first at postnatal day 0, (birth, P0) in the perikarya of the cerebellar Purkinje cells, followed at P4 by the hippocampal CA1 pyramidal cells and granule cells of the dentate gyrus and finally, at P9, by a majority of the neurons in the cortical layers II-III and V, especially in the frontal cortex and cingulate cortex; claustrum; caudate, putamen, accumbens, olfactory tubercle and calleja islets; anterior olfactory nucleus; taenia tecta; piriform piriform cortex; dorsolateral septum; bed nucleus stria terminalis; amygdala; hippocampal CA2-4 sectors and subiculum. By immunohistochemistry, the enzyme was initially found in the periphery of the cell bodies of the neonatal neurons; was progressively enriched in the developing dendritic arborization during the first postnatal weeks where it remained exclusively localized in the adult. In conclusion, in the developing brain, InsP3 3-kinase was first detected at birth, and thereafter its concentrations increased to reach adult levels around 2-3 postnatal weeks. At the cellular level, the kinase was exclusively found in the neurons. The small amounts of transcripts found per neuron in the neonate increase during synaptogenesis and the protein became progressively enriched in the developing dendritic arborization, where it is localized in the adult.

Animals↗
PubMed1980

Efferent connections of the parabrachial nucleus in the rat.

The efferent connections of the parabrachial nucleus have been analyzed in the rat using the anterograde autoradiographic method. Fibers originating from the lateral parabrachial nucleus (PBl) ascend in the periventricular system, the dorsal tegmental bundle and the central tegmental tract. The PBl projects to the dorsal raphe nucleus, the superior central raphe nucleus, and the Edinger-Westphal nucleus. It also innervates the intralaminar (centromedian, centrolateral, paracentral, parafascicular), the midline (paraventricular, reuniens), and the ventromedial basal (VMb) thalamic nuclei as well as much of the hypothalamus, including the dorsomedial, the ventromedial, the arcuate and the paraventricular nuclei, the lateral hypothalamic and the lateral preoptic areas. The PBl sends fibers via the ansa peduncularis into the amygdala, innervating the anterior, the central, the medial, the basomedial, and the posterior basolateral nuclei. In addition, it projects to the lateral part of the bed nucleus of the stria terminalis. Descending PBl fibers travel mainly through the ventrolateral medulla, passing through the region of the A1 and A5 catecholamine cell groups, the ventrolateral reticular formation and the region that contains parasympathetic preganglionic neurons. A small component travels in Probst's bundle to the ventral part of the nucleus of the solitary tract. Only a few PBl axons continue caudally into the lateral funiculus of the spinal cord, but these could not be followed beyond the first few cervical segments. The projections of the medial parabrachial nucleus (PBm) are similar to those of PBl, but two major differences have been noted. One difference is that the PBm provides a direct input to 4 regions of cerebral cortex: (1) the granular insular cortex; (2) the deep layers of the frontal cortex; (3) the septo-olfactory area; and (4) the infralimbic cortex. The other difference is that unlike the PBl, the PBm appears to provide almost no input to the medial hypothalamic nuclei (dorsomedial, ventromedial, arcuate nuclei) nor to the medial amygdaloid nucleus. The PBm projects heavily to the nucleus ambiguus and there was no evidence for an input to the nucleus of the solitary tract. The projections of the Kölliker-Fuse nucleus (KF) are distinct from those of either PBm or PBl. The KF projects via the central tegmental tract to the lateral hypothalamic area, the lateral preoptic area, and the central nucleus of the amygdala. The contralateral projection to the zona incerta, the lateral hypothalamic area, and the lateral preoptic areas is more prominent than the ipsilateral projections. Descending KF fibers travel mainly through the ventrolateral medullary reticular formation passing through regions which give rise to parasympathetic preganglionic fibers of the VIIth, IXth and Xth cranial nerves and the A1 and A5 catecholamine cell groups. In one experiment, fibers could be followed to the intermediolateral cell column of the upper thoracic spinal cord.

Animals↗
PubMed1982

Origin of cocaine- and lidocaine-induced spindle activity within the olfactory forebrain of the rat.

Cocaine and other local anesthetics produce a characteristic form of electrical activity in the olfactory forebrain consisting of bursts of sinusoidal potentials (spindles) in the range of 20-50 c/sec. The purpose of the present experiment was to determine if this drug-induced spindle activity is generated by the same neuronal elements in the olfactory bulb (OB) and prepyriform cortex (PPC) which generate naturally occurring olfactory spindles. Rats with chronically implanted electrodes in the OB and PPC were injected with doses of cocaine or lidocaine hydrochloride sufficient to produce spindles (5 mg/kg i.v. or 40 mg/kg i.p.). Drug-induced and naturally occurring spindles exhibited similar anterior-posterior amplitude profiles, with the highest amplitude in the OB and the lowest in the posterior PPC. Multipolar recordings from the PPC indicated that the amplitude of naturally occurring and drug-induced spindles was highest at sites near the superficial pyramidal cell layer of the PPC and lower at sites 1-2 mm more dorsal. Furthermore, both naturally occurring and drug-induced spindles exhibited a polarity reversal near the superficial pyramidal cell layer of the PPC and the mitral cell layer of the OB. Finally, neither form of spindle occurred when nasal air flow (olfactory stimulation) was prevented. These observations suggest that cocaine- and lidocaine-induced spindles are generated in the OB and PPC by the same neuronal elements which also produce naturally occurring olfactory spindles.

Animals↗
PubMed1995

Distribution of neurotensin-containing neurons in the central nervous system of the dog.

The distribution of neurotensin-containing cell bodies and fibers was examined in the central nervous system of the dog using light microscopic immunohistochemistry. A very large population of neurotensin-containing cell bodies was observed in the septal nuclei, nucleus accumbens septi, preoptic areas, bed nucleus of the stria terminalis, olfactory tubercle, entorhinal cortex, ventral subiculum, anterodorsal thalamic nucleus, anteroventral thalamic nucleus, nucleus reuniens, lateral habenular nucleus, parabrachial nucleus, and nucleus of the solitary tract. Extremely dense networks of neurotensin-containing fibers were found in the globus pallidus, hypothalamus, infundibular stalk, ventral tegmental area, periaqueductal gray, interpeduncular nucleus, and spinal nucleus of the trigeminal nerve and substantia gelatinosa. However, the cerebral neocortex and cerebellum were negative for neurotensin in the present study. When the present findings are compared with those in other animals, it is clear that the major species-specific differences in distribution involve three immunonegative regions and four immunopositive regions in the dog: The former are the cerebral neocortex, mammillary body, and hippocampus; the latter are the cell bodies in the pyramidal layer of the olfactory tubercle, the superficial and middle layers of the entorhinal cortex and ventral subiculum, and the nerve fibers in the interpeduncular nucleus. The present study indicates a rather extensive network of neurotensin neurons in the central nervous system of the dog.

Animals↗
PubMed1989

Chronic phenobarbital administration affects GABA and benzodiazepine receptors in the brain and periphery.

Chronic phenobarbital administration for 20 days to mice resulted in significant increases in the density of peripheral benzodiazepine binding sites in the heart, kidney and cerebellum, but did not affect the density of these sites in the olfactory bulb. No alteration in the affinity (KD) of peripheral benzodiazepine binding sites for their ligand [3H]PK 11195 was observed in any of the organs examined. Phenobarbital treatment did not affect the maximal binding capacity or the affinity of the central benzodiazepine receptors for [3H]flunitrazepam in the cerebral cortex, hippocampus and olfactory bulb. A significant reduction in [3H]muscimol binding in the hippocampus was obtained following chronic phenobarbital treatment. Such an alteration was not detected in the cerebral cortex. The KD values remained unaltered in both tissues. The modulatory effect of phenobarbital on peripheral benzodiazepine binding sites could be related to alterations in the functions of these organs or to the neurochemical effects of the drug.

Animals↗
PubMed1981

Central connections of the olfactory bulb in the American opossum (Didelphys virginiana): a light microscopic degeneration study.

Destructive lesions were made in the right olfactory bulb of 16 adult opossums. Following postoperative survival periods of 4 to 31 days, the animals were sacrificed and perfused with 10% Formalin. Frozen sections of the brain were cut in either the coronal, horizontal, or sagittal plane and processed by the Fink-Heimer II method. Degenerating axons of olfactory bulb neurons were traced caudally in the ipsilateral lateral olfactory tract (LOT). Small lesions revealed a topographic representation of the olfactory bulb within the LOT. The dorsal, lateral, and ventral parts of the bulb were, respectively, represented in the dorsal, intermediate, and ventral parts of the LOT. Terminal degeneration was observed in the superficial half of the molecular layer ipsilaterally in the following structures: anterior olfactory nucleus, anterior hippocampal rudiment, olfactory tubercle, piriform cortex, ventrolateral frontal neocortex, lateral entorhinal cortex, nucleus of the LOT, and the lateral aspect of the cortical amygdaloid nucleus. No degeneration was observed in the anterior limb of the anterior commissure. Dorsal and lateral parts of the olfactory bulb projected to the anterolateral aspect of the olfactory tubercle, whereas the ventral part projected heavily to the entire tubercle. There was no evidence of topographic projections to other olfactory structures. The observations of the present investigation indicated that the olfactory bulb projections in the opossum, a primitive mammal, are essentially comparable with those of placental mammals.

Animals↗
PubMed2003

Immunolocalization of estrogen receptor beta in the mouse brain: comparison with estrogen receptor alpha.

Estrogen receptor alpha (ER alpha) and ER beta are members of the steroid nuclear receptor family that modulate gene transcription in an estrogen-dependent manner. ER mRNA and protein have been detected both peripherally and in the central nervous system, with most data having come from the rat. Here we report the development of an ER beta-selective antibody that cross-reacts with mouse, rat, and human ER beta protein and its use to determine the distribution of ER beta in the murine brain. Further, a previously characterized polyclonal antibody to ER alpha was used to compare the distribution of the two receptors in the first comprehensive description of ER distribution specifically in the mouse brain. ER beta immunoreactivity (ir) was primarily localized to cell nuclei within select regions of the brain, including the olfactory bulb, cerebral cortex, septum, preoptic area, bed nucleus of the stria terminalis, amygdala, paraventricular hypothalamic nucleus, thalamus, ventral tegmental area, substantia nigra, dorsal raphe, locus coeruleus, and cerebellum. Extranuclear-ir was detected in several areas, including fibers of the olfactory bulb, CA3 stratum lucidum, and CA1 stratum radiatum of the hippocampus and cerebellum. Although both receptors were generally expressed in a similar distribution through the brain, nuclear ER alpha-ir was the predominant subtype in the hippocampus, preoptic area, and most of the hypothalamus, whereas it was sparse or absent from the cerebral cortex and cerebellum. Collectively, these findings demonstrate the region-selective expression of ER beta and ER alpha in the adult ovariectomized mouse brain. These data provide an anatomical framework for understanding the mechanisms by which estrogen regulates specific neural systems in the mouse.

Amino Acid Sequence↗
PubMed1993

Expression of c-fos mRNA following seizures evoked from an epileptogenic site in the deep prepiriform cortex: regional distribution in brain as shown by in situ hybridization.

Using in situ hybridization histochemistry for the detection of c-fos mRNA, we examined the pathways activated by seizures evoked by a focal application of bicuculline into a highly discrete epileptogenic site in the deep prepiriform cortex, the area tempestas (AT). Thirty minutes after the initiation of limbic motor seizures evoked by bicuculline in AT, a marked increase in c-fos mRNA was detected in the hippocampal formation, amygdala, olfactory bulb, piriform cortex, and entorhinal cortex. The increase of c-fos mRNA was strictly dependent upon the infusion of the drug in AT. Infusions of bicuculline in the same dose outside the AT did not increase c-fos mRNA levels. The extent to which the mapping pattern of c-fos mRNA expression was specific to limbic seizures was evaluated by examining another focally evoked seizure model involving the application of bicuculline bilaterally into the inferior colliculus. The absence of any detectable c-fos induction in the limbic system after explosive running-bouncing clonic seizures evoked by bicuculline injected into the inferior colliculus indicates that the pattern of activation that we found in the AT-evoked seizure model is not common to all forms of convulsive activity. Furthermore these observations suggest that the pattern of activation we have observed is seizure dependent and not stress induced. Our results indicate that c-fos mRNA expression is useful in the functional mapping of pathways involved in seizure propagation and that the anatomic pattern of activation is selectively related to the type of seizure evoked.

Animals↗
PubMed2003

Insulin-like growth factor-II/mannose-6-phosphate receptor: widespread distribution in neurons of the central nervous system including those expressing cholinergic phenotype.

The insulin-like growth factor-II/mannose-6-phosphate (IGF-II/M6P) receptor is single transmembrane glycoprotein that plays a critical role in the trafficking of lysosomal enzymes and the internalization of circulating IGF-II. At present, there is little information regarding the cellular distribution of the IGF-II/M6P receptor within the adult rat brain. With the use of immunoblotting and immunocytochemical methods, we found that the IGF-II/M6P receptor is widely but selectively expressed in all major brain areas, including the olfactory bulb, striatum, cortex, hippocampus, thalamus, hypothalamus, cerebellum, brainstem, and spinal cord. Intense IGF-II/M6P receptor immunoreactivity was apparent on neuronal cell bodies within the striatum, deeper layers (layers IV and V) of the cortex, pyramidal and granule cell layers of the hippocampal formation, selected thalamic nuclei, Purkinje cells of the cerebellum, pontine nucleus and motoneurons of the brainstem as well as in the spinal cord. Moderate neuronal labeling was evident in the olfactory bulb, basal forebrain areas, hypothalamus, superior colliculus, midbrain areas, granule cells of the cerebellum and in the intermediate regions of the spinal gray matter. We also observed dense neuropil labeling in many regions, suggesting that this receptor is localized in dendrites and/or axon terminals. Double-labeling studies further indicated that a subset of IGF-II/M6P receptor colocalizes with cholinergic cell bodies and fibers in the septum, striatum, diagonal band complex, nucleus basalis, cortex, hippocampus, and motoneurons of the brainstem and spinal cord. The observed widespread distribution and colocalization of IGF-II/M6P receptor in the adult rat brain provide an anatomic basis to suggest a multifunctional role for the receptor in a wide-spectrum of central nervous system neurons, including those expressing a cholinergic phenotype.

Acetylcholine↗
PubMed1986

Autoradiographic localization of D1 dopamine receptors in the rat brain with [3H]SCH 23390.

The regional distribution of D1 dopamine (DA) receptors in the rat brain has been studied by quantitative autoradiography using the specific D1 antagonist [3H]SCH 23390 as a ligand. The binding of [3H]SCH 23390 to striatal sections was saturable, stereospecific, reversible and of high affinity (Kd = 2.05 nM); it occurred at a single population of sites and possessed the pharmacological features of the D1 DA receptor. The highest densities of [3H]SCH 23390 binding sites were found in the caudate-putamen, olfactory tubercle, nucleus accumbens and substantia nigra (especially in the pars compacta). High densities were also observed in the nucleus interstitialis striae terminalis, the anterior olfactory nucleus, the entopeduncular nucleus, the subthalamic nucleus, the claustrum and the amygdalohippocampal area. An intermediate labelling was found in the anteromedial and suprarhinal DA terminal fields of the cerebral cortex, the basolateral, medial and lateral amygdaloid nuclei, the endopiriform nucleus, the primary olfactory cortex, the globus pallidus, the superior colliculus (especially the superficial layer), the nucleus amygdaloideus corticalis and the dorsal hippocampus (molecular layer of the CA1 and dentate gyrus). In the anteromedial and suprarhinal cortices, [3H]SCH 23390 binding was more concentrated in layers V and VI. Moderate levels of [3H]SCH 23390 were found in the thalamus, hypothalamus, the habenula, the ventral tegmental area, the posterior cingulate and entorhinal cortices, the supragenual dopamine terminal system and the cerebellum (molecular layer). This regional distribution of [3H]SCH 23390 closely correlated (except for the cerebellum) with the reported distribution of dopaminergic terminals. The topographical distribution of [3H]SCH 23390 has also been studied in detail in striatal subregions. The density of D1 receptors was much greater in the ventrolateral sector and medial margin of the striatum than in the ventromedial and dorsolateral sectors. A rostrocaudal decrease in the densities of D1 sites was also found along the rostrocaudal axis of the caudate-putamen. These lateral to medial and anteroposterior gradients overlapped with the density of the dopaminergic afferents.

Animals↗
PubMed1992

Distribution of arginine vasotocin in the brain of the lizard Anolis carolinensis.

The distribution of immunoreactive arginine vasotocin (AVT-ir) was determined in the brain of the lizard Anolis carolinensis. Cells and fibers containing AVT-ir were found in the medial septal region, lamina terminalis, lateral forebrain bundle, preoptic area, supraoptic nucleus, anterior hypothalamus, paraventricular nucleus, periventricular nucleus, arcuate nucleus, and ventromedial nucleus of the thalamus. Occasional AVT-ir cells were found in the interpeduncular nucleus. Fibers containing AVT-ir were found in the cortex, around the olfactory ventricle, in the diagonal band of Broca, amygdala area, dorsal ventricular ridge, striatum, nucleus accumbens, septum, ventromedial hypothalamus, lateral hypothalamus, medial forebrain bundle, median eminence, pars nervosa, nucleus of the solitary tract, locus coeruleus, cerebellar cortex (granular layer), dorsal part of the nucleus of the lateral lemniscus, substantia nigra, and myelencephalon. The intensity of AVT-ir staining was, in general, greater in males than in females. Comparison of AVT-ir distribution in A. carolinensis with those previously published for other reptilian species revealed species-specific differences in distribution of AVT.

Animals↗
PubMed2003

Bioaccumulation and locomotor effects of manganese phosphate/sulfate mixture in Sprague-Dawley rats following subchronic (90 days) inhalation exposure.

Methylcyclopentadienyl manganese tricarbonyl (MMT) is an organic manganese (Mn) compound added to unleaded gasoline in Canada. The primary combustion products of MMT are Mn phosphate, Mn sulfate, and a Mn phosphate/Mn sulfate mixture. Concerns have been raised that the combustion products of MMT containing Mn could be neurotoxic, even at low levels of exposure. The objective of this study is to investigate exposure-response relationships for bioaccumulation and locomotor effects following subchronic inhalation exposure to a mixture of manganese phosphates/sulfate mixture. A control group and three groups of 30 male Sprague-Dawley rats were exposed in inhalation chambers for a period of 13 weeks, 5 days per week, 6 h a day. Exposure concentrations were 3000, 300, and 30 microg/m(3). At the end of the exposure period, locomotor activity and resting time tests were conducted for 36 h using a computerized autotrack system. Rats were then euthanized by exsanguination and Mn concentrations in different tissues (liver, lung, testis, and kidney) and blood and brain (caudate putamen, globus pallidus, olfactory bulb, frontal cortex, and cerebellum) were determined by neutron activation analysis. Increased manganese concentrations were observed in blood, kidney, lung, testis, and in all brain sections in the highest exposure group. Mn in the lung and in the olfactory bulb were dose dependent. Our data indicate that the olfactory bulb accumulated more Mn than other brain regions following inhalation exposure. Locomotor activity was increased at 3000 microg/m(3), but no difference was observed in resting time among the exposed groups. At the end of the experiment, rats exposed to 300 and 3000 microg/m(3) exhibited significantly decreased body weight in comparison with the control group. Biochemical profiles also revealed some significant differences in certain parameters, specifically alkaline phospatase, urea, and chlorate.

Alkaline Phosphatase↗
PubMed1984

Characterization and regulation of insulin receptors in rat brain.

An in vitro receptor binding assay, using filtration to separate bound from free [125I]insulin, was developed and used to characterize insulin receptors on membranes isolated from specific areas of rat brain. The kinetic and equilibrium binding properties of central receptors were similar to those of hepatic receptors. The binding profiles in all tissues were complex and were consistent with binding in multiple steps or to multiple sites. Similar binding properties were found among receptors in olfactory tubercle/bulb, cerebral cortex, hippocampus, striatum, hypothalamus, and cerebellum. High affinity [125I]insulin binding sites (KD = 3-11 nM) were distributed evenly between membranes isolated from P1 and P2 fractions of these brain areas, with the exception of the olfactory tubercle in which binding to P2 membranes was four-fold greater (Bmax = 150 fmol/mg protein). One difference between insulin receptors in brain and peripheral target tissues, however, was observed. Following exposure to 0.17 microM insulin for 3 h at 37 degrees C, the number of specific [125I]insulin binding sites on adipocytes decreased by 40%, while the number of binding sites on minces of cerebral cortex/olfactory tubercle remained constant. The results suggest that although the binding characteristics of central and peripheral insulin receptors are similar, these receptors do not appear to be regulated in the same manner.

Animals↗
PubMed1993

Regulation of protein kinase C activity by sensory deprivation in the olfactory and visual systems.

Environmental regulation of sensory function has provided an important model of plastic mechanisms mediating neural information processing. To define potential commonalities in information processing in different systems, we investigated molecular changes elicited by sensory deprivation in the developing rat olfactory and visual systems. Protein kinase C (PKC), an intracellular messenger implicated in synaptic plasticity and memory, was analyzed. Initial, developmental studies indicated that PKC activity in the soluble and particulate fractions of the olfactory bulb increased three- to fourfold from birth to 3 months of age. Unilateral olfactory deprivation prevented the developmental increase in both soluble and particulate PKC activities in the ipsilateral olfactory bulb and piriform cortex, the second-order relay. Phorbol ester binding localized PKC to intrinsic neuronal populations and their dendrites in the control and deprived bulbs. Moreover, PKC was similarly lower in the visual cortex of dark-reared rats than in light-reared controls. The changes in PKC were region specific, as activity was unchanged by either treatment in the parietal cortex, a control area that does not process primary olfactory or visual information. Our results suggest that the important intracellular messenger, PKC, is similarly regulated in entirely different sensory systems by different environmental stimuli. Consequently, different sensory systems may use common molecular mechanisms to process information.

Animals↗
PubMed1985

The regional distribution of cadmium in the brains of orally exposed adult rats.

Cadmium (Cd) levels were measured in 13 dissected brain regions of adult male rats from 3 treatment groups. Rats (approximately 200 g each) were each fed 10 g/day of diets containing either 20 or 100 micrograms/g (ppm) Cd or control diet to which no Cd was added but contained approximately 0.35 ppm Cd. After 67 days of treatment, the brain of each rat was removed and each was dissected into 13 anatomical regions including olfactory bulbs, frontal cortex, rest of cortex, corpus callosum, hippocampus, amygdalae, corpus striatum, colliculum, tegmentum, thalamus, hypothalamus, pons-medulla, and cerebellum. Cd residues (dry weight) in each sample were determined by flameless atomic absorption spectrophotometry. With exception of the thalamus and olfactory bulbs, each of the brain regions of the 100 ppm Cd rats had more Cd than did those from either the 20 ppm Cd rats or controls which did not differ. There was evidence of selective accumulation of Cd within the olfactory bulbs of control and treated animals. This selective accumulation may be related to anosmia reported in workers with industrial exposure to Cd.

Animals↗
PubMed1993

Migration of LHRH neurons derived from the olfactory placode in rats.

Using the olfactory placode of 12.5- and 14.5-day-old (E12.5, E14.5) rat embryos, we examined the migration of LHRH neurons by in vivo intraventricular transplantation and in vitro organotypic culture systems. In the transplantation, the olfactory placode of E12.5 embryos was co-transplanted with the cerebral cortex and also with medial basal hypothalamus (MBH). LHRH neurons that had migrated into the co-transplanted brain tissues were fusiform, but those that had moved into the neuro-mesenchymal tissue were polyhedral. The migration occurred most conspicuously in the MBH. In our in vitro studies, we used E14.5 embryos; their vomeronasal organ was cultured with MBH, the olfactory cortex, and the septum of the telencephalon in two systems (piled-culture with an intervening transferrable membrane and co-culture). Among these brain tissues, the MBH was the most effective in inducing the development and migration of LHRH neurons. We further found synaptic junctions of immunonegative nerve fibers on immunoreactive LHRH neurons located in the septum of E16.5 and 17.5 embryos. These findings suggest that the MBH may lead the intraseptal migration of LHRH neurons by yielding certain substances after introducing the neurons into the medial aspect of forebrain vesicles. The early development of the neuronal connection may further promote the migration of LHRH neurons.

Animals↗