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At least 1,099 records · Page 61Linked to original sources
PubMed1996

Effects of gestational or neonatal treatment with alpha-difluoromethylornithine on ornithine decarboxylase and polyamines in developing rat brain and on adult rat neurochemistry.

Pregnant rats were treated for five consecutive days during gestation with s.c. injections of the ornithine decarboxylase (ODC) inhibitor alpha-difluoromethylornithine (DFMO). Treatment beginning at gestational days 13 or 14 was effective in inhibiting ODC and altering polyamine levels, and resulted in relatively small decreases in body and forebrain weight, but not in significant differences in adult neurochemistry. Neonatal rats were treated with DFMO from postnatal day 0 (PD 0) to PD 24. In addition to some somatic effects (decreased body weight, delayed eyelid opening and delayed fur growth) the postnatal treatment resulted in a permanent decrease in brain weight, which was mainly due to a dramatic decrease in cerebellar size. During treatment, and 3 days after the end of it, the levels of putrescine and spermidine, but not those of spermine, were consistently lower in the cerebellum and forebrain of DFMO-treated rats than in controls. On the other hand, ODC appeared strongly inhibited only during the first phase of the treatment and showed recovery, and also rebound of the activity, during the second part of the treatment. A screening of neurochemical markers related to cholinergic, GABAergic and glutamatergic neurons, as well to astrocytes and oligodendrocytes was performed in several brain regions (cerebellum, olfactory bulbs, cortex, striatum, hippocampus) of some of these rats once they became adults. Significant alterations for all the parameters tested, with the exception of the marker for the glutamatergic transmission, were measured in the undersized cerebellum of the neonatally DFMO-treated rats. A shorter neonatal treatment with DFMO (from PD 1 to 6) resulted, in the adult, in decreased cerebellar size and in neurochemical alterations, both very similar to those occurring after the prolonged treatment. In the other brain regions a few minor differences were noticed. The present results show that: (1) the brain polyamine system is differently regulated in foetuses with respect to newborns; (2) the effects of chronic ODC blockade are different on prenatally or postnatally proliferating neurons, due either to a lower sensitivity of gestationally proliferating neurons or to a subsequent recovery; and (3) chronic postnatal ODC inhibition has a strong effect on proliferating neurons, but little effect on further maturation of postmitotic neurons.

Animals↗
PubMed1993

Dexamethasone target sites in the central nervous system and their potential relevance to mental illness.

1. The topical distribution of tritiated dexamethasone (DEX), a potent synthetic glucocorticoid of widespread use in the diagnosis and assessment of mental illness, was studied in rat CNS by autoradiography to obtain information on potential target sites for feedback and other centrally mediated effects of glucocorticoids. 2. The cells of the arcuate nucleus of the hypothalamus and the lateral thalamic nuclei displayed the most concentrated nuclear accumulation of silver grains. 3. Significant accumulation, exceeding that found in the hippocampal formation, also occurred in the cells of the ventromedial, periventricular, and paraventricular nuclei of the hypothalamus, the locus ceruleus, the nucleus tractus solitarii, and the area postrema, none of which are targeted by corticosterone, the native glucocorticoid of the rat. 4. Nuclear accumulation of silver grains was prominent in neural and glial cells of the cerebral cortex, the olfactory nucleus, the dorsolateral septum, the amygdala, the subfornical organ, the lateral parabrachial, medial trapezoid, and dorsal reticular nuclei, the nucleus centralis of the raphe, the cerebellum, and vascular tissues. 5. The localization of DEX in hypothalamic and brain-stem nuclei coincided with that of the glucocorticoid receptor, possibly implicating these sites in direct or modulating effects of glucocorticoids in various forms of mental disturbance, including depression, anxiety, panic disorders, and alcohol withdrawal. 6. The extent to which various CNS regions targeted by DEX feature in negative feedback control of adrenocortical secretion remains to be defined, as does the site of impaired feedback disclosed by the dexamethasone suppression test in psychiatric patients.

Animals↗
PubMed1989

Regionally-specific alterations in mesotelencephalic dopamine synthesis in diabetic rats: association with precursor tyrosine.

The effect of diabetes-induced chronic tyrosine (Tyr) deficiency on dopamine (DA) synthesis in different areas of the mesotelencephalic DA system was examined. Diabetes was induced using streptozotocin. In vivo Tyr hydroxylation was used as an index of DA synthesis. The brain areas examined were prefrontal cortex (PFC), pyriform cortex (PYR), olfactory tubercle (OT), caudate-putamen (CP), substantia nigra (SN), and ventral tegmental area (VTA). Significant decreases in Tyr hydroxylation were observed in PFC, CP, and PYR. The largest decrease was seen in the PFC. Variations in tissue Tyr levels were shown to account for 62% of the variability in Tyr hydroxylation in the PFC, and 23% of the variability in the CP; a significant correlation between Tyr levels and Tyr hydroxylation was not seen in the other brain areas. The mechanisms underlying this regionally selective effect, and possible clinical relevance are discussed.

Animals↗
PubMed1985

In vivo effects of anticonvulsant drugs on nerve terminal (synaptosomal) GABA levels in 11 brain regions of the rat.

The in vivo effects of two GABA-elevating drugs with anticonvulsant properties, namely valproic acid (VPA) and aminooxyacetic acid (AOAA), on nerve terminal GABA levels in discrete rat brain regions were studied by means of a newly developed synaptosomal model. The profile of synaptosomal GABA increases obtained with AOAA was quite different from that seen with VPA. Thus, AOAA (30 mg/kg i.p., 2 hours) caused significant increases in olfactory bulb, cortex, hippocampus, thalamus and cerebellum, whereas VPA (200 mg/kg i.p., 0.5 hour) significantly increased GABA also in hypothalamus, substantia nigra and superior and inferior colliculus. In contrast to the regional selectivity of both drugs with respect to synaptosomal GABA levels, AOAA in most regions was more potent than VPA in increasing whole tissue GABA levels determined prior to subcellular fractionation. The data thus demonstrate that comparison of GABA levels in synaptosomal fractions rather than homogenates from discrete brain areas provides a more sensitive index of the action of GABA-elevating drugs administered in vivo.

Aminooxyacetic Acid↗
PubMed2005

Tissue- and species-specific expression patterns of class I, III, and IV Adh and Aldh 1 mRNAs in rodent embryos.

Alcohol and aldehyde dehydrogenases (ADHs and ALDHs) may be of interest in the pathology of Parkinson's disease (PD) because of their role in protection against toxins and in retinoid metabolism, which is required for growth and development of the mesencephalic dopamine system. In the present study, the spatial and temporal expression patterns of Adh 1, Adh 3, Adh 4, and Aldh 1 mRNAs in embryonic C57BL/6 mice (E 9.5-E19.5) and Sprague-Dawley rats (E12.5-P0) have been investigated by using radioactive oligonucleotide in situ hybridization. High expression of Aldh 1 mRNA was found in the developing mesencephalic dopamine neurons of both mice and rats. Expression of Adh 1 and Adh 4 mRNAs was observed in adrenal cortex and olfactory epithelium in mice. Additionally, Adh 1 was expressed in epidermis, liver, conjunctival, and intestinal epithelium. In rat embryos, expression was less extensive, with Adh 1 mRNA being found in liver and intestines. Adh 3 expression was ubiquitous in both mouse and rat embryos, suggesting a housekeeping function of the gene. Consistent with previous studies in adult rats and mice, our data suggest that Adh 3 is the only ADH class present in rodent brain. Adh and Aldh gene activity in mouse and rat embryos indicate the possible involvement of the respective enzymes in retinoid metabolism and participation in defense against toxic insults, including those that may be involved in the pathogenesis of PD.

Alcohol Dehydrogenase↗
PubMed1985

Kainic acid-induced seizures: dose-relationship of behavioural, neurochemical and histopathological changes.

Behavioural, neurochemical and histopathological changes induced by systemic injection of kainic acid were investigated at various doses of the neurotoxin (3, 6 and 10 mg/kg s.c.). There was a positive correlation between the dose of kainic acid and the extent of both the acute neurochemical changes 3 h after the injection (increases of 3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid levels and a decrease in noradrenaline levels in all brain regions investigated), the acute histopathological changes (shrinkage and condensation of nerve cells and brain oedema in the entire forebrain) and the extent of behavioural alterations (immobility, 'wet dog shakes' and limbic seizures). However, the slope of the dose-response curves was very steep. Late and irreversible alterations included losses of the enzyme markers glutamic acid decarboxylase and choline acetyltransferase and, histopathologically, incomplete parenchymal necrosis and haemorrhages. These changes, however, were restricted to a few brain regions, the most important being the hippocampus, amygdala, entorhinal and pyriform cortex, and olfactory bulb, and they were seen only in animals which had undergone severe convulsions. It is suggested that the irreversible brain lesions in this animal model of limbic (temporal lobe) epilepsy are not solely induced by a direct action of kainic acid, but may be caused--at least in part--by additional, secondary pathogenetic mechanisms.

Animals↗
PubMed1985

Distribution of immunoreactive metorphamide (adrenorphin) in discrete regions of the rat brain: comparison with Met-enkephalin-Arg6-Gly7-Leu8.

The distribution of immunoreactive (ir)-metorphamide (adrenorphin) in 101 microdissected rat brain and spinal cord regions was determined using a highly specific radioimmunoassay. The highest concentration of metorphamide in brain was found in globus pallidus (280.1 fmol/mg protein). High concentrations of ir-metorphamide (greater than 120 fmol/mg protein) were found in 9 nuclei, including central amygdaloid nucleus, lateral preoptic area, anterior hypothalamic nucleus, hypothalamic paraventricular nucleus, interpeduncular nucleus, periaqueductal grey matter and nucleus of the solitary tract. Moderate concentrations of the peptide (between 60 and 120 fmol/mg protein) were found in 47 brain nuclei such as nucleus accumbens, bed nucleus of stria terminalis, several septal and amygdaloid nuclei, most of the hypothalamic nuclei, ventral tegmental area, red nucleus, raphe nuclei, lateral reticular nucleus, area postrema and others. Low concentrations or ir-metorphamide (less than 60 fmol/mg protein) were measured in 41 nuclei, e.g., cortical structures, hippocampus, caudate nucleus, thalamic nuclei, supraoptic nucleus, substantia nigra, vestibular nuclei, cerebellum (nuclei and cortex). The olfactory bulb has the lowest metorphamide concentration (5.8 fmol/mg protein). Spinal cord segments exhibit very low peptide concentrations.

Animals↗
PubMed1987

Localization of neurotensin receptors in the forebrain of the common marmoset and the effects of treatment with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

The distribution of neurotensin binding sites was mapped in the brain of the common marmoset using [3H]neurotensin as the ligand. Autoradiographic techniques show that the density of receptors is particularly high in the substantia nigra, ventral tegmental area, olfactory tubercle and cerebral cortex and that the distribution of neurotensin receptors in the cerebral cortex and striatum is heterogenous. In the cerebral cortex neurotensin receptors are concentrated in layers I, II, III and V, whilst receptor density is generally less in all layers of middle temporal cortex. Striatal neurotensin receptors conformed to a striosomal distribution as defined by acetylcholinesterase staining with the highest density of binding sites in the matrix. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine selectively destroyed over 80% of the dopaminergic neurons of the marmoset substantia nigra and almost 60% of those in the adjacent ventral tegmental area. The subsequent loss of a large proportion of neurotensin receptors from marmoset substantia nigra and striatum suggests their presence on the dopaminergic nigrostriatal pathway.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1992

Regional distribution of copper, zinc and iron in the brain in Long-Evans Cinnamon (LEC) rats with a new mutation causing hereditary hepatitis.

In Long-Evans Cinnamon (LEC) rats of three different ages (7, 13 and 32 weeks old) concentrations of Cu, Zn and Fe were measured in 8 regions of the brain. The LEC groups aged 7 and 13 weeks showed low concentrations of Cu in all regions compared to Long-Evans Agouti (LEA) rats. In 32-week-old LEC rats, however, Cu concentrations increased in 7 regions, in particular, significantly so in the striatum, hypothalamus, cerebellum, midbrain and cortex. Changes of Zn concentration were not found in any region. The Fe concentration increased in cortex and olfactory lobes. The three LEC groups showed a very high concentration of hepatic Cu and a low concentration of serum Cu compared to LEA rats. In LEC rats aged 32 weeks, however, hepatic Cu decreased and serum Cu increased compared to the other two LEC groups. These results suggest that the increase of the cerebral Cu concentration is closely related to the inherently abnormal Cu metabolism and then to the changes of Cu metabolism from about 13 weeks after birth.

Animals↗
PubMed1994

Localization of neurotrophin-3-like immunoreactivity in the rat central nervous system.

Neurotropin-3 (NT3) is a nerve growth factor (NGF) homologue whose function is presently unknown. The factor promotes the survival of a subpopulation of sensory and sympathetic neurons in vitro. NT3 mRNA is widely distributed in both the peripheral and central nervous system but the distribution of NT3 has not yet been examined. In the present study we have determined the regional distribution and cellular localization of NT3-like immunoreactivity (-IR) in the central nervous system by immunohistochemistry. Both glia and neurons were stained. NT3-IR glia were distributed in corpus callosum, substantia nigra, fimbria of hippocampus, subependymal areas of the ventricles and cerebellum. In the forebrain, NT3-IR was detected in a number of neuronal cells, including pyramidal cells in the fifth layer of the cerebral cortices, subpopulations of neurons in the septal nuclei, diagonal bands of Broca, olfactory primary cortex, amygdala and islands of Calleja. In the hippocampus, pyramidal cells in the CA1, CA2 and lateral regions of CA3 and granular cells in dorsal dentate gyrus were labelled with different intensities. Neurons in the bed nuclei of the striatum terminalis, mesencephalic trigeminal nuclei and motoneurons in the brain stem and spinal cord were intensively labelled. A subpopulation of neurons in the reticular thalamic nuclei and midbrain were moderately labelled. Finally, in the cerebellum, NT3-IR was also found in Purkinje cells and neurons in the deep cerebellar nuclei. In some brain regions such as hippocampus, the distribution of NT3-IR correlates with that of mRNANT3 as described by others. In contrast in other regions such as spinal cord and brain stem, little correlation was found between protein and mRNA. The results suggest that some NT3 immunoreactive neurons in the central nervous system accumulate NT3 in accord with a neurotrophic role for their maintenance or survival, while others may synthesize and secrete the factor to provide support for innervating neurons.

Animals↗
PubMed1994

mu-Opioid receptor mRNA expression in the rat CNS: comparison to mu-receptor binding.

The distribution of cells expressing mu-receptor mRNA and mu-receptor binding sites were compared in brain and spinal cord tissue sections using a combination of in situ hybridization and receptor autoradiographic techniques. mu-Receptor mRNA was visualized with a 35S-labeled cRNA probe directed to transmembrane III-VI of the rat mu-receptor, while mu-receptor binding sites were labeled with the mu-selective ligand [3H]DAMGO. A high correspondence between the mu-receptor mRNA and receptor binding distributions was observed in the nucleus of the accessory olfactory bulb, anterior olfactory nuclei, striatal patches of the nucleus accumbens and caudate-putamen, endopiriform nucleus, claustrum, diagonal band of Broca, globus pallidus, ventral pallidum, bed nucleus of stria terminalis, most thalamic nuclei, medial and posteriocortical medial amygdala, lateral, dorsomedial, posterior and mammillary nuclei of the hypothalamus, presubiculum, subiculum, rostral interpeduncular nucleus, median raphe, inferior colliculus, parabrachial nucleus, locus coeruleus, central grey, nucleus ambiguus, nucleus of the solitary tract, nucleus gracilis, nucleus cuneatus, and the dorsal motor nucleus of vagus. Differences in mu-receptor mRNA and receptor binding distributions were observed in several regions, including the olfactory bulb, cortex, hippocampus, superior colliculus, spinal trigeminal nucleus, cochlear nucleus and spinal cord, and may be due to mu-receptor transport to presynaptic terminals.

Animals↗
PubMed1985

Modulation of alpha 1-and alpha 2-adrenoceptor binding sites in the brain of audiogenic seizure susceptible mice (DBA/2J).

The binding of [3H]dihydroalprenolol ([3H]DHA), [3H]prazosin and [3H]clonidine was assayed in whole brain and various brain regions of audiogenic seizure (AS) susceptible DBA/2J (D2) mice aged 10, 24 and 50 days (i.e. before, during and after their period of AS susceptibility, respectively) and in age-matched C57BL/6J (B6) controls. In whole brain, at 24 days, [3H]DHA binding was similar in the two strains, while the binding of [3H]prazosin and [3H]clonidine was significantly lowered in D2 mice. No difference could be detected in 10 and 50 day old mice with any of the ligands. Regional studies indicated an involvement of the cerebral cortex, the olfactory bulbs and the brain-stem. alpha- (but not beta-)adrenoceptor changes were concomitant with the AS susceptibility period. These changes were unevenly distributed in the brain of D2 mice; they suggest that alpha 1- and alpha 2-adrenoceptor subtypes might play different roles in the AS of the D2 mouse strain.

Acoustic Stimulation↗
PubMed1988

Changes in the limbic neurotensin systems induced by dopaminergic drugs.

Single or multiple high doses of the dopamine-releasing drug, methamphetamine, induced 100-150% increases in the content of neurotensin-like immunoreactivity (NTLI) in the nucleus accumbens, but was without effect on the NTLI level in the ventral tegmental area. The increases in NTLI content in the nucleus accumbens were selectively blocked by the dopamine D-1 receptor antagonist, SCH 23390, which failed to exert any significant effect of its own in the same area. In contrast, haloperidol or the selective dopamine D-2 antagonist, sulpiride, when administered alone, significantly raised the NTLI level in the nucleus accumbens and when given concomitantly with methamphetamine, their effects on the amount of NTLI appeared to be additive. Very different patterns of response were observed in neurotensin systems associated with the mesocortical dopaminergic terminal fields of the frontal cortex and olfactory bulbs. Changes in NTLI contents occurred following only multiple doses of methamphetamine and consisted of decreases in levels of this peptide. However, like the nucleus accumbens, these methamphetamine-induced alterations were blocked completely by D-1 antagonism, while D-2 blockade appeared to be additive with the effects of methamphetamine.

Animals↗
PubMed1995

Expression of the mouse and rat mas proto-oncogene in the brain and peripheral tissues.

We isolated the mas proto-oncogene from a mouse genomic library. Sequence analysis showed that it contains an open reading frame without intervening sequences. The amino acid sequence deduced confirms the seven-transmembrane-domain structure and exhibits 97% and 91% amino acid homology with the rat and the human Mas, respectively. In mice and rats, mas mRNA was detected in the testis, kidney, heart, and in the brain regions: hippocampus, forebrain, piriform cortex, and olfactory bulb. Testicular mas mRNA from rats increases markedly during development, while cerebellar mRNA is high postnatally but completely disappears at later stages. We conclude that the product of the mouse mas gene may be involved in the development of the brain and testis.

Amino Acid Sequence↗