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PubMed1999

Acute regulation and long-term modulation of presynaptic serotonin output.

This contribution summarizes the present knowledge about the mechanisms involved in the regulation of presynaptic serotonin release. Under conditions of a permanently altered environmental, (psychosocial, drug-induced, nutritional etc.) input, each one of these mechanisms may be adaptively adjusted to the novel use-dependent requirements. Examples of such long-term alterations of the 5-HT-output pattern in distant projection fields of the raphe-neurons are the downregulation of cortical serotonin-transporters after long-term food restriction, the loss of serotonergic nerve terminals caused by substituted amphetamines, the serotonergic hyperinnervation of the frontal cortex seen after olfactory bulbectomy in rats, or the long lasting changes in the levels of tryptophanhydroxylase, of serotonin-transporter depression or in the density of serotonergic nerve terminals in distant projection fields caused by long-term antidepressant treatments. All these long-lasting alterations and imbalances of a previously established serotonin-output-pattern will not only affect the impact of individual regional networks on whole brain information processing but also the established synaptic connectivity in distant projection fields of the central serotonergic system.

Animals↗
PubMed1988

Immunocytochemical study of the hypothalamic magnocellular neurosecretory nuclei of the snake Natrix maura and the turtle Mauremys caspica.

An immunocytochemical study of the magnocellular neurosecretory nuclei was performed in the snake Natrix maura and the turtle Mauremys caspica by use of antisera against: (1) a mixture of both bovine neurophysins, (2) bovine oxytocin-neurophysin, (3) arginine vasotocin, and (4) mesotocin. Arginine vasotocin- and mesotocin-immunoreactivities were localized in individual neurons of the supraoptic and paraventricular nuclei, with a distinct pattern of distribution in both species. The same cells appeared to be stained by the anti-oxytocin-neurophysin and antimesotocin sera. The supraoptic nucleus can be subdivided into rostral medial and caudal portions. In N. maura, but not in M. caspica, neurophysin-immunoreactive neurons were found in the retrochiasmatic nucleus. No immunoreactive elements were seen in the suprachiasmatic nucleus of both species after the use of any of the antisera. A dorsolateral aggregation of neurophysin-containing cells, localized over the lateral forebrain bundle, was present in both species. Magnocellular and parvocellular neurophysin-immunoreactive neurons were present in the paraventricular nucleus of both species. In the turtle, the paraventricular neurons were arranged into four distinct layers parallel to the ependyma; these neurons were bipolar with the major axis perpendicular to the ventricle, and many of them projected processes toward the cerebrospinal-fluid compartment. In N. maura a group of large neurons of the paraventricular nucleus was found in a very lateral position. The posterior lobe of the hypophysis and the external zone of the median eminence contained arginine vasotocin- and mesotocin-immunoreactive nerve fibers. The lamina termialis of both species was supplied with a dense bundle of fibers containing immunoreactive neurophysin. Neurophysin-immunoreactive fibers were also present in the septum, some telencephalic regions, including the cortex and the olfactory tubercule, in the paraventricular organ, and the periventricular and periaqueductal gray of the brainstem.

Animals↗
PubMed1984

A functional link between the limbic cortex and ventral striatum: physiology of the subiculum accumbens pathway.

Parallel electrophysiological and anatomical tracing studies on the projections from the hippocampal formation to the ventral striatum in the cat, were carried out with the aim of defining the nature and organization of the motor interfaces of the limbic cortex. In this context the main pathway was found to be that from the subiculum to the N. Accumbens; electrophysiological characteristics of this pathway are reported in the present study. This well organized pathway is primarily of an excitatory nature and consists of slow conducting fibers (1-2 ms-1). Three types of response patterns of single Accumbens units to subicular simulation were found: units which responded with a burst of action potentials (the majority); units which responded with iterative bursting; units responding primarily with an inhibition of firing. Often the primary excitatory response was followed by a decrease in firing rate. Analysis of Evoked Potentials indicate that the subicular inputs induce a monopolar positive field within the N. Accumbens; in combination with the evidence obtained from current source density (CSD) analysis these data suggest the following activation model: subicular inputs evoke depolarization of synapses lying peripherally in the dendrites of stellate neurons provoking peripheral sinks which form a concentric shell around sources at and in the neighbourhood of the cell bodies. In addition to the subiculum-Accumbens pathway evidence was also obtained for an excitatory input from the Entorhinal cortex to the N. Accumbens. Furthermore, an excitatory pathway from the prepyriform cortex to the olfactory tubercle was also electrophysiologically identified.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Neuro-toxic interaction in alcohol-treated, thiamine-deficient mice.

Groups of adult male mice were either fed a thiamine-deficient diet for 10 weeks and thereafter treated with ethanol by making them inhale vapourized cane spirit for 10 weeks, or given both treatments simultaneously. The brains of these mice were then searched for degeneration using both light and electron microscopy. No degenerating nerve cells were observed in any animal in the cerebral cortex, hippocampus, cerebellum, olfactory bulbs, midbrain or hindbrain. However, axon terminal degeneration was seen in the olfactory bulbs and deep cerebellar nuclei in mice given the combined treatment. No cerebellar degeneration was found and only little degeneration was present in the olfactory bulbs of mice given the two treatments at different times. Thus, the combined treatment of alcohol and thiamine deficiency produced more brain damage than the sum of that produced by the two treatments given separately. This represents the first experimental in vivo demonstration of a biochemical interaction between these two factors in alcohol-related brain damage. The findings of long-term animal treatment with models using thiamine antagonists are compared.

Animals↗
PubMed1995

The effect of ethanol on HSP70 in cultured rat glial cells and in brain areas of rat pups exposed to ethanol in utero.

Prenatal exposure to alcohol is associated with a cluster of symptoms called Fetal Alcohol Syndrome with a characteristic pattern of neuroanatomy and biochemical changes. In recent years it has been shown, that stress exposed cells rapidly increase transcription and translation of heat shock protein genes resulting in an increased appearance of these proteins. It has also been found that heat shock proteins, especially the HSP70 family play a role as molecular chaperons maintaining the native conformation of proteins and participating in protein transport in particular cellular compartments. The aim of this study was to determine the effect of chronic maternal alcohol consumption on HSP70 content in the different regions of the brain of the newborn rats as well as to examine in vitro the effect of ethanol on HSP70 content in cultured glial cells. Chronic maternal ethanol consumption resulted in increased HSP70 in the following regions of developing brain: hippocampus, cerebellum, olfactory bulbs, frontal cortex and septum. Moreover, ethanol applied in vitro, increased HSP70 content in primary astroglial cultures and astrocytes but not in oligodendrocyte cultures. The above described changes may be important in brain maturation and may play a role in Fetal Alcohol Syndrome.

Alcoholism↗
PubMed1987

Activation of striatal neurons by dexamphetamine is antagonized by degeneration of striatal dopaminergic terminals.

Unilateral degeneration of nigrostriatal dopaminergic terminals by the intranigral infusion of 6-OHDA produced a decrease in spontaneous multiple unit activity (MUA) in both the ipsilateral and contralateral striata of freely moving rats. Nigral lesions also attenuated the dexamphetamine-induced increase in MUA in the ipsilateral but not in the contralateral striatum. The magnitude of the attenuation in the ipsilateral striatum was directly proportional to the percent depletion of dopamine. Similarly degeneration of dopaminergic terminals produced by a unilateral application of 6-OHDA into the striatum lowered spontaneous MUA and completely antagonized the dexamphetamine-induced increase in MUA in the dopamine-depleted striatum. Although the spontaneous MUA in striata contralateral to a local 6-OHDA treatment was significantly reduced, the response to dexamphetamine was normal. Both striatal and nigral application of 6-OHDA produced dopamine depletion in the ipsilateral striatum and an increase in striatal dopamine levels on the contralateral side. Striatal application of 6-OHDA did not alter dopamine levels in either the olfactory tubercles, piriform cortex or cingulate cortex. It is concluded that the increase in MUA observed in the striatum following dexamphetamine treatment is critically dependent upon the release of dopamine in the striatum. These results support the concept that dopamine may have an excitatory action on some striatal neurons.

Animals↗
PubMed1996

Persisting changes in brain glucose uptake following neurotoxic doses of phencyclidine which mirror the acute effects of the drug.

Phencyclidine (PCP) can induce a model psychosis which has a number of similarities to dementias and schizophrenia. In some cases the psychosis persists for prolonged periods after drug discontinuation. N-Methyl-D-aspartate (NMDA) antagonists such as PCP induce increases in glucose metabolism in a variety of brain structures but most notably in limbic regions such as retrosplenial, piriform, and entorhinal cortex, hippocampus, and olfactory tubercle. When given continuously for several days, these NMDA antagonists induced neural degeneration in these same critical limbic areas. In the present study regional 2-fluorodeoxyglucose (FDG) uptake was measured in rats at both 24 h and 10 days after neurotoxic, 5-day "binge" PCP administration. At 24 h after minipump removal there were persisting and large increases in glucose uptake in many brain regions, with maximal changes in the same limbic structures in which neurotoxicity has been observed. Surprisingly, many of these regions still showed elevated glucose metabolism after 10 days of recovery. These findings suggest an anatomical and neurochemical substrate for the persisting psychosis which can occur following PCP.

Animals↗
PubMed1998

Ontogeny of NADPH-diaphorase in rat forebrain and midbrain.

This study characterizes the developmental expression of NADPH-diaphorase from embryo to adulthood in the forebrain, midbrain and cerebellum of rat brain via histochemical staining. On embryonic day 12 no neurons stained. Labeling was observed in certain nuclei from E15 through the postnatal period to adulthood. Labeling in neurons increased or maintained a constant level with increased age. The embryo demonstrated substantial labeling in neurons of the caudate putamen, bed nucleus of the stria terminalis, preoptic area, lateral hypothalamic area, paraventricular thalamic nucleus, ventromedial hypothalamic nucleus, magnocellular nucleus posterior commissure, and periaqueductal central gray. Additional neuronal labeling was observed postnatally in the olfactory bulb, cerebral cortex, amygdala, various nuclei of the thalamus, interpeduncular nucleus, linear nucleus of the raphe, pretectal area and superior colliculus. In the cerebellum, labeling appeared only after P14 in cells of the molecular cell layer and granular cell layer. The sizes of labeled neurons developed significantly from P4 to P14 in several nuclei. The distinctive temporal and spatial expression pattern of NADPH-diaphorase implies that the NO/cGMP system may play an important role in physiological and developmental functions.

Age Factors↗
PubMed2006

Three types of tyrosine hydroxylase-positive CNS neurons distinguished by dopa decarboxylase and VMAT2 co-expression.

1. We investigate here for the first time in primate brain the combinatorial expression of the three major functionally relevant proteins for catecholaminergic neurotransmission tyrosine hydroxylase (TH), aromatic acid acid decarboxylase (AADC), and the brain-specific isoform of the vesicular monoamine transporter, VMAT2, using highly specific antibodies and immunofluorescence with confocal microscopy to visualize combinatorial expression of these proteins. 2. In addition to classical TH, AADC, and VMAT2-copositive catecholaminergic neurons, two unique kinds of TH-positive neurons were identified based on co-expression of AADC and VMAT2. 3. TH and AADC co-positive, but VMAT2-negative neurons, are termed "nonexocytotic catecholaminergic TH neurons." These were found in striatum, olfactory bulb, cerebral cortex, area postrema, nucleus tractus solitarius, and in the dorsal motor nucleus of the vagus. 4. TH-positive neurons expressing neither AADC nor VMAT2 are termed "dopaergic TH neurons." We identified these neurons in supraoptic, paraventricular and periventricular hypothalamic nuclei, thalamic paraventicular nucleus, habenula, parabrachial nucleus, cerebral cortex and spinal cord. We were unable to identify any dopaergic (TH-positive, AADC-negative) neurons that expressed VMAT2, suggesting that regulatory mechanisms exist for shutting off VMAT2 expression in neurons that fail to biosynthesize its substrates. 5. In several cases, the corresponding TH phenotypes were identified in the adult rat, suggesting that this rodent is an appropriate experimental model for further investigation of these TH-positive neuronal cell groups in the adult central nervous system. Thus, no examples of TH and VMAT2 co-positive neurons lacking AADC expression were found in rodent adult nervous system. 6. In conclusion, the adult mammalian nervous system contains in addition to classical catecholaminergic neurons, cells that can synthesize dopamine, but cannot transport and store it in synaptic vesicles, and neurons that can synthesize only L-dopa and lack VMAT2 expression. The presence of these additional populations of TH-positive neurons in the adult primate CNS has implications for functional catecholamine neurotransmission, its derangement in disease and drug abuse, and its rescue by gene therapeutic maneuvers in neurodegenerative diseases such as Parkinson's disease.

Animals↗
PubMed1987

Effect of ketamine on local cerebral glucose utilization in fetal sheep.

Ketamine hydrochloride was infused intravenously in eight near-term fetal sheep, in doses ranging from 4.6 to 62.2 mg/kg. Local cerebral glucose utilization was determined by the [14C]deoxyglucose method. Heterogeneity in density of autoradiographs, a prominent feature in untreated fetal brains, was greatly diminished in animals receiving greater than 18 mg/kg, with differences between cerebral cortical gray and white matter virtually disappearing at high doses. In striking contrast to the pale, washed-out appearance in autoradiographs of most cerebral, cerebellar, and brain stem structures was a relatively high density of entorhinal cortex, hippocampus, lateral olfactory tract, and olfactory bulbs. Local cerebral glucose utilization of most gray and white matter structures was elevated in one ketamine-treated fetus experiencing a marked drop in PO2 during the study.

Animals↗
PubMed1985

Regional heterogeneity of rat brain phencyclidine (PCP) receptors revealed by photoaffinity labeling with [3H] azido phencyclidine.

Photoaffinity labeling of rat brain phencyclidine (PCP) receptors with [3H] azido phencyclidine ([3H]AZ-PCP) reveals the existence of five polypeptides which are specifically labeled by the affinity probe (Mr's 90,000, 62,000, 49,000, 40,000 and 33,000). These labeled components are unevenly distributed in rat brain. In the frontal cortex, thalamus and olfactory bulb, the major bands labeled are the Mr's 90 K and 62 K polypeptides; in the cerebellum most of the labeling is in the 90 K and 33 K bands; and in the hippocampus all but the Mr 40 K band are heavily labeled. Together with dexoxadrol/[3H]PCP competition binding data, which indicated the existence of high and low affinity dexoxadrol/PCP binding sites, these results suggest regional heterogeneity of PCP receptors. The regional distribution of the high affinity dexoxadrol binding sites correlates best with that of the Mr 90 K polypeptide.

Affinity Labels↗
PubMed1985

In vivo effects of aminooxyacetic acid and valproic acid on nerve terminal (synaptosomal) GABA levels in discrete brain areas of the rat. Correlation to pharmacological activities.

A newly developed synaptosomal model was used to evaluate the in vivo effects of the GABA-elevating drugs aminooxyacetic acid (AOAA, 30 mg/kg i.p.) and valproic acid (VPA, 200 mg/kg i.p.) on GABA levels in nerve endings of 11 brain regions in rats as a function of time after administration. The data obtained were compared with the magnitude and time course of the effects of both drugs in rats on body temperature, pain response and against seizures induced by electroshock, pentylenetetrazol and 3-mercaptopropionic acid. Following AOAA, maximum increases in synaptosomal GABA levels of brain regions were observed 6 hr after administration. At this time, GABA was significantly elevated up to 300% over control values in synaptosomal fractions from all 11 regions. However, the hypothermic and antinociceptive effects of the drug as well as its anticonvulsant action against electroshock and pentylenetetrazol induced seizures were maximal 1 hr after injection and had vanished after 6 hr, i.e. at the time of maximum GABA increases in synaptosomes. The only pharmacological effect of AOAA which paralleled the time course of the synaptosomal GABA elevation was the attenuation of seizures induced by 3-mercaptopropionic acid. Following VPA, the effect on synaptosomal GABA levels was much more rapid in onset and significant increases were already determined 5 to 30 min after administration. Significant increases of up to 80% over control values were found in synaptosomal fractions from olfactory bulb, frontal cortex, hippocampus, hypothalamus, tectum, substantia nigra and cerebellum. In contrast to AOAA, the time course of the synaptosomal GABA increases, at least in some regions, was similar to the time course of VPA's antinociceptice effects and its anticonvulsant effects in the three seizure models studied. The data may suggest that AOAA and VPA increase different pools of GABA within nerve terminals, only one of which is involved in GABA-mediated neurotransmission.

Acetates↗
PubMed1983

Cholecystokinin peptides in the brain and pituitary of the bullfrog Rana catesbeiana: distribution and characterization.

The distribution of CCK peptides in the bullfrog brain was determined with a CCK radioimmunoassay. Frog brain CCK distribution resembles rat porcine and human brain in that CCK concentration is moderate to high in hypothalamus, diencephalon, and medulla (3 18.4 ng/mg protein) and low in cerebellum (0.6 ng/mg protein). However, unlike all mammalian species examined, the CCK content of frog cerebral cortex, hippocampus and olfactory lobe is quite low (0.03 0.23 ng/mg protein). The elution of CCK-like peptides in frog brain extracts was determined on two HPLC systems. On both systems the bulk of the CCK-like material eluted with CCK 8 sulfate and separated from gastrin and other CCK peptides. These data suggest that though the chemical structure of CCK appears to be the same in the brains of frogs and mammals, the distribution of CCK in the brain appears to have shifted during the course of evolution, becoming a cortical, hippocampal, and olfactory system peptide only in more evolved organisms.

Animals↗
PubMed1985

Biochemical characterization and autoradiographic localization of central substance P receptors using [125I]physalaemin.

The binding of [125I]physalaemin to rat brain slices was investigated. Radiolabeled physalaemin bound with high affinity (Kd = 0.3 nM) to a single class of sites (Bmax = 22 fmol/mg protein). Kinetic studies indicated that binding was time-dependent and all specific binding was reversible. Pharmacology studies indicated that specific [125I]physalaemin binding was inhibited by structurally related peptides such as substance P and eledoisin. Biochemical studies indicated that specific binding of radiolabeled physalaemin was greatly reduced if the brain slices were pretreated with heat, trypsin or N-ethyl maleimide. Autoradiographic studies indicated that the [125I]physalaemin binding sites were discretely distributed throughout the brain. Highest grain densities were present in the olfactory bulb, dentate gyrus, amygdala, superficial layers of the superior colliculus, subiculum, dorsal parabrachial nucleus, locus coeruleus, nucleus tractus solitarii and dorsal horn of the spinal cord. Moderate grain densities were present in the nucleus accumbens, olfactory tubercle, pyriform cortex, striatum, hippocampus, inferior colliculus and central gray of the midbrain. Low grain densities were present in most thalamic nuclei, the substantia nigra and cerebellum. The corpus callosum and controls treated with 1 microM unlabeled physalaemin had negligible levels of binding. The unique pharmacological and regional distribution data obtained suggest that [125I]physalaemin may serve as a valuable probe to study central substance P receptors.

Animals↗
PubMed1985

Quantitative autoradiographic mapping of serotonin receptors in the rat brain. II. Serotonin-2 receptors.

The distribution of serotonin-2 (5-HT2) receptors in the rat brain was studied by light microscopic quantitative autoradiography. Receptors were labeled with four ligands: [3H]ketanserin, [3H]mesulergine, [3H]LSD and [3H]spiperone, which are reported to show high affinity for 5-HT2 receptors. Co-incubation with increasing concentrations of several well-known 5-HT2-selective drugs, such as pirenperone, cinanserin and ketanserin, resulted in an inhibition of the binding of the four 3H-labeled ligands to the same areas. However, all of them recognized, in addition to 5-HT2 sites, other populations of binding sites. Receptor densities were quantified by microdensitometry with the aid of a computer-assisted image-analysis system. Our results reveal a heterogeneous distribution of 5-HT2 receptor densities in the rat brain. Very high concentrations were localized in the claustrum, olfactory tubercle and layer IV of the neocortex. The anterior olfactory nucleus, piriform cortex and layer I of neocortex were also rich in 5-HT2 receptors. Intermediate concentrations of receptors were found in caudate putamen, nucleus accumbens, layer V of neocortex, ventral dentate gyrus and mammillary bodies. Areas containing only low concentrations of receptors included the thalamus, hippocampus, brainstem, medulla, cerebellum and spinal cord. The specificity of the different ligands used is discussed in terms of the other populations of sites recognized by them. The distribution of 5-HT2 receptors here reported is discussed in correlation with (a) the known distribution of serotoninergic terminals, (b) the specific anatomical systems and (c) the central effects reported to be mediated by 5-HT2-selective drugs.

Animals↗
PubMed1987

Dopamine-like action of nicotine: lack of tolerance and reverse tolerance.

Rats with unilateral 6-hydroxydopamine lesions of the substantia nigra became briefly sedated and hypothermic after the acute injection of nicotine s.c. (0.4 or 0.8 mg/kg free base). When nicotine was repeated 5 days per week there was rapid tolerance for the sedation and slower tolerance for the hypothermia and the lesioned animals began to rotate ipsiversively after each injection. Stereotypic behavior was also noted. Rats injected with nicotine 5 days per week and nigrally lesioned on the 24th day rotated promptly on their first postoperative injection of nicotine. The nicotinic antagonist, mecamylamine (1.0 mg/kg i.p.), completely blocked the induced rotation. The appearance of rotation did not seem to depend on tolerance to sedation. The direction of rotation indicated enhancement of activity in the intact nigrostriatal system. However, 10 min after the acute injection of 0.8 mg/kg nicotine no change was found in the ratios of dopamine to its metabolites DOPAC and homovanillic acid in the substantia nigra, caudate-putamen, nucleus accumbens, olfactory tubercle, frontal cortex, or ventral tegmental area. Rats given 0.4 or 0.8 mg/kg nicotine 5 days per week and either lesioned prior to nicotine or lesioned during the third week rotated during the sixth week without any sign of tolerance. One day after the 30th injection in intact or lesioned rats the ratios of dopamine to its metabolites did not differ from those in saline controls on either the right or left side of any of the regions examined. There was no evidence of a change in dopamine metabolism after an acute challenge with nicotine or of a sustained change after repeated injection. The possibility remains that repeated nicotine modifies the dopaminergic response to nicotine without causing a sustained change in metabolism.

Animals↗
PubMed1988

Autoradiographic visualization in rat brain of receptors for omega-conotoxin GVIA, a newly discovered calcium antagonist.

Putative N-type voltage-sensitive calcium channels were localized autoradiographically in thaw-mounted rat brain slices using [125I]omega-conotoxin GVIA as a ligand. Density of the toxin binding sites were highly heterogeneous throughout the brain. The highest density of the binding sites was observed in the glomerular layer of the olfactory bulb, cerebral cortex, molecular layer of the hippocampus, amygdaloid complex, reticular part of the substantia nigra, molecular layer of the cerebellar cortex, and nucleus of the solitary tract. White matter tract regions such as the internal capsule, corpus callosum, fimbria of the hippocampus, fornix, and fasciculus retroflexus showed an extremely low density.

Animals↗
PubMed1990

Glial localization of adenylate-cyclase-coupled beta-adrenoceptors in rat forebrain slices.

Fluorocitrate (FC), a selective inhibitor of glial cell respiration, was used to estimate the extent to which glial cells contain adenylate cyclase-coupled beta-adrenoceptors in rat brain slices. The drug blocked 75-95% of the elevation of cyclic AMP caused by the beta-agonist, isoproterenol, in the 4 forebrain regions sampled (frontal and parietal cortex, caudate nucleus, olfactory tubercle). Intracellular recording of neurons in the treated slices confirmed that they were unaffected by FC. Treatment with the neurotoxin, kainic acid, eliminated all electrophysiological activity but did not affect the cAMP response. The results indicate that glial cells contain the preponderance of adenylate-cyclase-coupled beta-adrenoceptors in slices of the rat forebrain and may constitute an important target of the central noradrenergic system in vivo.

Adenosine Triphosphate↗