bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of destruction of serotonin neurons on basal and fenfluramine‐induced serotonin release in striatum
Authors: Kirby Lynn G. , Kreiss Deborah S. , Singh Ashish , Lucki Irwin 
Published: December 2004

AbstractThis study examined the relationship between the magnitude of tissue serotonin (5‐HT)depletion produced by treatment with the neurotoxin 5,7‐dihydroxytryptamine (5,7) and basal and fenfluramine‐induced 5‐HT release in the striatum. Separate groups of rats were treated with either vehicle or 5,7‐DHT (100μ 76% striatal 5‐HT depletion; or 200μ 93% styriatal 5‐HT depletion). four weeks after treatment 5‐HT release was measured in the ventral striatum using in vivo microdialysis in animals anesthetized with chloral hydrate. Basal 5‐HT levels were not significantly altered in any lesion group, whereas basal 5‐hydroxyindoleacetic acid levels were dosedependently reduced by 5,7‐DHT. In contrast, the increase of 5‐HT release produced by fenfluramine treatement (10 mg/kg) wa diminished significantly after 5‐HT neuronal destruction in correlation with the reduction of striatal tissue 5‐HT content. Fractional 5‐HT efflux, a measure of the 5‐HT release from surviving striatal nerve terminals, was also significantly elevated when tissue depletion of 5‐HT exceeded 95%. This study suggests that compensatory mechanisms may enable surviving 5‐HT terminals to maintain basal 5‐HT levels in th striatum with as little as 5% of the terminals remaining, but those mechanisms are not sufficient to allow the damaged system to respond to a pharmacological challenge. © 1995 Wiley‐Liss, Inc.
Brain somatostatin receptors in a rat model of acute liver failure
Authors: Boyano‐Adánez Maria Del Carmen , Barrios Vicente , Afulla Eduardo 
Published: December 2004

AbstractThe present study examines the effect of acute liver failure induced by a single intraperitoneal (i.p.) injection of D‐galactosamine‐HC1(3 gkg) on somatostatin (SS) binding and levels in the rat frontoparietal cortex and hippocampus. Neurobehavioural changes were evaluated by the method of Zieve et al. (1984)J. Lab. Clin. Med., 1046554641.The rats were decapitated as soon as they reached neurobehavioural stage I or 11. In stage I, rats had lethargy and in stage I1 they showed mild ataxia, mainly in the hind limbs. The administration of D‐galactosamine elevated serum transaminase levels (mean peak level 2,242 IU/1) but hypoglycemia, gross cerebral edema, or signs of sepsis were not detected in any of the animals studied. In addition, D‐galactosamine did not affect somatostatin‐like immunoreactivity (SSLI) levels in either brain area in any of the experimental groups as compared to the control groups. The rats sacrificed in stage I showed no change in the number or affinity of specific 125I‐Tyr11‐somatostatin(125I‐Tyr11‐SS)receptors in synaptosomes from the frontoparietal cortex and hippocampus. The rats sacrificed in stage II showed a decrease in the number of specific 125I‐Tyr11‐SS receptors in synaptosomes from both brain areas, with no change in receptor affinity. Binding studies were also conducted on synaptosomes from the frontoparietal cortex and hippocampus of rats that received D‐galactosamine but did not develop acute liver failure and consequently did not develop neurobehavioural changes. The SS receptors in these synaptosomes did not change in comparison with controls, indicating that the D‐galactosamine was not directly responsible for the changes in the cerebral SS receptors. SS caused a significantly lower inhibition in AC activity in frontoparietal cortex and hippocampal membranes of D‐galactosamine‐treated rats sacrificed in stage II. No significant differences were seen for the basal or for the forskolin (FK)‐stimulated AC activities in all groups. The results of this study indicate that D‐galactosamine‐induced acute liver failure in rats is associated with a decrease of the number of SS receptors and the inhibitory effect of SS on adenylyl cyclase (AC) activity in frontoparietal cortex and hippocampus when the animals showed neurobehavioural stage II from Zieve et al. [(1984)J. Lab. Clin. Med., 104:655‐664]. © 1995 Wiley‐Liss, Inc.
Biochemical and electrophysiological effects of 7‐OH‐DPAT on the mesolimbic dopaminergic system
Authors: Devoto Paola , Collu Maria , Muntoni Anna Lisa , Pistis Marco , Serra Gino , Gessa Gian Luigi , Diana Marco 
Published: December 2004

AbstractSystemic administration of the putative selective D3 receptor agonist 7‐hydroxy‐2‐(N, N‐di‐n‐propylamino)tetralin(7‐OH‐DPAT) consistently decreased extracellular dopamine and 3,4‐dihydroxyphenylacetic acid (DOPAC) levels in the nucleus accumbens and dopaminergic neuronal activity in the ventral tegmental area. 7‐OH‐DPAT inhibited dopamine release in the nucleus accumbens also when locally perfused through the dialysis probe. The results suggest the possibility that stimulation of dopamine D2 receptors with 7‐OH‐DPAT mimic biochemical and electrophysiological actions previously ascribed to D2 autoreceptor stimulation; however the lack of selective D3 antagonist precludes any firm conclusion in this sense. © 1995 Wiley‐Liss, Inc.
Neuroprotective sigma ligands interfere with the glutamate‐activated NOS pathway in hippocampal cell culture
Authors: Lesage Anne S. , De Loore Katrien L. , Peeters Luc , Leysen Josee E. 
Published: December 2004

AbstractWe studied neuroprotective properties of 12 structurally different sigma site ligands in primary rat hippocampal cell cultures and analyzed whether they interfere with glutamate‐induced activation of the nitric oxide synthase (NOS) pathway. Neurotoxicity was triggered with 1mM glutamate on day 8 of culture. Cells were treated with various concentrations of the compounds for 7 days before glutamate exposure (prolonged pretreatment), or during glutamate exposure (acute treatment). Protection was seen after prolonged pretreatment (long‐term protection) with sabeluzole, opipramole, haloperidol, ifenprodil, fenpropimorph, carbetapentane, and tiospirone, with pIC50S of 7.30, 7.15, 6.87, 6.68, 6.66, 6.39, and 6.34, respectively. There was no protection with PD 128298, 1,3‐ortho‐di‐tolylguanidine, BMY‐14802, (+)3‐(3‐hydroxyphenyl)‐N‐l(propy1) piperidine, or dextromethorphan. Upon acute treatment, only ifenprodil was protective. Interference of the drugs with glutamate activation of the NOS pathway was determined by measuring glutamate‐activated cGMP formation and citrulline levels. Glutamate‐activated cGMP formation was reduced by all neuroprotective sigma ligands after prolonged pretreatment but not after acute treatment. Sigma ligands added to cell culture iysate did not reduce citrulline formation, evidence that there was no direct effect on the NOS enzyme. We conclude that some but not all sigma ligands exert long‐term protective properties against glutamate‐induced neurotoxicity in primary hippocampal cultures, and that this protection is accompanied by attenuation of cGMP formation in the NOS pathway. However, inhibition of cGMP formation by itself appeared not sufficient for obtaining neuroprotective effects, as inhibition of glutamate‐activated cGMP formation by N‐nitro‐L‐arginine, haemoglobin, or PD128298 did not provide neuroprotection. © 1995 Wiley‐Liss, Inc.
Neuropharmacology of the nucleus accumbens: Iontophoretic applications of morphine and nicotine have contrasting effects on single‐unit responses evoked by ventral pallidal and fimbria stimulation
Authors: Hakan R. L. , Eyl C. 
Published: December 2004

AbstractExtracellular recordings within the nucleus accumbens (NAS) of halothane anesthetized rats have revealed that iontophoretically applied morphine and nicotine have contrasting effects on neuronal responses evoked by fimbria or VP stimulation. Iontophoretically applied morphine inhibited NAS single‐unit responses evoked by VP stimulation but did not affect unit responses evoked by fimbria stimulation. In contrast, iontophoretically applied nicotine had no effect on NAS single‐unit responses evoked by VP stimulation but inhibited single‐unit responses evoked by fimbria stimulation. Spontaneously active NAS units were inhibited by iontophoretically applied morphine but were unaffected by nicotine.In addition, experiments were conducted to determine whether NAS unit responses to electrical stimulation of the VP were likely to involve cell body as opposed to axonal activations. Selective cell body stimulation by glutamate microinfusions into the VP region excited spontaneously active VP single‐units. Concurrently recorded NAS unit responses to electrical stimulation of the VP were also excited. These results are consistent with the idea that NAS evoked responses to VP electrical stimulation involve somal activation.Generally, these results suggest a specific neuropharmacological organization of the NAS. Analysis of the effects of morphine and nicotine on other NAS circuits will establish a systems level understanding of NAS responses to reinforcers. © 1995 Wiley‐Liss, Inc.
Corticosteroid‐mediated modulation of carbachol responsiveness in CA1 pyramidal neurons: A voltage clamp analysis
Authors: Hesen W. , Joëls M. 
Published: December 2004

AbstractPyramidal neurons in the rat hippocampal CA1 area contain mineralocorticoid (MRs) and glucocorticoid (GRs) receptors for corticosterone. Previous current clamp experiments showed that depolarizations evoked by carbachol(1–3 μM) depend on relative MR/GR occupation: carbachol responses are small with predominant MR‐activation and larger when both receptor types are occupied. Multiple K‐conductances underlie the carbachol‐induced depolarization. In the present study we used the single electrode voltage clamp technique to examine which K‐conductances modulated by carbachol are sensitive to corticosteroid treatment in vitro. We observed that 1 μM carbachol significantly reduced the IK, Leak while the IM was hardly affected; carbachol effects on the IK, Leak were significantly reduced under conditions of predominant MR activation compared to simultaneous activation of MRs and GRs. With a higher (10 μM) carbachol dose, steroid modulation of the IK, Leak showed a similar tendency. The amplitude of the IM was largely reduced by 10 μM carbachol but appeared to be not affected by steroid treatment. We conclude that the previously described suppression of the carbachol‐induced depolarization with predominant activation MRs is caused by an attenuation of the carbachol action on the IK, Leak. © 1995 Wiley‐Liss, Inc.
Time‐dependent changes in dopamine agonist‐induced striatal fos immunoreactivity are related to sensory neglect and its recovery after unilateral prefkontal cortex injury
Authors: Vargo J. M. , Marshall J. F. 
Published: December 2004

AbstractThis study examined interactions between the corticostriatal glutamatergic system and the nigrostriatal dopaminergic system via immunocytochemical examination of dopamine (DA) agonist induction of the striatal immediate early gene product Fos following cortical injury. After unilateral aspiration of the medial agranular cortex (AGm) region of prefrontal cortex, rats were tested for orientation to visual, tactile, and auditory stimuli. Fos immunoreactivity induced by d‐amphetamine (5 mg/kg) or apomorphine (5 mg/kg) was quantified in dorsolateral and ventrolateral regions of caudate‐putamen (CPu) in rats still demonstrating sensory neglect (5 days postsurgery) and in rats recovered from sensory neglect produced by AGm ablation (29+ days postsurgery). The pattern of immunoreactivity of rats still demonstrating neglect differed from that of unlesioned rats or recovered AGm‐ablated rats. In rats demonstrating sensory neglect, d‐amphetamine or apomorphine induction of Fos in the ipsilateral CPu was reduced by about 40% compared to the contralateral CPu or to comparable readings in unlesioned controls. These asymmetries were restricted to dorsolateral CPu, the region receiving the densest input from AGm. In contrast, recovered AGm‐ablated rats had DA agonist‐induced striatal Fos immunoreactivity that was symmetrical between the two hemispheres and comparable to control values. These findings indicate that adaptations involving the striatal medium spiny neuron, a site of convergence of cortical glutamatergic and nigral dopaminergic afferents, may contribute to recovery from behavioral deficits resulting from neocortical injury. © 1995 Wiley‐Liss, Inc.
In vivo characterization of two cell types in the rat globus pallidus which have opposite responses to dopamine receptor stimulation: Comparison of electrophysiological properties and responses to apomorphine, dizocilpine, and ketamine anesthesia
Authors: Kelland Mark D. , Soltis Robert P. , Anderson Lisa A. , Bergstrom Debra A. , Walters Judith R. 
Published: December 2004

AbstractExtracellular single‐unit recording techniques were used to examine the rat globus pallidus (GP). In both locally anesthetized, paralyzed rats and ketamine‐anesthetized rats, we observed two distinct biphasic extracellular waveforms, which we have labeled Type I (negative/positive waveform) and Type II (positive/negative waveform). No significant differences were observed in the firing pattern or number of cells per track between these cell types, although the Type II neurons had a faster mean firing rate in the locally anesthetized animals. A portion of both cell types could be antidromically activated from the subthalamic nucleus, although Type II neurons had significantly slower conduction velocities. The most striking pharmacological difference between the two cell types was that Type I GP neurons were inhibited by systemic administration of the dopamine agonist apomorphine; previous studies have repeatedly shown that Type II. GP cells are excited by this treatment. Pretreatment with a subthreshold dose of apomorphine reduced the responsiveness of Type I cells to a subsequent high dose of apomorphine, as has been shown for Type II cells. However, pretreatment with the NMDA antagonist dizocilpine (MK 801) produced a significant change in the pattern of response to apomorphine for Type II GP neurons only. Relative to observations in locally anesthetized, paralyzed rats, ketamine anesthesia reduced the firing rate of both cell types, but did not significantly alter their direction of response to apomorphine. Thus, this study has confirmed the existence of two GP cell types with distinct extracellular waveforms and different responses to dopamine receptor stimulation. These data may necessitate a reevaluation of general theoretical models of basal ganglia function in order to account for these opposite effects of dopamine receptor stimulation on pallidal output. © 1995 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Comparison of the action of the stereoisomers of the psychostimulant 4‐methylaminorex (4‐MAX) on midbrain dopamine cells in the rat: An extracellular single unit study
Authors: Ashby Charles R. , Pan Helen , Minabe Yoshio , Toor Alon , Fishkin Lyle , Wang Rex Y. 
Published: December 2004

AbstractIn this study, we examined and characterized the action of the stereoisomers of 2‐amino‐4‐methyl‐Δ2‐5‐phenyl‐oxazoline (4‐methylaminorex, 4‐MAX) on spontaneously active dopamine (DA) neurons in the substantia nigra pars compacta (SNC or A9) and ventral tegmental area (VTA or A10) in anesthetized male rats. This was accomplished using the technique of extracellular single unit recording. The intravenous (i.v.) administration of the stereoisomers of 4‐MAX (0.1−6.4 mg/kg) produced a dosedependent suppression of the basal firing rate of A10 DA cells with the following rank order of potency: trans 4S,5S > cis 4R,5S ≈︁ cis 4S,5R ≫ trans 4S,5S 4‐MAX. The rank order of potency of the isomers of 4‐MAX to suppress the firing of A9 DA cells was trans 4S,5S = cis 4R,5S = cis 4S,5R ≫ trans 4R,5R. The trans 4S,5S isomer was 5‐fold more potent in suppressing DA cell firing in the A10 compared to the A9 area.The suppressant action of the isomers on A9 and A10 DA cells was reversed by the i.v. administration of haloperidol and the D2/D3receptor antagonists (−)‐sulpiride and (−)‐eticlopride but not by the D1receptor antagonists SCH 23390 and SCH 39166. In addition, the suppressant action of the trans 4S,5S isomer on A10 DA cells was not antagonized or reversed by the i.v. administration of the receptor antagonists granisetron (5‐HT3), ritanserin (5‐HT2A, C), idazoxan (α2), phentolamine (peripheral α1), (±)‐pindolol (5‐HT1A, Bβ) or prazosin (α1). The pretreatment of animals with either α‐methyl‐p‐tyrosine (AMPT) or reserpine, but not p‐chlorophenylalanine (PCPA), (±)‐fluoxetine or tomoxetine, significantly attenuated the suppression of A10 DA cell firing produced by trans 4S,5S 4‐MAX. Overall, our results suggest that the suppressant action of 4‐MAX on midbrain DA cell firing may be mediated by the release of DA, which subsequently interacts with D2/D3receptors. © 1995 Wiley‐Liss, Inc.
Regulation and functional characterization of a rat recombinant dopamine D3 receptor
Authors: Cox Barbara A. , Rosser Mary P. , Kozlowski Michal R. , Duwe Kevin M. , Neve Rachael L. , Neve Kim A. 
Published: December 2004

AbstractWe stably expressed a rat D3 receptor cDNA in C6glioma cells (C6‐D3 cells), quantifying receptor expression with the radioligands [125I]epidepride (KD= 0.1 nM) and [3H]spiperone (KD= 0.7 nM). As reported previously for D2 receptors, quinpirole induced a 9–16% increase in the rate of extracellular acidification by C6‐D3 cells. The acidification was inhibited by epidepride and by the Na+/H+antiporter inhibitors, amiloride and methylisobutylamiloride, but pertussis toxin treatment had no effect on quinpirole‐induced extracellular acidification. These data suggest that D3 receptor stimulation of Na+/H+exchange in C6glioma cells is not mediated by the pertussis toxinsensitive G proteins, Gior Go. Overnight treatment of C6‐D3 cells with N‐propylnorapomorphine, dopamine, or quinpirole resulted in large concentration‐dependent increases (up to 500%) in the density of D3 receptors on membranes prepared from the cells. Antagonists had smaller, variable effects on the density of D3 receptors in C6‐D3 cells, except for domperidone, which significantly increased the density of D3 receptors. Treatment with pertussis toxin had no effect on the agonist‐induced receptor up‐regulation, indicating that an interaction with pertussis toxin‐sensitive G proteins was not required. Densitometry analysis of Northern blots of RNA prepared from C6‐D3 cells showed no significant N‐propylnorapomorphine‐induced increase in D3 receptor message. Treatment with cycloheximide, however, completely prevented receptor up‐regulation by N‐propylnorapomorphine. Pretreatment of C6‐D2 cells with 1'0 pM DA resulted in a substantial heterologous sensitization, in which isoproterenol‐stimulated adenylyl cyclase activity was enhanced more than twofold. In contrast, isoproterenol‐stimulated enzyme activity was inhibited by greater than 50% in C6‐D3 cells pretreated with dopamine. These results confirm one functional response to activation of D3 receptors and demonstrate that the density of D3 receptors, like D2 receptors, is increased after incubation of intact cells with agonists. © 1995 Wiley‐Liss, Inc.This article is a US Government work and as such, is in the public domain in the United States of America.
Identification of age‐related changes of dopamine D1‐like receptors in the rat cerebellar cortex
Authors: Ricci Alberto , Zaccheo Damiano , Amenta Francesco 
Published: December 2004

AbstractThe present study was designed to characterize the pharmacological profile of dopamine D1‐like receptors in the rat cerebellar cortex and to assess if these receptor sites undergo age‐related changes. Cerebella of young (3 months), adult (12 months), and old (27 months) male Wistar rats were examined by using radioligand binding techniques and light microscope autoradiography. The non‐selective dopamine D1‐like radioligand [3H]SCH 23390 was specifically bound to sections of rat cerebellum. The findings that dopamine displaced [3H]SCH 23390 binding in the submicromolar range suggest the labelling of a dopamine D5 (or D1B) receptor subtype. The affinity of [3H]SCH 23390 for dopamine D1‐like receptors was similar in the cerebellar cortex of the three animal groups investigated, whereas radioligand binding techniques revealed a gradual age‐related reduction of the density of binding sites. Light microscope autoradiography showed the localization of [3H]SCH 23390 binding sites primarily in the molecular layer and to a lesser extent in the Purkinje neuron layer of the cerebellar cortex. Aging was accompanied by a loss of [3H]SCH 23390 binding sites affecting mainly the molecular layer. The age‐dependent loss of dopamine D1‐like receptors is more pronounced if detected with radioligand binding techniques than with light microscope autoradiography. This suggests that the decrease of dopamine D1‐like receptors observed in aging rat cerebellar cortex may depend in part on changes in the receptor expression and in part on cortico‐cerebellar structural changes. © 1995 Wiley‐Liss, Inc.
Ontogeny of fos protein‐like immunoreactivity in the suprachiasmatic nucleus
Authors: Joyce Myra P. , Barr Gordon A. 
Published: December 2004

AbstractThis study examined the normal development of neuronal activity in the suprachiasmatic nuclei (SCN) of rats between age 3–60 days, using Fos protein‐like immunoreactivity (Fos‐LI) as a marker. At age 3 days, Fos‐positive nuclei are sparsely distributed throughout the SCN. Between age 3–10 days, the density of labeled nuclei increases significantly. Fos‐LI labeling is maximal at 10 days. Between age 10–14 days, the number of labeled nuclei decreases and remains relatively constant thereafter, although the intensity of the reaction product diminishes as the animal matures. By age 60 days, the number of Fos‐LI labeled nuclei in the SCN is substantially decreased and is essentially the same as in the 3‐day‐old rat. The appearance of Fos‐LI nuclei in the SCN during development appears to reflect the development of visual system afferents to the nucleus as well as the development of intrinsic SCN synaptology. © 1995 Wiley‐Liss, Inc.
Effects of the putative antidepressant, ABT 200, on the clearance of exogenous norepinephrine in rat cerebellum
Authors: Cass Wayne A. , Friedema Marilyn N. , DeBernardis John F. , Kerkman Daniel J. , Gerhardt Greg A. 
Published: December 2004

AbstractABT 200 [(RR,SS)‐3‐phenyl‐l‐[l′,2′,3′,4′‐tetrahydro‐5′,6′‐methylenedi‐ oxy‐1′‐naphthalenyl‐methyl]‐pyrrolidine methanesulfonate] is a potent alpha2‐adrenoceptor antagonist (Ki = 1.2 nM) with modest norepinephrine uptake‐blocking activity (IC50 = 841 nM) that is currently under clinical evaluation as an antidepressant. The effects of ABT 200, nomifensine (an inhibitor of catecholamine uptake), and rauwolscine (a selective alpha2‐adrenoceptor antagonist) on the clearance of exogenous norepinephrine in the cerebellum of urethane‐anesthetized rats was investigated using a vivo electrochemistry. Chronoamperometric recordings were continuously made at 5 Hz using Nafion‐coated, single carbon fiber electrodes. When a calibrated amount of norepinephrine was pressure‐ejected at 5‐min intervals from a micropipette adjacent (290–330 μM) to the electrode, transient and reproducible norepinephrine signals were detected. In response to systemic ABT 200 (30 mg/kg i.p.) or nomifensine (30 mg/kg i.p.1, the signals increased in both amplitude and time course, indicating significant inhibition of the norepinephrine transporter. A lower dose (15 mg/kg i.p.) of either ABT 200 or nomifensine had no effect in this paradigm. Local application of ABT 200 (400 μM) or nomifensine (400 μM) prior to pressure‐ejection of norepinephrine also significantly increased the amplitude and time course of the norepinephrine signals. In contrast, systemic administration of rauwolscine (30 mgkg i.p.) or vehicle solution, and local application of vehicle solution, had no effect on the norepinephrine signals. These data indicate that at the higher dose evaluated, both ABT 200 and nomifensine inhibit cerebellar norepinephrine uptake in vivo. © 1995 Wiley‐Liss, Inc.