bluuebunny/crossref_metadata_2025_split huggingface dataset:
Loss of D1/D2 dopamine receptor synergisms following repeated administration of D1 or D2 receptor selective antagonists: Electrophysiological and behavioral studies
Authors: Hu Xiu‐Ti , White Francis J. 
Published: December 2004

AbstractMany effects resulting from D2 dopamine (DA) receptor stimulation are manifest only when D1 DA receptors are stimulated by endogenous DA. When D1 receptor stimulation is enhanced by administration of selective D1 receptor agonists, the functional effects of selective D2 agonists are markedly increased. These qualitative and quantitative forms of D1/D2 DA receptor synergism are abolished by chronic DA depletion when both D1 and D2 DA receptors are supersensitive. Using both electrophysiological and behavioral methods, the present study examined the effects of selective D1 and D2 renaptnr supersensitivity, induced by repeated administration of selective D1 or D2 receptor antagonists, on the synergistic relationships between D1 and D2 receptors. Daily administration of the selective D2 antagonist eticlopride (0.5 mg/kg, s.c.) for 3 weeks produced a selective supersensitivity of both dorsal (caudate‐putamen) and ventral (nucleus accumbens) striatal neurons to the inhibitory effects of the D2 agonist quinpirole (applied by microiontophoresis). This treatment also abolished the normal ability of the D1 agonist SKF 38393 to potentiate quinpirole‐induced inhibition, and relieved D2 receptors from the necessity of D1 receptor stimulation by endogenous DA (enabling), as indicated by significant electrophysiological and behavioral (sterotypy) effects of quinpirole in eticlopride‐pretreated, but not saline‐pretreated, rats that were also acutely depleted of DA. Daily administration of the selective D1 receptor antagonist SCH 23390 (0.5 mg/kg, s.c.) caused supersensitivity of striatal neurons to the inhibitory effects of SKF 38393 and also abolished both the ability of SKF 38393 to potentiate quinpirole‐induced inhibition and the necessity of D1 receptor stimulation for such inhibition. However, both quinpirole‐induced inhibition of striatal cells and stereotyped responses were also somewhat enhanced in SCH 23390‐pretreated rats. When such Dl‐sensitized rats were acutely depleted of DA, the behavioral effects of quinpirole were intermediate between saline‐pretreated rats with acute DA depletion and SCH 23390‐pretreated rats without acute DA depletion. Based upon these and related results, it is argued that the enhanced effects of quinpirole in D1‐sensitized rats are due to a heterologous sensitization of D2 receptors rather than to enhanced enabling resulting from supersensitive D1 receptors. It is suggested that supersensitivity of either D1 or D2 receptors can lead to an uncoupling of normal qualitative and quantitative D1/D2 synergisms and that the heterologous regulation of D2 receptor sensitivity by D1 receptors may be related to uncoupling of functional D1/D2 synergisms.
Metabotropic glutamate receptor agonist ACPD inhibits some, but not all, muscarinic‐sensitive K+ conductances in basolateral amygdaloid neurons
Authors: Womble Mark D. , Moises Hylan C. 
Published: December 2004

AbstractMuscarinic agonists produce membrane depolarization and losses of spike frequency accommodation and the slow afterhyperpolarization (AHP) when applied to neurons of the basolateral amygdala (BLA). Underlying these changes are the muscarinic‐induced inhibitions of several K+ conductances, including the voltage‐activated M‐current (IM), a slowly decaying Ca2‐activated current (IAHP), a voltage‐insensitive leak current (ILeak), and the hyperpolarization‐activated inward rectifier current (IIR) Similar depolarizations and losses of the slow AHP have been observed in other neuronal cell types following stimulation of metabotropic glutamate receptors. Therefore, we tested the effects of the metabotropic glutamate receptor agonist, 1‐aminocyclopentanels, 3r‐dicarboxylic acid (ACPD), on pyramidal neurons impaled with a single microelectrode for current‐ and voltage‐clamp recordings in a brain slice preparation of the rat BLA. Application of ACPD (20 or 100 μM) to BLA neurons inhibited IM and IA HP, resulting in membrane depolarization and reductions in the amplitude and duration of the slow AHP. However, ACPD did not inhibit the muscarinic‐sensitive current IIR, nor was ILeak blocked in the majority of neurons examined. These findings suggest the possibility that muscarinic cholinergic and metabotropic glutamatergic receptor agonists may activate separate intracellular transduction pathways which have convergent inhibitory effects onto IM and IAHP in BLA pyramidal neurons. © 1994 Wiley‐hiss, Inc.
Ethanol acts via the ventral tegmental area to influence hippocampal physiology
Authors: Criado Jose R. , Steffensen Scott C. , Henriksen Steven J. 
Published: December 2004

AbstractEthanol selectively alters hippocampal dentate physiology, in part by increasing recurrent inhibition and suppressing long‐term potentiation (LTP), a result of ethanol modulation of subcortical inputs. One of these inputs includes the ventral tegmental area (VTA) in the midbrain, whose neurons have been shown to discharge faster following systemic ethanol. To further understand how subcortical inputs regulate hippocampal physiology and their modulation by ethanol, we studied the effects of acute intoxicating levels of ethanol on VTA facilitation of the perforant path to dentate (PPD) responses. Furthermore, to test the role of the VTA on known pharmacological effects of ethanol on hippocampal physiology, we studied the effects of disruption of the VTA‐dentate inpute on ethanol actions on recurrent inhibition. Stimulation of the perforant path produced well‐characterized evoked responses in the ipsilateral dentate gyrus. Whereas VTA stimulation had no effect on PPD population EPSPs, VTA conditioning markedly increased perforant path‐evoked PS amplitudes (140%). The maximum facilitation was observed at VTA conditioning intervals of 30‐40 ms. PS amplitudes returned to baseline levels immediately following cessation of VTA conditioning. Intraperitoneal injections of ethanol (1.2 g/kg) markedly decreased VTA facilitation of PPD PS amplitudes. Lesions of the VTA blocked the ethanol‐mediated increase in PPD paired‐pulse inhibition. These results demonstrate that, to a great extent, the effects of intoxicating doses of ethanol on hippocampal physiology are mediated by remote pharmacological effects on the ventral tegmental area, whose direct or indirect influences on dentate physiology are described. © 1994 Wiley‐Liss, Inc.
No direct correlation between behaviorally active doses of the dopamine D2 agonist LY 171555 and displacement of [123I]IBZM as measured with SPECT in MPTP monkeys
Authors: Vermeulen R. Jeroen , Drukarch Benjamin , Verhoeff N. Paul L. G. , Goosen Cornelis , Sahadat M. C. Rob , Wolters Erik Ch. , Van Royen Eric A. , Stoof Johannes C. 
Published: December 2004

AbstractAlmost no information is available concerning the link between clinical effects of dopamine D2 receptor agonists in the treatment of Parkinson's disease (PD) and the extent of D2 receptor occupancy in the brain. Therefore, we investigated the possible correlation between adminis tration of behaviorally active doses of the selective D2agonist LY 171555 and in vivo D2 receptor occupancy in the unilateral 1‐methyl‐4‐phenyl 1,2,3,6‐tetrahydropyridine(MPTP)‐lesioned rhesus monkey model of PD. Single photon emission computed tomography (SPECT) with the D2 receptor antagonist (123I)IBZM (iodobenzamide) as radioligand was used to estimate the receptor occupancy.The MPTP‐lesioned monkeys consistenty showed signs of unilateral parkinsonism. LY 171555 (0.01 or 0.3 mg/kg) significantly increased contralateral rotation (away from the lesion), being most effective at the lower dose.In the MPTP‐lesioned monkeys [123]IBZM activity in the left (lesioned) striatum was significantly higher as compared to that in the right striatum. Only upon administration of 0.3 mg/kg LY 171555 a significant amount of receptor occupancy by LY 171555, as measured with [123I]IBZM SPECT, at both lesioned and non‐lesioned side, was detected. Using D2 receptor mediated inhibition of the evoked release of [3H]acetylcholine from rat striatal tissue as a functional model, we showed that the lack of effect with 0.01 mg/kg LY 171555 was not due to non‐competitive interaction between LY 171555 and IBZM at the D2 receptor.We conclude that the D2 antagonist [123I]IBZM is not a suitable SPECT ligand to study the relationship between behavioral effects of the selective D2 agonist LY 171555 in unilaterally MPTP‐lesioned monkeys and the D2 receptor occupancy in vivo in this animal model of PD. © 1994 Wiley‐Liss. Inc.
Localization and developmental pattern of vasoactive intestinal polypeptide binding sites in the human hypothalamus
Authors: Sarrieau Alain , Najimi Mohamed , Chigr Fatiha , Kopp Nicolas , Jordan Daniel , Rostene William 
Published: December 2004

AbstractUsing a quantitative in vitro autoradiographic approach, vasoactive intestinal polypeptide (VIP) binding site densities were compared in the post‐mortem hypothalamus of human neonate/infant and adult. The densities were similar during development in most of the hypothalamic nuclei and areas examined underlying the stability of 125I‐VIP binding sites in the post‐mortem hypothalamus of young and adult individuals. However, the ventral part of the medial preoptic area, the medial, lateral, and supramammillary nuclei were characterized by an increase of 125I‐VIP binding with age. In young and adult individuals, the highest densities of hypothalamic 1251‐VIP binding sites were detected in the supraoptic and infundibular nuclei; the ependyma; the organum vasculosum of the lamina terminalis; the horizontal limb of the diagonal band of Broca; the ventral part of the medial preoptic area (in adult); the suprachiasmatic, paraventricular, and periventricular nuclei; and the medial and lateral mammillary nuclei in adult. Moderate densities were found in the vertical limb of the diagonal band of Broca, the bed nucleus of the stria terminalis, the ventral part of the medial preoptic area in neonate/infant, the medial and lateral mammillary nuclei in neonate/infant, the supramammillary nucleus in adult, the dorsal hypothalamic area, and the ventromedial nucleus. Low to moderate binding site densities were observed in the other hypothalamic regions of young or adult individuals. The nonspecific binding ranged from 15% of the total binding in the anterior hypothalamus to 20% in the mediobasal and posterior hypothalamic levels. Taken together, these results provide evidence for a large distribution of VIP binding sites in neonate/infant and adult human hypothalamus suggesting the implication of VIP in the development of this brain structure and the maintenance of its various functions. © 1994 Wiley‐Liss, Inc.
Effects of chronic ethanol ingestion on long‐term potentiation remain even after a prolonged recovery from ethanol exposure
Authors: Tremwel Margaret F. , Hunter Bruce E. 
Published: December 2004

AbstractPrevious work in our laboratory has demonstrated that memory formation, a behavioral process thought to be at least in part attributed to hippocampal functioning, is severely attenuated following 5 months of chronic ethanol treatment (CET) and 2 months of recovery from CET. Additionally, 48 h following CET, a well‐recognized physiological correlate of memory formation, long‐term potentiation (LTP), is reduced in the hippocanipus. We hypothesized that the reduction in LTP may in part contribute to the behavioral deficit in memory formation, which is a permanent consequence of CET. In order for the reduction of LTP to be involved with the permanent deficit in memory acquisition, it too must be present following a prolonged period of ethanol abstinence. The present study examined the permanent effect of CET on LTP. Animals were fed a nutritionally complete, ethanol containing diet for 28 weeks and then allowed a 5‐7 month abstinence period. A control group was fed the same diet except sucrose was isocalorically substituted for ethanol. Neurophysiological methods measured the capacity of synaptic connections onto CA1 pyramidal cells to support LTP in response to a variety of conditioning trains. The magnitude of LTP was reduced in CET animals as compared with pair‐fed controls. LTP induction is mediated by activation of the N‐methyl‐D‐aspartate (NMDA) receptor complex and is modulated by activation of β‐amino‐butyric acid (GABA)ergic synaptic transmission. The effect of CET on LTP magnitude may be due to effects on the NMDA‐induced induction itself or on the GABAergic modulation of induction. To distinguish between these possibilities, the induction of LTP was tested in the presence of bicuculline methiodide (a specific antagonist to the GABAA receptor). Under these conditions, the ethanol‐induced deficit in LTP was abolished. On the basis of these results we hypothesized that the CET reduction in LTP magnitude observed in the absence of bicuculline was due to a permanent alteration of GABAergic modulation of LTP induction. Portions of this paper have been presented previously in abstract form [Tremwel and Hunter (1990), Soc. Neurosci Abstr., 980]. © 1994 Wiley‐Liss, Inc.
Attenuation of the locomotor‐sensitizing effects of the D2 dopamine agonist bromocriptine by either the D1 antagonist SCH 23390 or the D2 antagonist raclopride
Authors: Wise Roy A. , Carlezon William A. 
Published: December 2004

AbstractInjections of the selective D2 dopamine agonist bromocriptine (5.0 mg/kg, IP) produced progressively stronger locomotion over 10 days of repeated testing. Concurrent treatment with either the D1 antagonist SCH 23390 (0.01 or 0.1 mg/kg, IP) or the D2 antagonist raclopride (0.1 or 1.0 mg/kg, IP) suppressed bromocriptine‐induced locomotion on treatment days and attenuated or blocked the progressive increases in locomotion that accompanied repeated injections of bromocriptine alone. The fact that D1 and D2 antagonists each block the acute actions of bromocriptine and attenuate the development of bromocriptine sensitization is suggested to imply a striatal rather than a ventral tegmental mechanism for the sensitization produced by repeated treatments with direct dopamine agonists. © 1994 Wiley‐Liss, Inc.
Electrophysiological verification of the presence of D1 and D2 dopamine receptors within the ventral pallidum
Authors: Napier T. Celeste , Maslowski‐Cobuzzi Renata J. 
Published: December 2004

AbstractThe ventral pallidum is a basal forebrain region recently shown to receive dopaminergic projections from the midbrain. Binding sites for the D1 and D2 dopamine receptor families have been identified within the ventral pallidum, yet the consequences of activating these receptors have not been studied. Thus, to characterize the physiological pharmacology of D1 and D2 receptor subtypes for the ventral pallidum, extracellular single‐neuron recording and microiontophoretic techniques were used in chloral hydrate‐anesthetized rats. Half of the 93 ventral pallidal neurons tested were sensitive to iontophoresis of dopamine (DA), and both rate increases and decreases were observed. Co‐iontophoresis of either the D1 antagonist SCH23390, or the D2 antagonist sulpiride, generally attenuated the DA‐induced rate changes. Like DA, about half of the ventral pallidal neurons tested were sensitive to the D1 agonist, SKF38393. Yet in contrast to DA, rate suppression was observed almost exclusively, and the magnitude of this decrease was greater than that produced by DA. SKF38393‐induced suppressions were antagonized by SCH23390, but not by sulpiride, demonstrating the specificity of the D1 agonist. Most of the neurons tested were not affected by quinpirole, but when responsive to the D2 agonist, rate increases were observed most often. The increases were antagonized by the D2 antagonist sulpiride, but not SCH23390, demonstrating that this response resulted from an activation of D2 receptors. These results support binding studies demonstrating that both D1 and D2 receptors are present in the ventral pallidum, and reveal that the independent activation of each of these is sufficient to alter neuronal activity. © 1994 Wiley‐Liss. Inc.
Effects of haloperidol, quinelorane, and lithium on regional neurotensin/neuromedin N concentrations: Further evidence for neurotensin/neuromedin N‐Dopamine interactions
Authors: Clement Rita , Griff Dan , Banks Beth , Nemeroff Charles , Kitabgi Patrick , Bissette Garth 
Published: December 2004

AbstractIn order to further characterize the pharmacologic mechanisms that mediate the antipsychotic drug‐induced increase in neurotensin (NT) in nucleus accumbens and striatum, the effects of three weeks treatment with psychotherapeutic levels of lithium alone or in conjunction with haloperidol were compared to the ability of haloperidol alone to alter NT and neuromedin N (NMN) regional brain concentrations in rats. A separate experiment examined the ability of a selective dopamine D2 receptor agonist, quinelorane, to alter NT/NMN regional concentrations after three weeks of treatment as compared to haloperidol, a D2 receptor antagonist. Haloperidol (1 mg/kg) increased both NT and NMN concentrations in several brain regions and these parallel peptide increases were highly correlated. Lithium chloride (0.4 mM) had no effect, either alone or with haloperidol, on NT/NMN concentrations. Quinelorane (1 mg/kg), however, effectively increased both NT and NMN concentrations in the caudate nucleus and nucleus accumbens, as did haloperidol (2 mg/kg). These data indicate that the induction of NT and NMN, whose adjacent sequences are contained in a pro‐hormone product of a single gene, occurs in tandem and remains proportional, as well as demonstrating that putative D2 receptor agonists can produce effects on NT/NMN systems that are similar to D2 receptor antagonists. © 1994 Wiley‐Liss, Inc.
Local communication within dendritic spines: Models of second messenger diffusion in granule cell spines of the mammalian olfactory bulb
Authors: Woolf Thomas B. , Greer Charles A. 
Published: December 2004

AbstractDendritic spines are generally believed to play a role in modulating synaptically induced electrical events. In addition, they may also confine second messengers and thus topologically limit the distance over which second messenger cascades may be functionally significant. In order to address this possibility, computer simulations of transient second messenger concentration changes were performed. The results show the importance of spine morphology and binding and extrusion mechanisms in controlling second messenger transients. In the presence of intrinsic cytoplasmic binding sites and kinetic rates similar to that expected for calcium, second messengers were confined to the spine head. In the absence of binding/extrusion mechanisms, the size and time course of the input transient to the spine head influenced the second messenger transients that might be seen at the base of the spine neck and in other spines. Large and/or sustained increases in second messenger concentration in the spine head were communicated to the spine base and to other spine heads. The results emphasize the importance of a knowledge of breakdown pathways, concentrations and kinetics of binding sites, and extrusion mechanisms for understanding the dynamics of local chemical changes for dendritic spine function. © 1994 Wiley‐Liss, Inc.
Nitric oxide inhibits 3H‐glutamate transport in synaptosomes
Authors: Pogun Sakire , Dawson Valina , Kuhar Michael J. 
Published: December 2004

Abstract3H‐glutamate (GLU) uptake was measured in hippocampal synaptosomes from rat brain. Addition of sodium nitroprusside (SNP) (Sodium nitroferricyanide), a generator of nitric oxide (NO), produced a time‐, temperature‐, and dose‐dependent inhibition of 3H‐GLU uptake. The inhibition was due to changes in both Kd and Vmax of GLU uptake, and it was at least partially reversible upon washing. Addition of reduced hemoglobin (Hb), a substance that binds NO, prevented the SNP‐induced depression of uptake. Potassium ferricyanide, a compound similar to SNP, did not cause a reduction in 3H‐GLU uptake. Utilization of another generator of NO, S‐nitroso‐N‐acetylpenicillamine (SNAP), produced similar results as did NO itself. Decreases in uptake were also observed in the striatum and cerebellum. Similar treatments did not consistently affect 3H‐norepinephrine (NE) uptake, suggesting some selectivity in the NO effect. Thus, the observed inhibition of 3H‐GLU uptake appears to be produced by NO, and it may represent a novel type of transynaptic retrograde regulation of transport. If found in vivo, inhibition of uptake activity could also be involved in the toxic effects of NO, the neurotoxicity of glutamate, and other potential neuronal changes associated with NO such as hippocampal long‐term potentiation. © 1994 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Ultrastructural organization of the noradrenergic innervation of the superficial gray layer of the hamster's superior colliculus
Authors: Arce Erick A. , Bennett‐Clarke Carol A. , Rhoades Robert W. 
Published: December 2004

AbstractImmunocytochemistry with an antibody‐directed tyrosine hydroxylase (TH) was combined with electron microscopy and serial‐section analysis to examine the synaptic organization of the catecholaminergic projection to the stratum griseum superfciale (SGS) of the hamster's superior colliculus (SC). A total of 250 TH‐immunoreactive profiles within SGS were examined. Of these, 114 (45.6%) made synaptic contacts; 81 (71.1%) were axodendritic, and the remainder (33, 28.9%) were axo‐axonic. Serial‐section analysis was employed to evaluate the presence or absence of synaptic contacts for 26 profiles. Overall, 19 (73.1%) of the profiles followed through serial sections exhibited synaptic contacts. Double staining of single sections with antibodies directed against TH and dopamine‐ß‐hydroxylase (DßH) and examination in the light microscope indicated that virtually all TH‐positive fibers also contained DßH. This indicated that the fibers examined at the electron microscopic level were noradrenergic rather than dopaminergic. These results suggest that norepinephrine may have both pre‐ and postsynaptic actions in the hamster's SC and that at least some of these effects are mediated by conventional synapses.