bluuebunny/crossref_metadata_2025_split huggingface dataset:
Selective induction of Fos and FRA immunoreactivity within the mesolimbic and mesostriatal dopamine terminal fields
Authors: Dilts Roger P. , Helton Todd E. , McGinty Jaqueline F. 
Published: December 2004

AbstractThe influence of the mesencephalic dopaminergic projections on the neurons within the basal forebrain and prefrontal cortex is not well understood although it has been intensely investigated. The purpose of this study was to evaluate the expression of Fos‐like and FRA‐like (Fos Related Antigens) immunoreactivity (IR) as a qualitative and quantitative marker of neuronal activity within the mesolimbic and mesostriatal dopamine terminal fields. Following the administration of apomorphine (5.0 mg/kg S.C.), a rapid increase in FRA‐IR, accompanied by Fos‐IR, was observed within the striatum in a patchy distribution. Apomorphine also induced the expression of FRA‐IR within the nucleus accumbens, cortex, septum, and the islands of Calleja complex. This broad pattern of activation contrasts with the limited expression of Fos‐IR and FRA‐IR within the dorsolateral striatum, dorsomedial shell of the nucleus accumbens, and cingulate cortex following haloperidol administration (2.0 mg/kg, S.C.). Finally, it was observed that nuclei expressed Fos‐IR rapidly and transiently within the striatum following haloperidol, whereas the number of FRA‐IR nuclei remained elevated but changed in distribution and intensity over time. In conclusion, different regions within the dopamine terminal fields express varying concentrations of Fos‐IR and FRA‐IR after stimulation or blockade of dopamine receptors. These data indicate that Fos, as well as selective FRAs, can be used to delineate populations of neurons with altered metabolic activity resulting from the administration of dopaminergic agents. Furthermore, the data support the concept of segregated mesostriatal and mesolimbic projections, in particular the divison of the nucleus accumbens into the shell and core compartments. © 1993 Wiley‐Liss, Inc.
Electrophysiological evidence for the existence of NMDA and non‐NMDA receptors on rat ventral tegmental dopamine neurons
Authors: Wang Ting , French Edward D. 
Published: December 2004

AbstractIn vitro extracellular single‐unit recordings from rat midbrain slices were used to assess the effects of excitatory amino acid agonists on the activity of A10 dopamine neurons. N‐methyl‐D‐aspartic acid (NMDA), kainic acid (KA), and β‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA) elicited dose‐dependent increases in firing rates. The relative potencies for the 3 compounds was AMPA > KA > NMDA. None of the excitations was accompained by burst firing, but frequently periods of nonrecordable activity occurred following pronounced stimulation. Concurrent application of the excitatory amino acid antagonist CGS 19755 (cis‐4‐phosphonomethyl‐2‐piperidine carboxylate) selectively blocked the excitations elicited by NMDA but not by KA or AMPA. Likewise the selective non‐NMDA antagonist NBQX [2,3‐dihydroxy‐6‐nitro‐7‐sulfamoyl‐benzo(F)quinoxaline] blocked only the excitatory effects of AMPA and KA but not those elicited by NMDA. NBQX appeared to be less optent at antagonizing KA than AMPA. These results suggest that mesolimbic‐mesocortical dopamine neurons possess both NMDA and non‐NMDA receptors, and possibly distinct AMPA and KA recognition sites. © 1993 Wiley‐Liss, Inc.
CNS signal transduction in the pathophysiology and pharmacotherapy of affective disorders and schizophrenia
Authors: Hudson Craig J. , Young L. Trevor , Li Peter P. , Warsh Jerry J. 
Published: December 2004

AbstractUntil recently, research on the neurochemical basis of affective disorders (AD) and schizophrenia (SCZ) focused on detecting postulated disturbances in presynaptic neurotransmitter release and metabolism, or postsynaptic receptor function. New insights into the molecular mechanisms involved in the propagation of neurotransmitter signals across biological membranes and in the regulation of neuronal responses have allowed the development of novel hypotheses, which may explain the altered postsynaptic neuroreceptor responsivity thought to be integral to the pathophysiology of these disorders. In this review we evaluate evidence from both basic science and clinical research implicating disturbances in postreceptor signal transduction in the pathophysiology and pharmacotherapy of AD and SCZ. Specific findings regarding potential postreceptor sites of pathophysiology are highlighted in each of these disorders, together with the growing body of data on the possible postreceptor loci of psychotropic drug action, especially lithium and antidepressants. © 1993 Wiley‐Liss, Inc.
Locomotor activity following intra‐accumbens microinjections of dopamine D1 agonist SK&F 38393 in rats
Authors: Meyer Merle E. , van Hartesveldt Carol , Potter Thomas J. 
Published: December 2004

AbstractThe present study examined the effects of the dopamine D1 receptor subtypes agonist SK&F 38393 on locomotor activities after bilateral microinjection (0.00, 0.01, 0.1, 10.0 μg) into the nucleus accumbens (Acb). The dose of 0.1 μg elicited the highest response rate across measures of locomotion, rearing and stereotypy behavior. On the other hand, the largest dose of 10.0 μg was associated with significant increase in center time behaviors. The data were supportive of the hypothesis that dose‐related locomotor activities elicited by microinjections of SK&F 38393 into the Acb are independently mediated by D1 receptors. © 1993 Wiley‐Liss, Inc.
Glutamate effects on calcium homeostasis in cerebellar granule cells in primary cultures grown under depolarizing and nondepolarizing conditions
Authors: Zhao Zhong , Peng Liang 
Published: December 2004

AbstractCerebellar granule cell culture are normally grown under partly depolarizing conditions (in a medium with ∼25 mMK+), but these cultures can also be grown at a normal potassium concentration (5.4 mM k+), although some of their characteristics are altered. In this study, intracellular free calcium concentration and 45Ca uptake were measured in cerebellar granule cell cultures grown at either 25 or 5.4 mM extracellular potassium in the presence of glutamate, and/or some of its subtype‐specific agonists and antagonists. Granule cells in cultures grown at 25mM K+ responded to glutamate, but not to quisqualate, with an increase in free cytosolic calcium concentration and in 45Ca uptake. This increase in free cytosolic calcium concentration was dependent on extracellular calcium and it was antagonized by AP5 and Ketamine, NMDA receptor antagonists. In contrast, granule cells in cultures grown at 5.4 mM K+ responded to both glutamate and quisqualate, and these responses were independent of extracellular calcium and not sensitive to AP5 and ketamine. In agreement with this, 45Ca uptake was not affected by glutamate. Neither of the two culture types responded to kainate with an increase in calcium concentration or uptake. These observations indicate that calcium uptake in granule cells in cultures grown at 25mM K+ reflect NMDA activation of calcium influx, whereas the cells in cultures grown at 5 mM K+ increase cytosolic calcium concentration on account of intracellular release of bound calcium, caused by activation of the metabotropic receptor. The two types of cultures may constitute valuable experimental tools for investigation of physiological and pathological effects of calcium releas from intracellular stores induced by glutamate via the metabotropic receptors and of calcium uptake induced by NMDA. © 1993 Wiley‐Liss, Inc.
Serotonin‐induced increase in cAMP in ganglia isolated from the myenteric plexus of the guinea pig small intestine: Mediation by a novel 5‐HT receptor
Authors: Fiorica‐Howells Elena , Wade Paul R. , Gershon Michael D. 
Published: December 2004

AbstractSerotonin (5‐HT) is a mediator (through 5‐HT1P receptors) of slow EPSPs in myenteric ganglia of the small intestine. The effect of 5‐HT can be mimicked by elevating cAMP; therefore, we tested the hypothesis that the slow EPSP‐like response to 5‐HT is cAMP‐mediated. Guinea pig gut was enzymatically dissociated; myenteric ganglia remained intact and were collected by filtration. Neurons in the isolated ganglia retained their ability to manifest the slow EPSP‐like response to 5‐HT. Exposure to 5‐HT raised the ganglionic level of cAMP (ED50 0.3 μM). This effect was not antagonized by the 5‐HT1P antagonist, N‐acetyl‐5‐hydroxytryptophyl‐5‐hydroxytryptophan amide (100.0 μM), or mimicked by the 5‐HT1P agonist, 5‐hydroxyindalpine (10.0 μM). Increases in cAMP were also evoked by the 5‐HT1 agonist, 5‐carboxyamidotryptamine (10.0 μM), the 5‐HT2 agonist, (±)‐1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI; 1.0–10.0 μM), and by the 5‐HT4 agonists, renzapride (1.0–10.0 μM) and 5‐methoxytryptamine (1.0–10.0 μM); however, neither the 5‐HT1/5‐HT2 antagonists, spiperone, methysergide, and methiothepin, nor the 5‐HT4 antagonist, tropisetron (ICS 205–930; 10.0 μM), were able to inhibit the rise in cAMP evoked by these compounds or by 5‐HT (0.1–10.0 μM). The 5‐HT‐evoked elevation of cAMP was antagonized by ketanserin (10.0 μM), which also blocked the effects of 5‐methoxytryptamine and DOI, but not those of renzapride. The effective concentration of DOI, however, was higher than that needed for activation of 5‐HT2 receptors, and Northern analysis using a cDNA probe encoding the rat 5‐HT2 receptor failed to reveal the presence of 5‐HT2 mRNA in myenteric ganglia, although it hybridizes with mRNA of the right size in the guinea pig brain. Compounds that failed to change levels of cAMP or to antagonize the action of 5‐HT included 8‐hydroxy‐di‐n‐propylamino tetralin, R58639, R88226, and sumatriptan. It is concluded that the receptor responsible for the 5‐HT‐induced rise in cAMP in ganglia isolated from the guinea pig myenteric plexus is not a known subtype of 5‐HT receptor. Since the pharmacology of this novel receptor is different from that of the slow EPSP‐like response to 5‐HT, the receptor probably does not mediate the slow EPSP. © 1993 Wiley‐Liss, Inc.
Striatal binding of the PET ligand 11C‐raclopride is altered by drugs that modify synaptic dopamine levels
Authors: Dewey Stephen L. , Smith Gwenn S. , Logan Jean , Brodie Jonathan D. , Fowler Joanna S. , Wolf Alfred P. 
Published: December 2004

AbstractBilatera decreases in striatal 11C‐raclopride binding were observed in adult female baboons with high resolution PET following administration of drugs that act centrally on dopaminergic neurons. At baseline and following administration of d‐amphetamine (a dopamine‐releasing drug), GBR‐12909 (a potent dopamine reuptake inhibitor), or tetrabenazine (a biogenic amine depleting drug) PET scans of 11C‐raclopride binding were obtained in a CTI 931 positron tomograph. In all studies, the ratio of the distribution volumes for the striatum to the cerebellum for 11C‐raclopride binding decreased significantly by an average of 16.2% for d‐amphetamine, 22.1% for GBR‐12909, and 28.3% for tetrabenazine while there were no significant changes observed in the cerebellum or in the rate of systemic metabolism of the radiotracer. These decreases exceed the test/retest variability of striatal 11C‐raclopride binding measured in the same animals under identical experimental conditions (Dewey et al., 1992b). Together these studies demonstrate that PET measurements of striatal 11C‐raclopride binding can be used to indirectly and non‐invasively monitor changes in synaptic dopamine concentrations that result from a variety of neurophysiologic mechanisms. © 1993 Wiley‐Liss, Inc.
Further studies concerning the role of nitric oxide in LTP induction and maintenance
Authors: Musleh Wael Y. , Shahi Kavian , Baudry Michel 
Published: December 2004

AbstractNitric oxide (NO) has recently been proposed to act as a retrograde messenger to produce long‐term potentiation (LTP) in hippocampal area CA1. This notion is based largely on the absence of LTP when hippocampal slices are incubated in the presence of inhibitors of NO synthase (NOS) or of NO scavengers. In the present study, we tested the effects of such compounds on both the induction and maintenance of LTP in field CA1 of hippocampal slices. Incubation of slices in the presence of N‐methyl‐L‐arginine (MLA) or L‐nitroarginine (LNA), two inhibitors of NOS, or in the presence of hemoglobin (Hb), a NO scavenger, produced a large reduction in the magnitude of LTP induced by a theta burst stimulation (TBS) paradigm. These compounds had no effect on the degree of paired‐pulse facilitation but produced a significant reduction of the facilitation of postsynaptic responses occuring during TBS. On the other hand, MLA did not prevent the potentiation induced by application of tetraethylammonium (TEA). These results suggest that the inhibition of LTP produced by these agents could be due to an effect on a physiological mechanism that triggers LTP and not necessarily on an event that follows the triggering step. © 1993 Wiley‐Liss, Inc.
Withdrawal following cocaine self‐administration decreases regional cerebral metabolic rate in critical brain reward regions
Authors: Hammer R. P. , Pires W. S. , Markou A. , Koob G. F. 
Published: December 2004

AbstractThe quantitative [14C]‐2‐deoxyglucose autoradiographic method was utilized to assess regional cerebral metabolic rate for glucose (rCMRglc) in rat brain during withdrawal from cocaine self‐administration. RCMRglc was determined in 62 regions from brains of naïve rats which were placed into an empty operant chamber for 12 hr continuously, and rats trained to self‐administer cocaine during 3 hr training sessions and subsequently placed into the operant chamber for 12 hr continuously with or without access to cocaine. Animals placed into the chamber without access to cocaine were examined 6 hr later, while animals allowed access to the 12 hr cocaine binge were examined either 6 or 72 hr post‐cocaine. Metabolic activity was reduced during withdrawal in the nucleus accumbens, olfactory tubercle, islands of Calleja region, basolateral and central amygdaloid nuclei, medial septum, piriform and cingulate cortices, rostral caudatoputamen, entopeduncular nucleus and the adjacent lateral hypothalamus, somatosensory, auditory, and motor cortices compared to the naïve state. These effects were usually more severe at 72 than at 6 hr after binge exposure, with intermediate values observed in cocaine trained animals without binge exposure. The response was negatively correlated with the amount of cocaine consumed during binge exposure in the striatum, olfactory tubercle, piriform, cingulate, somatosensory, and motor cortices. Thus, the amount of cocaine consumed can affect the extent of metabolic depression after sustained drug exposure. The pattern of regional effects suggests that mesolimbic and rostral extrapyramidal dopamine terminal regions and certain of their efferent pathways are preferentially affected during cocaine withdrawal. The reduction of basal metabolic rate observed in these brain regions during cocaine withdrawal may become more severe with time despite the apparent recovery of certain behavioral‐motivational responses. © Wiley‐Liss, Inc.
Cocaine actions on rat prefrontal cortical and hippocampal dentate granule neurons in vitro
Authors: Jahromi Shokrollah S. , Schertzer Stephen , Carlen Peter L. 
Published: December 2004

AbstractThe electrophysiological actions of cocaine hydrochloride (COC) on medial prefrontal cortical (mpfc) and hippocampal dentate granule (DG) neurons were investigated in rat brain slices with intracellular recording techniques. The following parameters were measured: resting membrane potential (RMP), spike threshold, spike firing adaptation, postspike train afterhyperpolarization (AHP), excitatory postsynaptic potentials (EPSPs), and inhibitory postsynaptic potentials (IPSPs). In the mpfc, COC appeared to have both inhibitory and excitatory effects. In the majority of cells examined, the EPSP amplitude was attenuated by COC (200 nM–20 μM), whereas the amplitude of the postspike train afterhyperpolarization (AHP) was reduced (an excitatory effect). In DG neurons, 1 μM COC caused a small depolarization. COC potentiated the EPSPs at 1 μM but attenuated EPSPs and IPSPs at 10–100 μM. The amplitude of antidromically evoked EPSPs was also increased by 20 μM COC. At concentrations of 10 μM and greater, COC increased spike threshold. It is concluded that COC actions on mpfc and DG neurons are both excitatory and inhibitory and that these effects may be mediated by multiple neurotransmitters/modulators. © 1993 Wiley‐Liss, Inc.
Quantitative autoradiographic analysis of [3H]carfentanil binding to mu opiate receptors in the rat brain
Authors: Fitzgerald Lawrence W. , Teitler Milt 
Published: December 2004

AbstractFentanyl and its derivatives are considered among the most potent opiate analgesic/euphoriants. The pharmacological literature generally supports a μ opiate receptor site of action for the fentanyl derivatives, but some observations suggest that other sites of action may be involved in producing the extremely potent fentanyl effects. In order to investigate the mechanism of action of fentanyl‐like drugs further, [3H]carfentanil was used as a radioligand to image high‐affinity carfentanil binding sites in slidemounted sections of the rat brain (receptor autoradiography). In parallel studies the prototypical μ opiate agonist radioligand [3H]DAMGO ([D‐Ala2‐MePhe4‐Glyol5]enkephalin) was also used. The working hypothesis was that if carfentanil was acting through another high‐affinity site besides the μ opiate receptor, the distribution pattern of the autoradiographic image produced by [3H]carfentanil should be significantly different than the autoradiographic image produced by [3H]carfentanil should be significantly different than the autoradiographic pattern displayed by the well‐characterized and selective μ opiate [3H]DAMGO. Thirty‐five brain regions were examined for specific [3H]carfentanil and [3H]DAMGO binding. The absolute and relative densities of the sites were essentially identical. The highest levels of binding were observed in the “patch” areas of the striatum (131 ± 5 fmol/mg T. E. for [3H]carfentanil; 162 ± 13 fmol/mg T. E. for [3H]DAMGO). The lowest levels were observed in the cerebellum where no specific binding of either radioligand was observed. The overall distribution pattern of the two radioligands produced a correlation coefficient of 0.95; the distribution pattern was prototypical for the μ opiate receptor as reported previously by other groups. Despite the nearly identical distribution patterns, an intriguing difference in the interaction of DAMGO and carfentanil with the μ opiate receptor was observed. The biologically active nonhydrolyzable analog of GTP, GTPγS, was able to completely abolish or greatly diminish specific [3H]DAMGO binding depending on brain region; GTPγS had little or no effect on specific [3H]carfentanil binding. This latter difference in the molecular interaction of DAMGO and carfentanil with the μ opiate receptor may indicate that some of the observed differences in the effects of fentanyl‐like opiates may be due to a difference in the intrinsic activity of the fentanyl derivatives at the μ opiate receptor. © 1993 Wiley‐Liss, Inc.
Identification of tryptamine and tryptamine‐serotonin neurons in the rat dorsal raphe nuclei using specific antibodies
Authors: Dabadie Henry , Geffard Michel 
Published: December 2004

AbstractPrevious studies have shown that tryptamine (T) is closely associated with the serotonergic system but have failed to determine whether neurons containing only T exist in the raphe nuclei (RN) and/or if T colocalizes with serotonin (5‐HT). The use of rabbit‐conjugated T antisera (TAS) and rat‐conjugated 5‐HT antisera (5‐HTAS) in a double‐labelling technique has made the study of the colocalization of T and 5‐HT in neurons of the rat dorsal RN (DR) possible. Slices taken from the same zone of the DR were treated following four different procedures of double‐immunolabelling: DAB coloration for the rabbit TAS and DAB‐nickel coloration for the rat 5‐HTAS either first or second; or DAB coloration for the 5‐HTAS and DAB‐nickel coloration for the TAS first or second. Control sections were treated according to a single immunoperoxidase staining in the same zone. The immunolabelled neurons were computed using the Biocom 200 program at the same magnification. The results of this double‐immunolabelling show that three different cell types exist in the rat DR: (1) T‐only‐containing neurons, (2) 5‐HT‐only‐containing neurons displaying either homogeneous DAB or homogeneous DAB‐nickel, and (3) neurons where T colocalizes with 5‐HT (T‐positive/5‐HT‐positive neurons) displaying heterogeneous DAB‐nickel coloration. The results were identical whatever the procedure performed or the order of the DAB‐nickel revelation. In contrast, the single immunolabelling method failed to stain T‐only‐containing neurons (or 5‐HT‐only‐containing neurons); T‐immunoreactive cells (or 5‐HT‐immunoreactive cells) correspond in fact to neurons containing either T (or 5‐HT) or T and 5‐HT. © 1993 Wiley‐Liss, Inc.
Localization of 5‐HT1A receptors to astroglial cells in adult rats: Implications for neuronal‐glial interactions and psychoactive drug mechanism of action
Authors: Whitaker‐Azmitia Patricia M. , Clarke Colin , Azmitia Efrain C. 
Published: December 2004

AbstractAlthough tissue culture studies have shown a variety of neurotransmitter receptors on astroglial cells, verifying these observations in adult animals has been difficult and rarely accomplished. In the current study we have used double immunocytochemistry to localize 5‐HT1A receptors to astroglial cells in fixed sections of adult rat brain. The astroglial cells were identified using an antibody raised against the astroglialspecific protein glial fibrillary acidic protein (GFAP). To label the 5‐HT1a receptor, we used an antibody we recently raised against a unique peptide sequence occurring in the second extracellular loop of the receptor.Our results show that the 5‐HT1a receptor occurs in relatively high abundance on astroglial cells. There is regional specificity, the receptor being much more commonly found is septum and hippocampus than striatum. There are also intraregional differences in that even within a single brain region one astrocyte may have very high levels of the receptor while an adjacent cell has none.We propose that the cellular localization of this receptor could have significance in understanding the mechanism of action of 5‐HT1a receptor active drugs in alleviating anxiety and depression. The mechanism may be through the release of a neurotrophic agent, S‐100β, from astrocytes. This factor may then cause regeneration or sprouting of neuronal terminals which have been lost due to a disease process. © 1993 Wiley‐Liss, Inc.