bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intracellularly recorded response of rat striatal neurons in vitro to fenoldopam and SKF 38393 following lesions of midbrain dopamine cells
Authors: Twery M. J. , Thompson L. A. , Walters J. R. 
Published: December 2004

AbstractThe effect of long‐term (6–19 weeks) 6‐hydroxydopamine‐induced (6‐OHDA) lesions of midbrain dopamine cells on dopamine D1‐like agonist‐induced changes in the excitability of rat striatal neurons was investigated in vitro using tissue slices and intracellular recording techniques. Fenoldopam and (±)‐SKF 38393 predominantly decreased excitability in control preparations including striatal neurons located contralateral to 6‐OHDA injection sites and neurons obtained from rats receiving sham injections or no treatment. Fenoldopam also inhibited neurons ipsilateral to lesions of midbrain dopamine cells. (±)‐SKF 33393, unlike fenoldopam, produced predominantly increases in the excitability of ipsilateral striatal neurons. Superfusion of the D1 receptor antagonist, SCH 23390, blocked fenoldopam‐induced decreases in excitability but not the (±)‐SKF 38393‐induced excitation of neurons ipsilateral to the lesion. Sequential application of fenoldopam and quinpirole, a D2/D3 receptor agonist, produced responses to both drugs in a majority of neurons. The results demonstrate that inhibitory responses to fenoldopam are mediated by D1 receptors, while excitatory effects of (±)‐SKF 38393 in the striatum ipsilateral to the lesion are apparently not dependent on D1 receptor activation. These findings also suggest that dopamine D1 and D2/D3 receptors are able to concurrently influence the excitability of striatal neurons in the dopamine deafferentated striatum. Similar regulation of striatal neurons in vivo may contribute to dopaminergic regulation of basal ganglia output and the ability of dopaminomimetic agents to ameliorate symptoms of dopaminergic deficiency in Parkinson's disease. © 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.
Transient increase in the in vivo binding of the benzodiazepine antagonist [3H]flumazenil in deafferented visual areas of the adult mouse brain
Authors: Madar Igal , Scheffel Ursula , Frost J. James 
Published: December 2004

AbstractFlumazer it is an imidazobenzodiazepine, an antagonist of central benzodiazepine (BDZ) receptors. BDZ binding sites are a modulatory component located on the gamma‐aminobutyric acid (GABA) receptor macromolecule. We studied the effect of monocular enucleation on [3H]flumazenil binding in deprived and intact visual areas and nonvisual areas of the adult mouse brain under in vivo conditions. [3H]flumazenil binding was examined at seven time points up to 56 days postenucleation. In some monocularly deprived mice, changes in local blood flow accompanied with the BDZ receptor response were evaluated by coinjection of [3H]flumazenil and 9mTc‐HMPAO. Monocular enucleation produced a transient increase in [3H]flumazenil binding in the deprived visual cortex and superior colliculus. At 17 days postenucleation, [3H]flumazenil binding in the anterior and posterior portions of the visual cortex and the superior colliculus increased by 28%, 15% and 23%, respectively, and declined to control levels at 45 days postenucleation. The increase in [3H]flumazenil was accompanied with a decrease in blood flow. Alterations in BDZ receptors and blood flow were selective to deprived visual structures. The regional correlation between the metabolic deficit and the BDZ response provides further support that the increase in BDZ receptor binding is confined to regions of reduced neuronal activity. [11C]flumazenil is an excellent radiotracer for in vivo imaging of benzodiazepine receptors in human brain using positron emission tomography (PET). This study suggests the suitability of [11C]flumazenil for in vivo PET study of BDZ receptor response to deafferentation of visual structures in human brain. © 1994 Wiley‐Liss, Inc.
Slow recovery of human brain MAO B after L‐Deprenyl (Selegeline) withdrawal
Authors: Fowler Joanna S. , Volkow Nora D. , Logan Jean , Wang Gene‐Jack , Mac Gregor Robert R. , Schlyer David , Wolf Alfred P. , Pappas Naomi , Alexoff David , Shea Colleen , Dorflinger Ernest , Kruchowy Lesia , Yoo Kisook , Fazzini Enrico , Patlak Clifford 
Published: December 2004

AbstractL‐Deprenyl (Selegeline) is an enzyme‐activated irreversible inhibitor of monoamine oxidase B (MAO B; EC 1.4.3.4). It is used to treat Parkinson's disease at a dose of 5 mg twice a day. Since enzyme inhibition is irreversible, the recovery of functional enzyme activity after withdrawal from L‐deprenyl requires the synthesis of new enzyme. We have measured a 40 day half‐time for brain MAO B synthesis in Parkinson's disease and in normal subjects after withdrawal from L‐deprenyl. This is the first measurement of the synthesis rate of a specific protein in the living human brain. L‐Deprenyl is currently used by 50,000 patients with Parkinson's disease in the United States and its use is expected to increase with reports that it may be beneficial in Alzheimer's disease. The slow turnover of brain MAO B suggests that the current clinical dose of L‐deprenyl may be excessive and that the clinical efficacy of reduced dosing should be evaluated. Such an evaluation may have mechanistic importance as well as an impact on reducing the side effects and the costs arising from excessive drug use. © 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.
Pharmacokinetics and in vivo specificity of [LLC]dl‐threo‐methylphenidate for the presynaptic dopaminergic neuron
Authors: Ding Yu‐Shin , Fowler Joanna S. , Volkow Nora D. , Gatley S. John , Logan Jean , Dewey Stephen L. , Alexoff David , Fazzini Enrico , Wolf Alfred P. 
Published: December 2004

Abstractdl‐threo‐Methylphenidate (Ritalin) was labeled with carbon‐11 (t1/2:20.4 minutes) in order to measure its pharmacokinetics, to evaluate it as a radiotracer for the presynaptic dopaminergic neuron, and to examine its sensitivity to the loss of dopaminergic neurons. Positron emission tomographic (PET) studies were carried out in the baboon to determine specificity for the presynaptic dopaminergic neuron and in humans to assess sensitivity to neuronal loss. Studies with [llC]dl‐threo‐methylphenidate ([llC]MP) in baboon demonstrated high regional uptake in the striatum. Peak uptake (0.04%/cc) occurred at 5‐15 minutes post‐injection. The half‐time for clearance from peak uptake for [11C]MP was 60 minutes and the ratio between the radioactivity in the striatum and that in the cerebellum (ST/CB) ranged from 2.2 to 2.6 at 40 minutes. Repeated measures in the same baboon showed ≤8% variability in the ST/CB ratio. Pretreatment with unlabeled methylphenidate (0.5 mg/kg) or GBR12909 (1.5 mg/kg) 30 minutes prior to [11C]MP injection markedly reduced the striatal but not the cerebellar uptake of [11C]MP, demonstrating the saturable and specific binding of [11C]MP to a site on the dopamine transporter in the brain. In both cases, the ratio of striatum to cerebellum (ST/CB) after pretreatment was reduced by about 43% The ratios of distribution volumes at the steady‐state for the striatum to cerebellum (ST/CB) for these two separate studies in the same baboon were reduced by 37 and 38%, respectively. In contrast, pretreatment with tomoxetine (1.5 mg/kg) or citalopram (2.0 mg/kg), inhibitors of the norepinephrine and serotonin transporter, respectively, did not produce a significant change in the kinetics of [11C]MP and the ST/CB after pretreatment was similar to that for control. In one patient with Parkinson's disease, the striatum to cerebellum ratio of [11C]MP was markedly lower than that of an elderly normal subject. These results demonstrate the saturable [11C]MP binding to the dopamine transporter in the baboon brain and that [11C]MP is sensitive to dopamine neuron degeneration in Parkinson's disease. © 1994 Wiley‐Liss, IncThis article is a US Government work and, as such, is in the public domain in the United States of America
.
Haloperidol‐induced morphological alterations are associated with changes in calcium/calmodulin kinase II activity and glutamate immunoreactivity
Authors: Meshul Charles K. , Tan Soon‐Eng 
Published: December 2004

AbstractAdministration of haloperidol for 2 weeks causes an increase within the caudate nucleus of asymmetrical synapses associated with a discontinuous or perforated, postsynaptic density (PSD) [Meshul et al. (1992), Psychopharmacology, 106:45–52; Meshul et al. (1992), Neuropsychopharmacology, 7:285–293]. Coadministration of the N‐methyl‐D‐aspartate noncompetitive antagonist, MK‐801, with haloperidol blocked the increase in striatal synapses containing a perforated PSD [Meshul et al. (1994), Brain Res., 648:181–195]. Examination of the caudate using immuno‐gold electron microscopy revealed the vast majority (90%) of asymmetrical synapses were labelled with a glutamate antibody [Meshul et al. (1994), Brain Res., 648:181–195]. The purpose of this study was to determine if there were any changes in the density of glutamate immunoreactivity within presynaptic terminals of asymmetric synapses within the striatum following treatment with haloperidol for 1 month that would correlate with the previously observed increase in synapses with perforated PSDs. We also determined the activity of striatal calcium/ calmodulin kinase II (CaMK II), an enzyme known to be localized within the synaptic region, after administration of haloperidol. We report here that haloperidol causes an increase in the activity of CaMK II and a decrease in the density of immuno‐gold labelling for glutamate within the nerve terminals of asymmetrical synapses containing a perforated or nonperforated PSD. These results are consistent with the hypothesis that the haloperidol‐induced increase in activity of CaMK II and the increase in glutamate release, as suggested by the decrease in presynaptic glutamate immunoreactivity, may ultimately lead to an increase in the number of synapses displaying a perforated PSD. These results support the speculation that the haloperidol‐induced increase in synapses containing a perforated PSD may be associated with enhanced activity at excitatory synapses. © 1994 Wiley‐Liss, Inc.
Differential influence of electrical blocking agents on embryonic acetylcholine receptor mRNA levels in long‐term cultures of aneural mammalian myotubes
Authors: Carlson C. George , Adkins Steven D. , Blake Michael J. , Hasan Abul K. Q. , Loyland Stacy 
Published: December 2004

AbstractThe influence of spontaneous muscle activity on acetylcholine receptor (AChR) expression was examined by exposing long‐term cultures of mammalian myotubes to two pharmacological agents that have similar effects on the rate of spontaneous contractile activity but pharmacologically distinct actions on voltage gated Na+ channels. Previous studies by other investigators have shown that tetrodotoxin upregulates and that veratridine downregulates surface AChR expression in short‐term mammalian muscle cultures. In order to determine whether these drugs have disparate actions on AChR mRNA levels, myotubes were exposed to either tetrodotoxin or veratridine for a period of 10 days, and measurements of the relative levels of embryonic AChR subunit mRNAs (alpha, beta, gamma, delta) were obtained during and following the period of drug exposure. Veratridine produced a substantial decrease (between 33% and 50% reduction), while tetrodotoxin produced a relatively small increase (between 17% and 23%), in each of the AChR subunit mRNAs after 6 days of drug exposure. At 23 days in culture, spontaneously active myotubes exhibited a decrease in the relative levels of each of the AChR subunit mRNAs. Myotubes previously exposed to either veratridine or tetrodotoxin exhibited elevated levels of beta, gamma, and delta AChR subunit mRNAs 6 days after cessation of drug treatment, thus suggesting that a period of muscle inactivity can induce sustained influences on some AChR mRNA levels. These results indicate that the disparate effects of veratridine and tetrodotoxin on surface AChR expression are partly mediated by opposing alterations in AChR subunit mRNA levels, and suggest that changes in the resting influx of sodium and/or calcium ions that are independent of spontaneous electrical or contractile activity can modulate intracellular levels of AChR subunit mRNAs. © 1994 Wiley‐Liss, Inc.
In vivo biogenic amine efflux in medial prefiontal cortex with imipramine, fluoxetine, and fluvoxamine
Authors: Jordan Shaun , Kramer Gerald L. , Zukas Paul K. , Moeller Melissa , Petty Frederick 
Published: December 2004

AbstractIn vivo brain microdialysis was used to determine the effects of the standard tricyclic antidepressant imipramine and the two selective serotonin reuptake inhibitors (SSRIs) antidepressants, fluoxetine and fluvoxamine, on extracellular levels of norepinephrine (NE), dopamine (DA), and serotonin (5‐HT) in rat medial prefrontal cortex. When given intraperitoneally (IP), imipramine increased NE in the microdialysis perfusate, and elevated DA and 5‐HT to a lesser extent. Similar dose‐dependent increases in DA and 5‐HT were detected after IP fluoxetine, although NE was less affected. In contrast, IP fluvoxamine produced no change in basal NE nor DA, although a large increase in 5‐HT occurred at an intermediate dose. When administered directly into cortex, all three antidepressants increased 5‐HT by the same amount in a dose‐dependent fashion. Intracortical imipramine and fluoxetine increased NE, and fluoxetine and fluvoxamine both increased DA, with fluoxetine doing so at a lower concentration. These data suggest that the SSRIs are not entirely selective for serotonin in vivo. © 1994 Wiley‐Liss, Inc.
Further characteristics of long‐term potentiation in piriform cortex
Authors: Jung Min Whan , Larson John 
Published: December 2004

AbstractMechanisms for the induction and expression of long‐term potentiation (LTP) were studied in slices of piriform cortex. Cooperativity among afferent inputs as a controlling factor for induction of LTP was tested by pairing stimulation of one input that normally does not induce LTP with stimulation of another input. Combined stimulation, given either to two weak inputs with simultaneous bursts or by pairing single pulses with bursts, did effectively induce LTP. Tests for expression of LTP by NMDA vs. non‐NMDA receptors indicated that non‐NMDA receptor‐mediated responses expressed much greater LTP than NMDA receptor‐mediated responses. Ratios for paired‐pulse facilitation and depression were not altered after induction of LTP. These characteristics are comparable to those exhibited by synapses in the CA1 field of hippocampus. © 1994 Wiley‐Liss, Inc.
Anesthetics block morphine‐induced increases in serotonin release in rat CNS
Authors: Tao Rui , Auerbach Sidney B. 
Published: December 2004

AbstractThe effect of morphine on serotonin (5‐HT) was examined by microdialysis in unanesthetized and anesthetized rats. In unanesthetized rats, morphine (10 mg/kg, s. c.) produced increases in extracellular 5‐HT in nucleus accumbens (n. accumbens) and dorsal raphe nucleus (DRN), but not in the dorsal hippocampus. Similarly, extracellular 5‐HT in the n. accumbens, but not the dorsal hippocampus, was increased after morphine (1 μM) was infused for 60 min by reverse dialysis into the DRN. Chloral hydrate, pentobarbital, and ketamine anesthesia had different effects on 5‐HT in the n. accumbens. Chloral hydrate induced a transient increase and ketamine a sustained increase in extracellular 5‐HT. Pentobarbital caused a sustained decrease. The effects of systemic and intraraphe administration of morphine were abolished by all three anesthetics. Infusion of muscimol, a GABAA receptor agonist, into the DRN also induced a decrease in 5‐HT and abolished the effects of morphine on 5‐HT in the DRN and n. accumbens. These results are consistent with other evidence suggesting that morphineinduced increases in monoamine neurotransmission are a disinhibitory effect resulting from opioid‐mediated inhibition of GABA release. More conclusively, it is apparent that anesthetized animals are inappropriate for testing the effect of morphine on 5‐HT neurotransmission. © 1994 Wiley‐Liss, Inc.
Quantal analysis of presynaptic inhibition, low [Ca2+]0, and high pressure interactions at crustacean excitatory synapses
Authors: Golan Hava , Moore Homer J. , Grossman Yoram 
Published: December 2004

AbstractThe cellular mechanisms underlying the effects of high pressure, GABAergic presynaptic inhibition, and low [Ca2+]0 on glutamatergic excitatory synaptic transmission were studied in the opener muscle of the lobster walking leg. Excitatory postsynaptic currents (EPSCs) were recorded with or without prior stimulation of the inhibitor using a loose macropatch clamp technique at atmospheric pressure and at 6.9 MPA helium pressure. High pressure reduced the mean EPSC amplitude and variance, decreased the quantal content (m), but did not affect the quantum current (q). Pressure shifted the median of the amplitude histogram to the left by 1–2 q. Under normal pressure conditions, presynaptic inhibition and low [Ca 2+]0 induced similar effects. However, quantal analysis using a binomial frequency distribution model revealed that high pressure and low [Ca 2+]0 diminished n (available active zones) and slightly increased p (probability of release), but presynaptic inhibition reduced p and slightly increased n. At high pressure, presynaptic inhibition was reduced, at which time the major contributor to the inhibitory process appeared to be reduction in n and not p. The similarity of the alterations in quantal parameters of release at high pressure, low [Ca 2+]0, and in some conditions of presynaptic inhibition is consistent with the hypothesis that pressure reduces Ca2+ inflow into the presynaptic nerve terminals to affect the Ca2+‐dependent quantal release parameters n and p. © 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.
In situ hybridization evidence for the synthesis of 5‐HT1B receptor in serotoninergic neurons of anterior raphe nuclei in the rat brain
Authors: Doucet Edith , Pohl Michel , Fattaccini Claude‐Michelle , Adrien Joëlle , Mestikawy Salah El , Hamon Michel 
Published: December 2004

AbstractThe regional distribution of the mRNA encoding the serotonin 5‐HT1B receptor was studied in the central nervous system of the rat by in situ hybridization histochemistry and Northern blot analysis. A 180 base pair probe, corresponding to a highly selective portion of the third intracellular loop of the rat 5‐HT1B receptor, was used. In most regions, a single 5 kb message was found by Northern blot analysis. However, two additional bands (2.5 and 4 kb) were detected in the striatum. The rank order of 5‐HT1B mRNA abundance was striatum ≥ septum = ventral tegmentum _‐ colliculi = hypothalamus = hippocampus > brain stem a cerebellum _‐ dorsal horn of the spinal cord > cerebral cortex a ventral horn of the spinal cord > olfactory tubercle. This distribution was confirmed by in situ hybridization, which further revealed that the 5‐HT1B mRNA was present in dorsal root ganglia, the layer IV of the cerebral cortex, the Purkinje cell layer of the cerebellum, the pyramidal neurons in the CAl area of the hippocampus, and the dorsal and median raphe nuclei. In situ hybridization was also performed in nomifensine (10 mg/kg/ i.p.)‐pretreated rats whose serotoninergic neurons were extensively and selectively lesioned by microinjection of 5,7‐dihydroxytryptamine (8 μg/1 μl) directly into the anteroventral vicinity of anterior raphe nuclei 3 weeks before sacrifice. In lesioned rats, 5‐HT1B mRNA was present in the same areas and at the same levels as in control rats, except in the dorsal and median raphe nuclei, where a marked decrease (–75%) in its local concentration was observed. These data provide the first demonstration of the synthesis of 5‐HT1B receptor within serotoninergic neurons, as expected of their presynaptic autoreceptor function at the level of serotoninergic terminals. ©1995 Wiley‐Liss, Inc.
Cellular colocalization of dopamine D1 and D2 receptors in rat medial prefrontal cortex
Authors: Vincent Stephen L. , Khan Yusuf , Benes Francine M. 
Published: December 2004

AbstractIn a recent study in rat medial prefrontal cortex (mPFC), a fluorescently coupled, high‐affinity ligand for the D1 receptor subtype was localized to nonpyramidal neurons, while a ligand selective for the D2 subtype was found on neurons with a size distribution overlapping with both small pyramidal and large nonpyramidal cells. These observations raised the possibility that a subpopulation of cortical neurons with an intermediate size range may coexpress both the D1 and D2 receptor subtypes. In the present study, the D1 and D2 receptor subtypes have been simultaneously localized in layer VI of rat mPFC using 20 nM SCH 23390‐Bodipy and 20 nM N‐(p‐aminophenethyl) spiperone‐Texas red, respectively, in the presence of 100 nM mianserin (5‐HT2 receptor antagonist). The localization of receptor binding fluorescence was assessed in paired images using fluoresceiN isothiocyanate (FITC) and rhodamine dichroic filters for the D1 and D2 subtypes, respectively. Under the conditions employed here, most cell bodies showed either Dl‐like or D2‐like receptor binding fluorescence, while a colocalization of both fluoroprobes was observed on only 25% of the labeled cells. When the size of each single‐labeled cell body was measured using the respective FITC (D1‐probe) and rhodamine (D2‐probe) epifluorescence filters, the distribution of cells showing only D1‐like receptor binding fluorescence was similar to nonpyramidal neurons (68.6 ± 1.8 μm2), while that for cells showing only D2‐like receptor binding fluorescence was similar to that of both large interneurons and small pyramidal cells (106.9 ± 2.4 μm2). Cells showing both D1‐ and D2‐like receptor binding fluorescence were found to overlap in size only with nonpyramidal cells when either fluorescent filter was used. These findings are consistent with the hypothesis that the D1 and D2 receptor subtypes are most often found on different populations of neurons in mPFC, although approximately 25% of all such cells appear to be nonpyramidal neurons having both D1 and D2 receptor binding activity. These findings suggest that the dopamine projections to rat cortex probably engage in a complex interplay with intrinsic cortical neurons and their respective neurotransmitter systems. © 1995 Wiley‐Liss, Inc.