bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spinal cord transection produces a long‐term increase in GABAB binding in the rat substantia gelatinosa
Authors: Kroin Jeffrey S. , Bianchi Gregory D. , Penn Richard D. 
Published: December 2004

AbstractQuantitative autoradiography was used to determine changes in GABAB receptor binding in the substantia gelatinosa of the lumbar spinal cord at 4 days and at 6 weeks after a midthoracic spinal transection in rats.In the 4 day lesion animals, there was no significant change in either the density or the affinity of the GABAB binding. At 6 weeks, however, there was a 35% increase in binding density, with no significant change in affinity. The results suggest that alterations in spinal synaptic mechanisms can slowly evolve following loss of descending input to the spinal cord. © 1993 Wiley‐Liss, Inc.
Autoradiographic localization of [125I‐TYR8]‐bradykinin receptor binding sites in the guinea pig spinal cord
Authors: Lopes Paulo , Kar Satyabrata , Tousignant Christine , Regoli Domenico , Quirion Réami , Couture Réjean 
Published: December 2004

AbstractThe present study aimed to localize and characterize [125I‐Tyr8]‐BK binding sites in all major segments of the guinea pig spinal cord using in vitro quantitative receptor autoradiography. [125I‐Tyr8]‐BK specific binding sites were localized predominantly in superficial layers of the dorsal horn, with lamina II depicting the highest labelling. The density of specific binding in laminae I and III was moderate, whereas in other areas, i.e., laminae IV‐X, lower amounts of labelling were noticed. The B2 receptor antagonists D‐Arg[Hyp3,Thi5,D‐Tic7,Oic8]‐BK (Hoe 140),D‐Arg[Hyp3,D‐Phe7,Leu8]‐BK,Tyr0,D‐Arg[Hyp3,D‐Phe7,Leu8]‐BK, D‐Arg[Tyr3,D‐Phe7,Leu8]‐BK, D‐Arg[Hyp2,Thi5.8,DPhe7]‐BK, D‐Arg[Hyp3,Leu8]‐BK and D‐Arg[Hyp3,Gly6,Leu8]‐BK as well a., unlabelled [Tyr8]‐BK inhibited [1251‐Tyr8]‐BK binding with respective Ki values of 0.04, 12.4, 23.4, 34.5, 43.5, 33.5, 23.0, and 0.6 nM while B1 related molecules (Tyr0, des‐Arg10‐kallidin and [Leu8]‐des‐Arg9‐BK) did not significantly inhibit [125I‐Tyr8]‐BK binding up to micromolar concentrations. These results indicate that the specific [125I‐Tyr8]‐BK binding sites present in the guinea pig spinal cord belong to the B2 receptor subtype. The high density of B2 binding sites in the substantia gelatinosa provides an anatomical evidence in favour of a role for BK as a modulator of nociceptive information. © 1993 Wiley‐Liss, Inc.
Evaluation of 5‐[18F]Fluoropropylepidepride as a potential pet radioligand for imaging dopamine D2 receptors
Authors: Kessler Robert M. , Votaw John R. , de Paulis Tomas , Bingham Daniel R. , Ansari M. Sib , Mason N. Scott , Holburn George , Schmidt Dennis E. , Votaw Delicia B. , Manning Ronald G. , Ebert Michael H. 
Published: December 2004

AbstractThis study evaluated the utility of (S)‐N‐[(1‐ethyl‐2‐pyrrolidinyl)methyl]‐5‐(3‐[18F]fluoropropyl)‐2,3‐dimethoxybenzamide ([18F]fluoropropylepidepride), [18F]5‐FPrEpid, as a ligar d for PET studies of cerebral dopamine D2 receptors. The in vitro affinity for the rat striatal dopamine D2 receptor, KD 138 pM, was determined by Scatchard analysis of in vitro binding to rat striatal homogenate. The apparent lipophilicity, log kw 1.6, was measured with reverse phase HPLC at pH 7.5. The receptor specificity was determined by competitive displacement of [18F]5‐FPrEpid by a variety of neurotransmitter ligands. Only dopamine D2 ligands displaced [18F]5‐FPrEpid with high affinity. Positron tomographic imaging studies in primates of [18F]5‐FPrEpid demonstrated a stable striatal uptake. of 0.02% injected dose/ml for up to 5 h after injection. The striatal: cerebellar ratio increased from 2 at 15 min, to 7 at 200 min, and to 10 at 300 min. Striatal uptake was displaceable by haloperidol (1 mg/kg) or raclopride (2.5 mg/kg) to cerebellar levels with a t1/2 of washout of 9 or 15 min. Striatal uptake was mildly susceptible to displacement by d‐amphetamine (1–2 mg/kg) released endogenous dopamine; d‐amphetamine administration produced a 10%/h increase in the rate of striatal washout. Although uptake in the striatum is reversible, an equilibrium between receptor bound [18F]5‐FPrEpid in striatum and [18F]5‐FPrEpid in plasma is not reached within 5 h postinjection. © 1993 Wiley‐Liss. Inc.
Specific neurophysiological effects of systemic nicotine on neurons in the nucleus accumbens
Authors: Hakan R. L. , Hart C. , Eyl C. 
Published: December 2004

AbstractExtracellular recordings of single neurons within the nucleus accumbens (NAS) of halothane‐anesthetized rats have revealed that systemic nicotine injections (0.5 and 1.0 mg/kg, s.c.) inhibit the action potentials of normally inactive NAS neurons, evoked by fimbria stimulation (fimbria‐driven responses, n = 18). These nicotine inhibitions of fimbria‐driven NAS action potentials appear to be centrally mediated because they were reversed by subsequent systemic injections of the centrally acting nicotinic acetylcholine (nAch) antagonist, mecamylamine (1.0 mg/kg, s.c., n = 6), but not by the peripherally acting nAch antagonist, hexamethonium (2.0 mg/kg, s.c., n = 6). Fimbria‐driven NAS neurons were also tested with morphine (2.5 mg/kg, s.c.) in some experiments. Consistent with many past observations (Hakan et al., 1989), morphine did not affect these driven neurons. In other experiments, nicotine‐induced inhibition of NAS fimbria‐driven units was followed by haloperidol (0.5 mg/kg, s.c.), in attempts to reveal the possible role of dopamine in these effects. Haloperidol was successful at reversing nicotine inhibitions in only some cases (n = 2/6). Thus, the role of dopamine in these NAS responses to nicotine remains unclear. In contrast to the fimbria‐driven NAS responses, spontaneously active NAS neurons were not affected by nicotine injections yet were subsequently inhibited with systemic morphine. These results suggest a specific neuro‐pharmacological organization in the region of the nucleus accumbens that may relate to the qualitative and subjective differences in the experiential effects of different psychoactive drugs. Iontophoretic studies designed to localize further the site of these nicotine effects on NAS neurons are in progress. © 1993 Wiley‐Liss, Inc.
MK‐801 prevents the development of behavioral sensitization during repeated morphine administration
Authors: Jeziorski Michael , White Francis J. , Wolf Marina E. 
Published: December 2004

AbstractAcute administration of morphine (10 mg/kg) to rats elicited an increase in locomotion that became sensitized upon repeated treatment over 14 days. Administration of the noncompetitive N‐methyl‐D‐aspartate receptor (NMDA) antagonist MK‐801 (0.1 or 0.25 mg/kg) prior to each morphine injection prevented the development of behavioral sensitization to morphine, an effect that persisted even after a 7‐day withdrawal from repeated treatment. Sensitization was also prevented by coadministration of the competitive NMDA receptor antagonist CGS 19755 (10 mg/kg). In contrast, acute pretreatment with MK‐801 did not alter the response of sensitized rats to morphine challenge, indicating that MK‐801 does not prevent the expression of sensitization. When administered alone, MK‐801 produced stereotyped movements at moderate doses (0.25 rng/kg) and horizontal locomotion at higher‐ doses, (0.5 mg/kg). Repeated administration of 0.25 mg/kg MK‐801 elicited sensitization to its own locomotor stimulatory effects, such that this dose became capable of eliciting horizontal locomotion. Sensitization was not seen during repeated administration of 0.1 mg/kg MK‐801 or 10 mg/kg CGS 19755, although both of these pretreatments did produce a sensitized response to subsequent challenge with 0.25 mg/kg MK‐801. This effect was enhanced by coadministration of morphine, even though repeated administration of morphine alone failed to sensitize rats to MK‐801 challenge. These results suggest a complex interplay between NMDA and opioid receptors, such that NMDA antagonists prevent morphine sensitization while morphine enhances the ability of NMDA antagonists to elicit sensitization to their own locomotor stimulatory effects. © 1994 Wiley‐Liss, Inc.
Imaging endogenous dopamine competition with [11C]raclopride in the human brain
Authors: Volkow Nora D. , Wang Gene‐Jack , Fowler Joanna S. , Logan Jean , Schlyer David , Hitzemann Robert , Lieberman Jeffrey , Angrist Burton , Pappas Naomi , MacGregor Robert , Burr Gail , Cooper Thomas , Wolf Alfred P. 
Published: December 2004

AbstractThis study images dopamine release in response to a neurochemically specific challenge with the psychostimulant drug methylphenidate. Changes in synaptic dopamine induced by methylphenidate were evaluated with positron emission tomography and [11C]raclopride, a D2 receptor radioligand that is sensitive to endogenous dopamine. Methylphenidate significantly decreased striatal [11C]raclopride binding. The decrease was variable and was negatively correlated with age. Mood and anxiety at baseline, were also correlated with methylphenidate‐induced DA changes. This strategy provides a tool to investigate the responsiveness of the dopamine system in the normal and diseased human brain and to investigate the neurochemical correlates of behavior. © 1994 Wiley‐Liss, Inc.
Loss of paired‐pulse facilitation at the corticostriatal synapse of the aged rat
Authors: Walsh John P. , Ou Xiaorong 
Published: December 2004

AbstractChanges in calcium (Ca2+) homeostasis have been proposed to contribute to the aging process. Paired‐pulse facilitation, a form of synaptic enhancement that relies upon an accumulation of Ca2+ in the presynaptic terminal, was used to examine the effect of aging at the corticostriatal synapse. Intracellular recordings in striatal neurons from young rats demonstrated a consistent enhancement in the second of two synaptic responses evoked by stimulation of the corpus callosum. In contrast, neurons from aged rats showed a consistent depression of the second synaptic response at identical pairing intervals. These differences were not explained by an age‐dependent increase in synaptic depression and demonstrate an alteration in the Ca2+‐mediated process of presynaptic facilitation. © 1994 Wiley‐Liss, Inc.
Analysis of synaptic inputs and targets of physiologically characterized neurons in rat frontal cortex: Combined in vivo intracellular recording and immunolabeling
Authors: Cowan Ronald L. , Sesack Susan R. , Van Bockstaele Elisabeth J. , Branchereau Pascal , Chan June , Pickel Virginia M. 
Published: December 2004

AbstractUltrastructural immunocytochemical identification of transmitters in afferent terminals and targets of individual physiologically characterized neurons is essential for understanding the complex circuitry within the mammalian neocortex. For this type of analysis, we examined the utility of combining in vivo intracellular recording and biocytin injections with silver intensified 1 nm immunogold labeling of GABA and the catecholamine synthesizing enzyme, tyrosine hydroxylase (TH). These transmitters are found in local neurons and afferents known to prominently modulate the activity of pyramidal neurons in the neocortex. Individual neurons were physiologically characterlzea and filled with biocytin in the frontal cortex of anesthetized rats. The brains were then preserved by vascular perfusion with aldehydes. Single vibratome sections through the recording site were reacted (1) for immunoperoxidase detection of biocytin and (2) for immunogold labeling of GABA or TH. Dually labeled sections were processed for light microscopy or embedded in plastic for electron microscopy. The dense peroxidase product for biocytin was detected in pyramidal neurons. These were located in superficial as well as deep cortical laminae. and were readily distinguished from immunogold silver labeling. GABA labeled terminals formed symmetric synapses with larger biocytin filled dendrites, whereas the TH labeled terminals contacted distal dendrites and spines. Peroxidase labeling for biocytin also was seen in a few axon terminals forming synapses with unlabeled and with GABA immunoreactive dendrites. These results suggest that single pyramidal neurons of the rat frontal cortex receive dual input from both GABA and catecholamine terminals. Additionally, this study demonstrates the usefulness of silver enhancement of 1 nm coilloidal gold prior to plastic embedding for electron microscopic detection of neurotransmitters within afferents and targets of neurons physiologically characterized in vivo. © 1994 Wiley‐Liss. Inc.
Dopamine D2 receptors mapped in rat brain with [3H](+)PHNO
Authors: Nobrega Jose N. , Seeman Philip 
Published: December 2004

AbstractPrevious work with membrane preparations had demonstrated that the agonist (+)‐4‐propyl‐9‐hydroxynaphthoxazine (PHNO) labels the high‐affinity state of dopamine D2 receptors with 67‐fold selectivity over D1 sites. In this study, quantitative autoradiography was used to examine the binding of [3H](+)PHNO to rat brain sections. Highest binding densities were found in caudate‐putamen, accumbens, and olfactory tubercles, as expected, and also in specific layers of the olfactory bulb. In addition, a second group of brain regions, including lateral septum, entorhinal cortex, molecular layer of hippocampus, and several brainstem structures showed low but consistent levels of binding. In all brain regions [3H](+)PHNO binding (2 nM) was completely displaced by 10 μM sulpiride (>99%). Addition of 150 μM guanilylimidodiphosphate, which normally converts D2 receptors from high to low affinity states, abolished [3H](+)PHNO binding in all brain regions (>99%), except for the islands of Callejas. This is likely to reflect binding to D3 sites in this area. Omission of preincubation in binding assays decreased [3H](+)PHNO binding in a regionally dependent manner, with strongest effects (22%) seen in high‐density areas. These preincubation results confirm that (+)PHNO may have limitations for in vivo imaging studies. On the other hand, [3H](+)PHNOs negligible levels of non‐specific binding compared to other agonists and overall selectivity would make it an excellent tool for in vitro autoradiographic monitoring of the high affinity state of D2 receptors. © 1994 Wiley‐Liss. Inc.
Sigma‐1 and Sigma‐2 sites in rat brain: Comparison of regional, ontogenetic, and subcellular patterns
Authors: McCann David J. , Weissman Arthur D. , Su Tsung‐Ping 
Published: December 2004

AbstractRadioligand binding assay conditions were established for the selective labeling of sigma‐1 and sigma‐2 sites in membrane homogenates of rat brain. Selective sigma‐1 assays were conducted using 5 nM (+)[3H]SKF‐10,047 in the presence of 300 nM dizocilpine (MK‐801). Selective sigma‐2 assays were conducted using 5 nM [3H]DTG in the presence of 1 μM (+)SKF‐10,047. Distributions of sigma‐1 and sigma‐2 binding among brain regions were found to differ. While the brain stem yields the highest level of sigma‐1 binding, it yields among the lowest levels of sigma‐2 binding. The reverse is true in hippocampal membranes. Different ontogenetic patterns were also observed. Sigma‐2 binding decreases substantially during brain development, whereas sigma‐1 binding does not vary significantly. Patterns of distribution among subcellular fractions of rat brain homogenates were found to be similar. Both sigma‐1 and sigma‐2 sites are most enriched in microsomal fractions, and neither is enriched in synaptosomal or mitochondrial fractions. The present results suggest that sigma‐1 and sigma‐2 sites are distinct entities; they do not appear to be located on a common macromolecule, and they do not represent two different affinity states of a single type of binding site. While the precise subcellular locations (if sigma‐1 and sigma‐2) sites remain to be determined, we conclude that localization of either type of binding site to synaptic regions of plasma membrane or to mitochondria is highly unlikely © 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.
Dopamine displays an identical apparent affinity towards functional dopamine D1 and D2 receptors in rat striatal slices: Possible implications for the regulatory role of D2 receptors
Authors: Schoffelmeer Anton N. M. , Hogenboom Francois , Mulder Arie H. , Ronken Eric , Stoof Johannes C. , Drukarch Benjamin 
Published: December 2004

AbstractIn this study we examined the selectivity of dopamine (DA) for rat striatal DA D1 and D2 receptors. In a Krebs‐HEPES buffer, the Ki values of DA for D1 binding sites (labelled with [3H]SCH23390) and D2 binding sites (labelled with [3H]spiroperidol) in striatal membranes amounted to about 30 and.0.3 μM, respectively. However, the EC50s of DA (3 μM) and the DA releasing drug amphetamine (1 μM) were identical considering D1 receptor‐stimulated and D2 receptor‐inhibited adenylate cyclase activity in superfused striatal slices. Moreover, these EC50 values were also obtained studying DA‐ and amphetamine‐induced D2 receptor activation, resulting in inhibition of the electrically evoked release of [14C]acetylcholine from the slices. Therefore, with regard to the apparent affinity of exogenous and endogenous DA for D1 and D2 receptors in rat striatal slices, the ligand‐receptor binding data appeared to be misleading. Thus, our data show that in rat striatal slices DA has an identical apparent affinity towards functional D1 and D2 receptors, which is particularly intriguing in view of the very high receptor selectivity of synthetic D1 and D2 receptor agonists for these functional receptors in superfused brain slices as predicted on the basis of binding assays. This may have important implications for our understanding of central DA neurotransmission. For instance, since the inhibitory effect of opioid and muscarinic receptor activation on adenylate cyclase activity has been shown to be inversely related to the degree of DA D2 receptor activation, the degree of activation of D1 and D2 receptors by released DA is suggested to act as a functional gate allowing distinct neurotransmitters to play a role in striatal neurotransmission. © 1994 Wiley‐Liss, Inc.
Effects of prenatal cocaine exposure upon postnatal development of neostriatal dopaminergic function
Authors: Leslie Catherine A. , Robertson Matthew W. , Jung Anthony B. , Liebermann Jennifer , Bennett James P. 
Published: December 2004

AbstractPregnant rats were injected twice daily with 20 mg/kg cocaine (or saline) from gestational day 10 to parturition. Brains from offspring were examined with quantitative receptor autoradiography [D1 receptor (D1R), D2 receptor (D2R) and dopamine transporter (DAT)] and quantitative in situ hybridization [D1R mRNA, D2R mRNA, preproenkephalin (PPE) mRNA] for markers of neostriatal dopaminergic function. Prenatal cocaine exposure did not alter postnatal development of striatal D1R sites, but D1R mRNA levels were reduced by a third at days 14 and 35. D2R sites were increased over control in lateral striatum by day 6, and remained elevated through postnatal day 35. Total D2R mRNA was increased over control in both medial and lateral striatum at 7 and 14 days but was equal to control at 35 days. Prenatal cocaine exposure increased DAT density at postnatal days 1 through 5, but reduced it at days 14 and 35; PPE mRNA expression was reduced at days 7, 14 and 35. Many of these results are similar to those found in experimental animals and humans following cocaine withdrawal. © 1994 Wiley‐Liss, Inc.
GABA‐Ergic interneurons of the striatum express the shaw‐like potassium channel KvS3.1
Authors: Lenz S. , Perney T. M. , Qin Y. , Robbins E. , Chesselet M.‐F. 
Published: December 2004

AbstractIn addition to numerous GABA‐ergic efferent neurons, the striatum contains a subpopulation of fast‐firing GABA‐ergic interneurons characterized by the presence of immunoreactivity for the calcium‐binding protein, parvalbumin. Doublelabel in situ hybridization with digoxigenin‐ and radiolabelled cRNA probes was performed on striatal: sections of adult rats to identify mRNAs expressed by striatal GABAergic interneurons. In the dorsolateral striatum, only parvalbumin mRNA‐positive neurons expressed the mRNA encoding the potassium channel Kv3.1, a member of the Shaw family of potassium channels with rapid activation and inactivation kinetics, usually found in fast‐firing neurons such as the basket cells of the hippocampus. Colocalization of the parvalbumin and Kv3.1 proteins was confirmed by double‐label immunohistochemistry. Parvalbumin mRNA‐positive neurons expressed very high levels of the mRNA encoding glutamic acid decarboxylase (Mr 67,000: GAD67) in the dorsolateral striatum. A smaller proportion of double‐labelled neurons was found in the ventrolateral striatum. A small number of densely labelled neurons for GAD67 mRNA also expressed the mRNA encoding the dopamine D2 receptor, but none expressed detectable levels of the dopamine D1 receptor mRNA. This indicates major differences in the expression of dopamine receptor mRNA in a majority of GABA‐ergic interneurons vs. GABA‐ergic efferent neurons of the striatum. The results suggest that distinct molecular characteristics are associated with the distinct electrophysiological properties of striatal GABA‐ergic neurons. © 1994 Wi1ey‐Liss; Inc.
Modulation of dorsal thalamic cell activity by the ventral pallidum: Its role in the regulation of thalamocortical activity by the basal ganglia
Authors: Lavín Antonieta , Grace Anthony A. 
Published: December 2004

AbstractThe actions mediated by limbic system output projections of the basal ganglia were investigated by studying the effects of ventral pallidum (VP) stimulation on the activity of neurons in thalamic target nuclei, including several of the dorsal thalamic nuclei and the nucleus reticularis, using in vivo intracellular recordings in rats. Intracellular injection of Lucifer yellow was used in a subset of experiments to identify the neurons recorded and to confirm their location with respect to the specific thalamic nuclei targeted. Stimulation of the VP evoked ipsps in 79% of the mediodorsal cells recorded. In the reticular nucleus, 73% of the neurons tested responded with evoked ipsps. In contrast, in other dorsal thalamic nuclei VP stimulation evoked depolarizations in 58% of the cells recorded. The latency to onset of the ipsps in the mediodorsal nucleus and in the reticular nucleus were not substantially different (1.7 ± 1.1 msec vs. 2.7 ± 1.1 msec), whereas the depolarizing response evoked in dorsal thalamic nucleus neurons typically occurred at longer and more variable latencies (3.5 ± 2.7 msec).