bluuebunny/crossref_metadata_2025_split huggingface dataset:
Microinfusion of the Metabotropic Glutamate Receptor Agonist 1S, 3R–1‐Aminocyclopentane‐1, 3‐dicarboxylic Acid Into the Nucleus Accumbens Induces Dopamine‐dependent Locomotor Activation in the Rat
Authors: Attarian Shahram , Amalric Marianne 
Published: April 2006

AbstractAlthough the striatum has one of the highest densities of metabotropic glutamate receptor (mGluR) binding sites in the brain, little is known about their physiological role. In this study we characterized the contribution of mGluRs located in the ventral part of the striatum (the nucleus accumbens) to the control of extrapyramidal motor function. Activation of mGluRs by local infusion of the selective agonist 1S, 3R–1‐aminocyclopentane‐1, 3‐dicarboxylic acid (1 S, 3R‐ACPD; 25, 50 and 100 nmol/0.5 μl) into the nucleus accumbens induced a dose‐dependent increase in locomotor activity in rats. Intra‐accumbens infusion of a selective antagonist of mGluRs, a‐methyl‐4‐carboxyphenylglycine (MCPG) did not modify spontaneous locomotion but decreased the locomotor response to 1S, 3R‐ACPD. This effect appeared to be mediated by dopamine, since blockade of dopamine receptors with haloperidol (0.05 and 0.1 mg/kg i.p.) dose‐dependently reduced 1 S3R‐ACPD‐induced locomotor activation. Furthermore, D‐amphetamine (0.5 mg/kg, i.p.) combined with intra‐accumbens infusion of 1S, 3R‐ACPD (100 nmol) potentiated the locomotor hyperactivity response to a higher level than that seen with a single treatment with either drug. In contrast, D‐amphetamine‐induced hypermotility was abolished by infusion of MCPG (100 nmol) into the nucleus accumbens. These results demonstrate that glutamate may control extrapyramidal motor function through metabotropic receptors. Furthermore, activation of metabotropic glutamate receptors appears to act in synergy with the dopamine system at the level of the nucleus accumbens to produce a motor stimulant response.
Development of G Protein‐mediated Ca2+ Channel Regulation in Mouse Embryonic Stem Cell‐derived Neurons
Authors: Strübing Carsten , Rohwedel Jürgen , Ahnert‐Hilger Gudrun , Wiedenmann Bertram , Hescheler Jürgen , Wobus Anna M. 
Published: April 2006

AbstractBesides other mechanisms, the influx of Ca2+ into embryonic neurons controls growth and differentiation processes. To study the expression and regulation of voltage‐gated Ca2+ channels during early neurogenesis, we measured whole‐cell Ca2+ currents (Ica) in neurons developing from pluripotent embryonic stem cells. Various receptor agonists, including somatostatin and baclofen, reversibly inhibited ICa in embryonic stem cell‐derived neurons. The effects of somatostatin and baclofen were abolished by pretreatment of cells with pertussis toxin and mimicked by intracellular infusion of guanosine 5′‐O‐(3‐thiotriphosphate), suggesting the involvement of pertussis toxin‐sensitive G proteins in Ica inhibition. Investigations at different stages of neuronal differentiation showed that somatostatin efficiently suppressed L‐ and N‐type Ca2+ channels in immature as well as mature neurons. In contrast, inhibition of L‐ and N‐type channels by baclofen was rarely observed at the early stage. In terminally differentiated neurons, responses to baclofen were as prominent as those to somatostatin but were confined to N‐type Ca2+ channels. The stage‐dependent sensitivity of voltage‐gated Ca2+ channels to somatostatin and baclofen was not due to differential expression of Gαo isoforms, as revealed by reverse transcription‐polymerase chain reaction and immunofluorescence microscopy. These findings demonstrate that specific neurotransmitters such as somatostatin regulate voltage‐gated Ca2+ channels via G proteins during the early stages of neurogenesis, thus providing a mechanism for the epigenetic control of neuronal differentiation.
Stimulation of the Ventral Subiculum of the Hippocampus Evokes Glutamate Receptor‐mediated Changes in Dopamine Efflux in the Rat Nucleus Accumbens
Authors: Blaha Charles D. , Yang Charles R. , Floresco Stan B. , Barr Alasdair M. , Phillips Anthony G. 
Published: April 2006

AbstractThe effects of electrical stimulation of the ventral subiculum/CA1 region of the hippocampus on changes in dopamine oxidation current (corresponding to dopamine efflux) in the nucleus accumbens were examined using in vivo chronoamperometry with stearate‐graphite paste electrodes in urethane‐anaesthetized rats. Burst‐patterned monophasic pulses (10–100 Hz/burst delivered at 0.84 Hz) evoked a three‐component change in dopamine efflux in the nucleus accumbens with an initial transient increase in the dopamine signal above baseline, followed by an immediate decrease below baseline, and thereafter by a prolonged increase in the dopamine signal above baseline. 6–Hydroxydopamine lesions of the mesoaccumbens dopamine pathway or transection of the fimbria‐fornix blocked all of the evoked changes in the dopamine signal. Both the first and third components of enhanced dopamine efflux were blocked by microinfusion into the nucleus accumbens of the ionotropic glutamate receptor antagonists (±)‐2‐amino‐5‐phosphonopentanoic acid, 6,7‐dinitroquinoxaline‐2,3‐dione and kynurenate. Burst stimulation‐evoked decreases in the dopamine signal were abolished following microinfusions into the nucleus accumbens of the metabotropic glutamate receptor antagonist (+)‐α‐methyl‐4‐carboxyphenylglycine. These results suggest that ventral subiculum/CA1 glutamatergic inputs to the nucleus accumbens may presynaptically modulate dopamine efflux by synaptic activation of both ionotropic and metabotropic glutamate receptors in the nucleus accumbens. These glutamate‐dopamine interactions may constitute part of the mechanisms by which hippocampal signals are integrated through selective modulation of dopamine release in the nucleus accumbens in both physiological and pathological conditions.
Contribution of Area 17 to Cell Responses in the Striate‐recipient Zone of the Cat's Lateral Posterior‐Pulvinar Complex
Authors: Casanova C. , Savard T. , Darveau S. 
Published: April 2006

AbstractThe cat's lateral posterior‐pulvinar complex (LP‐pulvinar) contains three main representations of the visual field. The lateral part of the LP nucleus (LPI or striate‐recipient zone) is the only region of these extrageniculate nuclei which receives afferents from the primary visual cortex. We investigated the contribution of area 17 to the response properties (orientation and spatial frequency tuning functions) of LPI neurons by cooling or lesioning the visual cortex. Responses of 40 LPI cells were studied before, during and after the reversible cooling of the striate cortex. When tested for orientation, a total of 10 units out of 28 was affected (36%). For most of these cells (eight of lo), cooling the visual cortex yielded a reduction of the cells’ visual responses without altering their orientation‐selectivity (there was no significant change in the orientation tuning width). For only two cells, inactivation led to an increase in the response amplitude. Also, blocking the visual cortex never modified the direction‐selectivity of LPI cells. When tested for spatial frequency, 12 neurons out of 33 were affected (36%) by the experimental protocol. In most cases, we observed a reduction in the responses at each spatial frequency tested, with no change in tuning bandwidth. For only three LPI cells, the effects of inactivation of the visual cortex were restricted to specific spatial frequencies, altering the profile of the spatial frequency tuning function. In five cats, removing area 17 reduced the proportion of visual neurons in LPI and the spared visually evoked responses were noticeably depressed. Despite the reduction in responsiveness, a few LPI receptive fields within the cortical scotoma were still sensitive to the orientation and/or direction of a moving stimulus. This last observation suggests that some properties in LPI could be generated either by circuits intrinsic to the LPI or by afferents from extrastriate cortical areas. Overall, these results indicate that projections from the visual cortex to the striate‐recipient zone of the LP‐pulvinar complex are mainly excitatory. Despite the strong impact of the area 17 projections, our data suggest that the extrastriate cortex could also play a role in the establishment of response properties in the cat's LPI.
Tachykinin Actions on Deep Dorsal Horn Neurons In Wm: An Electrophysiological and Morphological Study in the Immature Rat
Authors: King A. E. , Slack J. R. , Lopez‐Garcia J. A. , Ackley M. A. 
Published: April 2006

AbstractTo assess whether functional neurokinin receptors exist in the deep dorsal horn of the rat, the actions of the selective neurokinin‐1 receptor (NK1R) agonist [Sar9,Met(O2)11]substance P [Sar9,Met(O2)11]]SP), the neurokinin‐2 receptor (NK2R) agonists [β‐Ala8]NKA4‐10 and GR64349 and the neurokinin‐3 receptor (NK3R) agonist senktide were examined intracellularly in vitro. [Sar9,Met(O2)11]]SP (1–4 μM) and senktide (1‐2 μM) elicited slow depolarizations (40 mV) associated with increased synaptic activity and cell firing. [β‐Ala8]NKA4‐10 (10‐20 μM) and GR64349 (0.25‐10 μM) caused small depolarizations (<2.0 mV) and no firing. Neurons were categorized as either ‘tonic’ or ‘phasic’ depending on their firing response to direct current step depolarizations. Tonic neurons, which, unlike phasic neurons, display no spike firing accommodation, generated a significantly larger depolarization to the NK1R and NK3R agonists. The putative contribution of these receptors to primary afferent‐mediated synaptic transmission was assessed by testing the NKIR antagonist GR82334 (1 μM), the NK2R antagonist MEN10,376 (1 μM) and the NK3R antagonist [Trp7,β‐Ala8]NKA4‐10 (1 μM) against the dorsal root‐evoked excitatory postsynaptic potential (DR‐EPSP). GR82334 and [Trp7,β‐Ala8]NKA4‐10 significantly reduced (P ≤ 0.05) the duration but not the amplitude of the DR‐EPSP. MEN10,376 (1 μM) had no effect on DR‐EPSP amplitude or duration. Morphological detail was obtained for seven biocytin‐filled deep dorsal horn neurons tested with [Sar9,Met(O2)11]SP. Five neurons responded to the NKIR agonist, and two of these had dorsally directed dendrites into the substantia gelatinosa. The other three [Sar9,Met(O2)11]SP‐sensitive neurons had dendrites within deeper laminae. These data support the existence of functional NK1Rs and NK3Rs in the deep dorsal horn which may be involved in mediating sensory afferent inputs from nociceptors.
Synaptic Plasticity in Dissociated Hippocampal Cultures: Pre‐ and Postsynaptic Contributions
Authors: Vogt Kaspar , Streit Jürg , Dityatev Alexander , Lüscher Hans‐Rudolf 
Published: April 2006

AbstractThe distinction between pre‐ or postsynaptic expression of synaptic plasticity is difficult to make, unless the postsynaptic receptors can be investigated in isolation. We have studied single synaptic contacts in dissociated cultures of rat hippocampus. The reaction of postsynaptic receptor assemblies to the induction of synaptic plasticity was measured and compared with changes in the rate of spontaneous miniature excitatory postsynaptic currents (mEPSCs), which can reflect changes in the transmitter release mechanism. The response of a receptor assembly to locally applied exogenous glutamate was measured before and after synchronized application of glutamate and a train of postsynaptic depolarizations (‘pairing’). Pairing induced a variety of changes: (i) the majority of the receptor assemblies showed no change in their response to glutamate before and after pairing; (ii) the postsynaptic current due to exogenous glutamate showed a rapid increase in five out of 26 cases. This was not due to changes in the single channel conductance; (iii) the rate of mEPSCs increased, if it had previously been below 25 Hz; (iv) the rate of mEPSCs decreased, if it had previously been above 25 Hz. Effects 2 and 3 were blocked by antagonists of NMDA receptors. These findings provide direct evidence for an increase of the number of glutamate receptors at a subset of the investigated postsynaptic sites during synaptic potentiation.
Nerve Growth Factor Treatment Increases Stimulus‐evoked Release of Sensory Neuropeptides in the Rat Spinal Cord
Authors: Malcangio Marzia , Garrett Neil E. , Tomlinson David R. 
Published: April 2006

AbstractIn the adult rat, nerve growth factor (NGF) upregulates the nociceptive peptide substance P (SP) and calcitonin gene‐related peptide (CGRP) in neuronal cell bodies of C fibres but the effects of NGF on release of these neuropeptides from the central afferent terminals have not been reported. Thus, this study compared rats treated with six doses of NGF over 2 weeks with controls and measured the release of the neuropeptides, SP and CGRP from the dorsum of the lumbar spinal cord in vitro. NGF (1.0 mg/kg s.c.) greatly increased basal and stimulus‐evoked SP and CGRP release; at 0.1 mg/kg, NGF did not affect SP release but significantly increased CGRP basal outflow and evoked release. In a different set of experiments, topical application of NGF (100 ng/ml) to cords from naive rats did not increase stimulus‐evoked release of SP or CGRP. These findings show marked stimulation by NGF treatment in vivo of release of sensory neuropeptides during stimulation of dorsal roots, albeit at relatively large doses of the neurotrophin.
Responses of Cortical EEG‐related Basal Forebrain Neurons to Brainstem and Sensory Stimulation in Urethane‐anaesthetized Rats
Authors: Détári László , Semba Kazue , Rasmusson Douglas D. 
Published: April 2006

AbstractThe basal forebrain can be considered to be a rostral extension of the ascending reticular activating system. A large number of neurons in the basal forebrain have been shown to display higher firing rates when low‐voltage fast activity is present in the cortical EEG as opposed to states characterized by large slow waves in both unanaesthetized and anaesthetized animals. However, a smaller number of cells with increased discharge rate during slow waves was also observed in most of these studies. While it is likely that these two types of neurons have opposite roles in the regulation of cortical activation, it is not known how they respond to inputs from the brainstem or the periphery. In the present study, extracellular recordings were made in the basal forebrain of urethane‐anaesthetized rats. A total of 52 neurons were studied in which the firing rate was significantly higher during fast cortical EEG waves (F‐cells), and 14 neurons in which activity was significantly greater during slow waves (S‐cells). The two cell types responded differently to stimulation of the pedunculopontine tegmental nucleus (PPT) and dorsal raphe nucleus (DRN) with short (0.5–1 s) trains of pulses and to noxious sensory stimuli (tail pinch). These stimulations excited most F‐cells (80–96%) and inhibited the majority of S‐cells (55–67%). In the few F‐cells that were inhibited by stimulation, the response varied with the background firing rate of the cell: the higher the firing rate at the time of stimulation, the higher the probability of observing an inhibitory response. In contrast, single electrical pulses delivered to the PPT and DRN excited the majority (72%) of both F‐ and S‐cells. Previous in vitro studies have shown that the application of acetylcholine or serotonin has predominantly inhibitory effects on basal forebrain cholinergic neurons. The predominantly excitatory effect of noxious, PPT and DRN stimulation on F‐cells therefore suggests that glutamatergic or other excitatory afferents play a more dominant role in regulating basal forebrain neurons. We have previously shown that F‐cells are more prevalent than S‐cells. In combination, these findings suggest that basal forebrain neurons, and F‐cells in particular, are important in mediating the ascending excitatory drive from the brainstem to the cerebral cortex.
GX/Z Is Regulated by μ But Not δ Opioid Receptors in the Stimulation of the Low Km GTPase Activity in Mouse Periaqueductal Grey Matter
Authors: Garzón Javier , Martinez‐Peña Yolanda , Sánchez‐Blázquez Pilar 
Published: April 2006

AbstractHigh affinity low Km GTPase activity was measured in membrane preparations of adult mouse mesencephalic periaqueductal grey matter (PAG). Opioids displaying selectivity towards μ‐ or δ‐opioid receptors (OR) activated the enzyme in a concentration‐dependent manner. Antibodies to μ‐OR greatly impaired the potential of μ‐agonists, [D‐Ala2,N‐MePhe4,Gly‐ol5]‐enkephalin (DAMGO) and morphine, to increase hydrolysis of GTP. The same antibodies had little effect on [D‐Pen2,5]enkephalin (DPDPE) and [D‐Ala2]deltorphin II, both agonists at δ‐OR. Stimulation of GTPase by DPDPE and [D‐Ala2]deltorphin II ‐ but not by morphine or DAMGO ‐ was diminished by antibodies to δ‐OR. The blockade of Gi2α subunits by specific antibodies impaired the activation of Gα‐related GTPase by all opioids. Antibodies in vitro, and oligodeoxynucleotides in vivo, prepared against Gx/zα subunits, reduced the release of Pi promoted by DAMGO and morphine. The impairment of Gx/z proteins also slightly reduced the effect of the δ2 agonist [D‐Ala2]deltorphin II. At δ1 receptors, DPDPE fully expressed its activation of GTPase. These results indicate that in the PAG, μ‐OR and δ‐OR couple with Gi2 transducer proteins. Notably, μ‐OR also regulates the pertussis toxin‐insensitive G‐protein Gx/z, an effect poorly exhibited by δ‐OR in this tissue.
The Whole Nucleotide Sequence and Chromosomal Localization of the Gene for Human Metabotropic Glutamate Receptor Subtype 6
Authors: Hashimoto Takao , Inazawa Johji , Okamoto Naoyuki , Tagawa Yoshiaki , Bessho Asumasa , Honda Yoshihito , Nakanishi Shigetada 
Published: April 2006

AbstractMetabotropic glutamate receptor subtype 6 (mGluR6) is restrictedly expressed in the retinal ON bipolar cells and ablation of mouse mGluR6 by gene targeting results in a loss of ON responses to light stimulus and impairs the detection of visual contrasts. We have isolated genomic clones containing the human mGluR6 gene and determined the whole nucleotide sequence of the mGluR6 gene. The transcription initiation site of the human mGluR6 gene has been identified using primer extension analysis in combination with reverse transcriptase‐mediated polymerase chain reaction analysis of human retinal RNA, while the termination of the mGluR6 mRNA has been assigned by the analysis of rapid amplification of 3′‐cDNA ends. The human mGluR6 gene consists of 16 742 base pairs with 10 exons separated by nine introns. The human mGluR6 is composed of 877 amino acid residues with a signal peptide of 24 amino acid residues and the mature protein shows a 94.6% homology with the rat counterpart. A CpG‐rich island is present at exon 1 and its preceding putative promoter region and this unusual sequence, like several tissue‐specific genes, may be important for a specific expression of the mGluR6 gene in the retinal bipolar cells. The human mGluR6 gene has been mapped to chromosome 5q35 by the analyses of blot hybridization of a DNA panel of human/mouse/hamster somatic cell hybrids and fluorescence in situ hybridization of human chromosomes. This study should provide the genetic basis for not only better understanding the molecular mechanism underlying a tissue‐specific expression of the mGluR6 gene but also exploring a potential defect in human mGluR6 in a certain inherited eye disease.
Figure‐Ground Segregation at Contours: a Neural Mechanism in the Visual Cortex of the Alert Monkey
Authors: Baumann R. , van der Zwan R. , Peterhans E. 
Published: April 2006

AbstractAn important task of vision is the segregation of figure and ground in situations of spatial occlusion. Psychophysical evidence suggests that the depth order at contours is defined early in visual processing. We have analysed this process in the visual cortex of the alert monkey. The animals were trained on a visual fixation task which reinforced foveal viewing. During periods of active visual fixation, we recorded the responses of single neurons in striate and prestriate cortex (areas V1, V2, and V3/V3A). The stimuli mimicked situations of spatial occlusion, usually a uniform light (or dark) rectangle overlaying a grating texture of opposite contrast. The direction of figure and ground at the borders of these rectangles was defined by the direction of the terminating grating lines (occlusion cues). Neuronal responses were analysed with respect to figure‐ground direction and contrast polarity at such contours. Striate neurons often failed to respond to such stimuli, or were selective for contrast polarity; others were non‐selective. Some neurons preferred a certain combination of figure‐ground direction and contrast polarity. These neurons were rare both in striate and prestriate cortex. The majority of neurons signalled figure‐ground direction independent of contrast polarity. These neurons were only found in prestriate cortex. We explain these responses in terms of a model which also explains neuronal signals of illusory contours. These results suggest that occlusion cues are used at an early level of processing to segregate figure and ground at contours.
Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
Authors: Naumann T. , Straube A. , Frotscher M. 
Published: April 2006

AbstractPrevious studies have suggested that target‐derived nerve growth factor (NGF) is essential for the survival of cholinergic basal forebrain neurons. Thus, axotomy of septohippocampal neurons in adult rats resulting in the withdrawal of target‐derived NGF caused a dramatic loss of choline acetyltransferase (ChAT)‐immunoreactive neurons in the medial septum‐diagonal band complex. We have recently shown that this loss of immunolabelled neurons does not indicate cell death, since many septohippocampal cholinergic neurons recover their immunoreactivity for ChAT after a long survival time despite disconnection from target‐derived neurotrophins. One possibility would be that these surviving ChAT‐immunoreactive neurons have gained access to other, probably local, NGF sources. Here we provide evidence that the recovery of ChAT immunoreactivity after axotomy is not accompanied by a similar recovery of NGF receptor expression in these neurons. In situ hybridization for p75NTR mRNA and trkA mRNA 6 months after bilateral fimbria‐fornix transection revealed a substantial loss of labelled cells. In addition, there was a persisting loss of p75NTR‐immunoreactive and NGF‐immunoreactive medial septal neurons. Cholinergic neurons in controls did not express NGF mRNA, but were heavily immunostained for NGF protein due to receptor‐mediated uptake. These data suggest that at least some cholinergic septohippocampal neurons re‐express ChAT either independently of NGF or with a reduced need for NGF.