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At least 577 records · Page 32Linked to original sources
PubMed1983

Propriospinal control of interneurons in spinal reflex pathways from tendon organs in the cat.

After chronic hemisection at C3, stimulation of propriospinal fibers in the dorsal quadrant at Th 10 facilitated disynaptic PSPs from Ib afferents in hindlimb motoneurons. Recording from interneurons monosynaptically activated from group I muscle afferents, and of extracellular focal synaptic potentials around them, revealed monosynaptic EPSPs from long propriospinal neurons. It is suggested that propriospinal neurons originating in the forelimb segments have direct excitatory connexions with inter-neurons of Ib reflex pathways to hindlimb motoneurons.

Animals↗
PubMed1985

Arecoline-induced elevations of regional cerebral metabolism in the conscious rat.

Local cerebral glucose utilization (LCGU) was measured, using the quantitative [14C]2-deoxy-D-glucose ([14C]DG) method, at 3 min after administration to 3-month-old, awake Fischer rats of the muscarinic agonist arecoline (AREC) 0.05, 0.5, 5, 15 or 50 mg/kg or saline i.p. Animals were pretreated with methylatropine (a cholinergic antagonist which does not enter the brain and has no effect on cerebral metabolism) 4 mg/kg s.c. to prevent parasympathomimetic side-effects of AREC. Tremor produced by AREC was rated subjectively. Intensity of tremor was dose-related, peaked at 2-5 min after AREC, and abated within 30 min. Elevations in LCGU (measured after [14C]DG injection during peak behavior) in extrapyramidal regions, which mediate tremor, were related to the intensity of tremor. The lowest dose of AREC selectively increased LCGU in the hippocampus and median raphe; higher doses produced more generalized metabolic enhancement. In the hippocampus and cortex, LCGU rose in layers in which cholinoceptive cells are located. Regions of the auditory pathway and superficial neocortical layers (I-III) were generally unaffected by AREC, but LCGU did not decrease in any region. The selective increase in LCGU produced by low doses of AREC in the hippocampus presumably is due to a specific action of AREC, and demonstrates the high sensitivity of this region to cholinomimetic stimulation.

Animals↗
PubMed1985

Regulation of intracellular pH in vertebrate central neurons.

The regulation of intracellular pH (pHi) was investigated in reticulospinal neurons of the lamprey using ion-selective microelectrodes. Steady-state pHi in 23 mM HCO-3-buffered Ringer was 7.44 +/- 0.03 with a membrane potential of 54 +/- 4 mV (mean +/- S.E.M., n = 6). In nominally HCO-3-free solutions, pHi recovery from acid loading was blocked by 10(-3)M amiloride. Recovery was stimulated by transition to HCO-3-containing solutions. Results suggest that pHi regulation in lamprey reticulospinal neurons is mediated by a Na+-H+ exchanger. The presence of a distinct, HCO-3-dependent pHi regulatory mechanism is postulated.

Amiloride↗
PubMed1985

Activity changes in nucleus reticularis gigantocellularis in relation to skilled forelimb movement in rats.

Adult hooded rats were trained to reach for food pellets into a narrow plexiglass tube and the movement of the preferred forelimb was photo-electrically detected. Multiple unit activity (MUA) or single unit activity in n. reticularis gigantocellularis (NGC) was recorded during reaching. Depression of MUA was observed about the onset of the forepaw movement and lasted during its execution. There was a correlation between MUA changes and the depression of activity of individual neurons observed in a part of NGC.

Action Potentials↗
PubMed1987

Long descending direct projection from the basal ganglia to the spinal cord: a revival of the extrapyramidal concept.

Our retrograde fluorescent labeling study shows that a distinct cell group of the subthalamic nucleus, posited in the basal ganglia, directly sends long descending axons contralaterally to the upper cervical segments (C1-C5) of the spinal cord in the rat. A large population (60-70%) of these subthalamic cells projecting to contralateral spinal levels give off axonal branches innervating the ipsilateral globus pallidus. Now, the classical concept of the 'extrapyramidal' motor system needs to be reconsidered. Furthermore, our results may provide a morphological substrate for the onset of a violent form of dyskinesia, 'hemiballism', which occurs in the contralateral limbs both clinically and experimentally following discrete lesions in the subthalamic nucleus or its fiber connections with the globus pallidus.

Animals↗
PubMed1990

3-Acetylpyridine results in degeneration of the extrapyramidal and cerebellar motor systems: loss of the dorsolateral striatal dopamine innervation.

3-Acetylpyridine (3-AP) administration to rats results in degeneration of the dopamine (DA) innervation of the striatum as well as degeneration of the olivocerebellar system. We now report that administration of this pyridine neurotoxin results in a decrease in striatal DA concentration which is restricted to the dorsolateral aspects of the caudatoputamen. 3-AP treatment did not alter DA levels in the ventromedial striatum, the nucleus accumbens, or the anteromedial prefrontal cortex. Both 3-AP and another pyridine neurotoxin, 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP), potently inhibited in vitro MAOB activity and in contrast weakly inhibited MAOA activity. However, in vitro inhibition of MAOB by the selective inhibitor deprenyl did not prevent or attenuate 3-AP-induced striatal DA depletion. These data indicate that 3-AP administration to rats not only results in degeneration of the olivocerebellar system, but also effects degeneration of the DA innervation of the dorsolateral striatum, the striatal sector thought to subserve motoric and sensorimotor function. 3-AP-induced nigrostriatal degeneration differs from that elicited by MPTP in that the former is not prevented by deprenyl pretreatment. The 3-AP-induced degeneration of both extrapyramidal and cerebellar motor systems may offer insight into the mechanisms involved in degeneration of the two motor systems in certain strains of rodents (such as the Weaver mutant mouse), and suggests that the sequelae of administration of this pyridine may serve as a useful model for olivopontocerebellar atrophy-associated parkinsonism.

Animals↗
PubMed1991

N-Methyl-D-aspartate receptors mediate dopamine-induced changes in extrapyramidal and limbic dynorphin systems.

The N-methyl-D-aspartate (NMDA)-type glutamate receptor was shown to mediate dopamine-induced dynorphin A (Dyn) changes in extrapyramidal and limbic structures. MK801, a potent noncompetitive antagonist of the NMDA receptor, blocked increases in striatal and nigral Dyn content following single and multiple administrations of methamphetamine (METH). Significant attenuation of the METH-induced increases occurred with MK801 doses of 0.1 mg/kg/dose with complete blockade at 2.5 mg/kg/dose. Similar to METH, NMDA itself caused significant increases in striatal and nigral Dyn content. The NMDA-induced increase in striatal Dyn content was blocked by coadministration of an intermediate dose of MK801. The Dyn system associated with the nucleus accumbens responded in a similar manner in that MK801 totally blocked the METH-induced increases; moreover, NMDA elevated the Dyn content in this structure. The inability of MK801 to alter the quinpirole-induced decrease in striatal Dyn content suggests that the NMDA receptor is not involved in the D2 receptor regulation of striatal Dyn systems.

Animals↗
PubMed1992

Scopolamine attenuates haloperidol-induced c-fos expression in the striatum.

Haloperidol increases the expression of Fos, the protein product of the proto-oncogene c-fos, in some parts of the central nervous system. Haloperidol also produces catalepsy in rodents and extrapyramidal side effects in humans, both of which are reduced by muscarinic receptor antagonists. In order to gain insight into the neurochemical and neuroanatomical substrates of haloperidol-induced catalepsy we examined the effects of the muscarinic receptor antagonist scopolamine on haloperidol-induced Fos expression in the striatum, nucleus accumbens and lateral septal nucleus. At a dose that reduced the cataleptic effect of haloperidol, scopolamine decreased the neuroleptic-induced Fos expression in the striatum and lateral septal nucleus but not the nucleus accumbens. These results indicate that haloperidol may increase c-fos expression in medium spiny striatal neurons indirectly by enhancing striatal acetylcholine release. They are also consistent with the hypothesis that neuroleptic-induced increases in striatal c-fos expression are predictive of extrapyramidal side effects produced by these compounds.

Animals↗
PubMed1992

Antagonism of limbic and extrapyramidal actions of intracerebrally injected dopamine by ergolines with partial D2 agonist activity in the rat.

Bromocriptine and a series of experimental ergoline D2 partial agonists (SDZ-208-911, SDZ-212-327, SDZ-208-912) were evaluated for their interactions with exogenous dopamine (DA, at ED50 = 16 micrograms) stereotaxically injected unilaterally into a limbic (superior-medial nucleus accumbens septi) or extrapyramidal (central corpus striatum) target site in rat brain. Behavioral measures to quantify responses were locomotor arousal induced by DA in accumbens and contralateral head turning with striatum. All agents, given systemically (i.p.), induced dose-dependent inhibition of behavioral responses to DA from both brain sites. In both accumbens and striatum, SDZ-212-327 was most potent and bromocriptine, least; however, bromocriptine was relatively much more potent in accumbens, and SDZ-208-912 somewhat more potent in striatum. These results add to the growing impression that agents with partial agonist actions at central DA receptors can show behaviorally inhibitory effects that may reflect paradoxical antidopaminergic actions against the full, natural agonist of DA receptors and that such effects can be regionally selective.

Animals↗
PubMed1993

Acrylamide-induced depletion of microtubule-associated proteins (MAP1 and MAP2) in the rat extrapyramidal system.

Acrylamide, an occupational neurotoxicant, reduced MAP1 and MAP2 distribution in different regions of rat brain. Different components of the extrapyramidal system (caudate-putamen, globus pallidus, substantia nigra and red nucleus) revealed differential distribution of MAP1 and MAP2 in acrylamide-treated animals. Rats were treated with acrylamide (estimated mean dose: 15 mg/kg/day) for 2 weeks and MAP1 and MAP2 were localized according to Sternberger's peroxidase-anti-peroxidase technique. MAP1 labelled neuronal perikarya and dendrites almost with a similar intensity, but MAP2 immunostaining was more intense in dendrites than neuronal perikarya. Acrylamide caused a near-total loss of MAP1 and MAP2 immunoreactivity in caudate-putamen. Other components of the extrapyramidal system were relatively less affected by acrylamide. These results indicate that caudate-putamen is more susceptible to the action of acrylamide than other components of the extrapyramidal system studied. The depletion of MAP1 and MAP2 immunoreactivity by acrylamide appears to be an early biochemical event preceding peripheral neuropathy. The loss of MAPs immunoreactivity occurs first in dendrites and proceeds toward the perikarya. This study indicates that acrylamide not only causes axonal damage but may also induce dendritic degeneration.

Acrylamide↗
PubMed1993

Assessing chronic brain damage by quantification of regional volumes in postischemic rat brains.

The present study provides data on fresh volumes of 39 anatomically defined brain regions after a 10 min transient forebrain ischemia in the rat. Ischemia was induced by occlusion of the carotid arteries and simultaneous hypotension. After a survival period of 3 months the rats were transcardially perfusion-fixed with Bodian's solution, and the brains processed for paraffin embedding and serially sectioned. The sections were Nissl-stained for delineation of the brain regions. The volume of a brain region was calculated from 8-10 equidistant sections, using the Cavalieri method and corrected for shrinkage of the brain. Fresh volumes were reduced by 27-50% in the layers of the hippocampal CA1 sector, by 40-46% in the substantia nigra, by 19% in the caudate nucleus, by 13% in the subiculum and the cingulate areas 1-3, by 12-14% in the retrosplenial and temporal areas. The results show that determination of fresh volumes is a sensitive method for quantification and localization of ischemic brain damage in the whole brain.

Animals↗
PubMed1995

Role of striatal dopamine D2 receptors in the paw test, an animal model for the therapeutic efficacy and extrapyramidal side effects of neuroleptic drugs.

The effect of administration of the D2 antagonist sulpiride in three striatal areas (dorsal striatum, DS; nucleus accumbens, ACC; olfactory tubercle; OT) was studied in the so-called paw test. In the paw test two parameters are measured (the hindlimb retraction time (HRT) and the forelimb retraction time (FRT)) that model the therapeutic efficacy and the extrapyramidal side effects of neuroleptics, respectively. Sulpiride significantly enhanced the HRT in each of the three structures. Identical doses of sulpiride administered in the three structures produced similar effects. The FRT was enhanced after administration of sulpiride in the DS and in the ACC. The minimal effective dose was lower for the DS. Administration of sulpiride in the OT did not affect the FRT. The effects on the FRT were very slow in onset (strong effects 4 h or more following administration of sulpiride), especially in comparison to the rapid effect on FRT following systemic administration of classical neuroleptics. To analyze this slowness of effect, two additional experiments were performed: first, the inter-trial time was changed so that it was identical to that used in systemic studies; second, sulpiride was administered simultaneously in the DS and the ACC. Neither experiment produced an earlier effect on the FRT. The present data provide additional evidence for the theory that regional selectivity of drugs determines their propensity to induce extrapyramidal side effects. However, the data also suggest that the generally held view that the dorsal striatum is solely responsible for the extrapyramidal side effects of neuroleptic drugs is too simple.

Animals↗
PubMed1994

Actions of (+/-)-7-hydroxy-N,N-dipropylaminotetralin (7-OH-DPAT) on dopamine synthesis in limbic and extrapyramidal regions of rat brain.

The proposed D3-selective ligand (+/-)-7-hydroxy-N,N-dipropylaminotetralin (7-OH-DPAT) inhibited tyrosine hydroxylase in vitro (IC50 = 0.6-0.7 microM) and dihydroxyphenylalanine (DOPA) accumulation in vivo (ID50 = 4.8-6.4 mg/kg) in two autoreceptor models in extrapyramidal and limbic tissue in rat forebrain, without consistent regional selectivity. Some limbic selectivity (ID50 = 10 vs. 29 mg/kg) was found in an in vivo model permitting expression of postsynaptic D3 and D2 receptor activity. The effects were partially blocked by S(-)-eticlopride alone, and fully after reserpine pretreatment. The results suggest that 7-OH-DPAT activates D3 or D2 autoreceptors, alters dopamine storage or release, and may interact with some limbic selectivity at postsynaptic D3 and D2 receptors as a partial agonist.

Animals↗
PubMed1994

Distribution of effects of the kappa-opioid agonist CI-977 on cerebral glucose utilization in rat brain.

The effects of the kappa-opioid agonist CI-977 upon local cerebral glucose utilization have been examined in conscious, lightly restrained rats to gain insight into the potential adverse effects of this neuroprotective agent. Cerebral glucose utilization was assessed quantitatively in 45 anatomically discrete brain regions by means of [14C]2-deoxyglucose autoradiography. The i.v. administration of CI-977 (0.03-3 mg/kg) induced relatively homogeneous patterns of altered cerebral glucose utilization with moderate statistically significant reductions (approximately 25%) being observed in 29 brain regions, and a statistically significant increase (approximately 40%) in one brain region, the lateral habenular nucleus. Glucose use throughout the entire neocortex and inferior colliculus was particularly sensitive to reduction (approximately 35%) following CI-977 administration, although there was only a limited dose dependency to the response. Minimal alterations in glucose use were observed in 15 of the 45 brain regions, particularly in the lower brain stem (e.g. superior olives, cochlear nucleus and median raphe) and forebrain limbic regions (e.g. septal nucleus, nucleus accumbens and mediodorsal thalamus). These data demonstrate that CI-977 produces widespread, anatomically organized alterations in function-related glucose use which contrast those seen previously with the NMDA receptor antagonists, thereby suggesting that CI-977 may be intrinsically safer as an in vivo neuroprotective agent.

Animals↗
PubMed1996

Comparison of the patterns of altered cerebral glucose utilisation produced by competitive and non-competitive NMDA receptor antagonists.

Recent studies indicate that competitive and non-competitive NMDA receptor antagonists can be readily distinguished by their effects on local cerebral glucose utilisation (1CGU). In the present study we compare the effects of the novel NMDA antagonist, (+)-1-methyl-1phenyl-1,2,3,4-tetrahydroisoquinoline (FR115427) on 1CGU, comparing its metabolic profile with that of the non-competitive NMDA receptor antagonist, dizocilpine (MK801) and of the competitive NMDA receptor antagonist CGS19755, using the 2-deoxyglucose metabolic mapping approach. Local cerebral glucose utilisation was measured in 80 anatomically discrete regions of the conscious rat brain using [14C]2-deoxyglucose quantitative autoradiography. Studies were initiated 10 min after the administration of FR115427 (0.1-3 mg/kg i.v.; n = 20), dizocilpine (0.03-0.3 mg/kg; n = 15), CGS19755 (1-30 mg/kg; n = 15) or saline (2 ml/kg; n = 5). Dizocilpine produced characteristic alterations in 1CGU with widespread increases in 1CGU in primary olfactory and limbic areas while reducing 1CGU in somatosensory and motor cortex. FR115427 produced a pattern of altered 1CGU which was broadly similar to that elicited by dizocilpine with increases in 1CGU in the pontine nuclei, presubiculum and hippocampus and reductions in somatosensory and motor cortex and within components of the auditory system. However, FR115427 was approximately 30-fold less potent than dizocilpine in this regard. In limbic structures, the effects of FR115427 were less pronounced than those produced by dizocilpine. Increases in 1CGU of 62-98% were found in retrosplenial, piriform and entorhinal cortex of dizocilpine-treated rats whereas these areas appeared relatively unaffected following FR115427 administration. A comparison of the pattern of metabolic response produced by each of these agents was performed by constructing a hierarchy of regional responsiveness using the f statistic: while focal differences in the metabolic profiles of dizocilpine and FR115427 were evident, a plot of the regional f values for dizocilpine and FR115427 revealed a strong overall relationship between the metabolic responses with a Pearson's product moment correlation of 0.78. In contrast, the correlation between the patterns produced by CGS19755 and that for dizocilpine or FR115427 was poor (r = 0.28 and 0.5 respectively).

Animals↗