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J F Marshall - One of the best experts on this subject based on the ideXlab platform.
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reduced Eticlopride induced fos expression in caudate putamen and globus pallidus after unilateral frontal cortex injury relation to neglect
Neuroscience, 1997Co-Authors: J.m Vargo, J F MarshallAbstract:Unilateral ablation of medial agranular cortex in rats results in neglect of contralateral stimuli and reductions in amphetamine-induced expression of the immediate early gene, c-fos, in both caudate-putamen and globus pallidus. Both unilateral neglect and the reductions in dopamine agonist induction of subcortical Fos immunoreactivity dissipate over a matter of weeks. Dopamine agonism induces Fos predominantly in striatonigral cells and in globus pallidus via striatopallidal disinhibition, whereas Fos is induced in striatopallidal cells by administration of antagonists of the D2 dopamine receptor subfamily. To examine more directly effects of cortical injury on striatopallidal function, induction of striatal Fos by the D2 antagonist Eticlopride (0.1 mg/kg, s.c.) was examined in rats with medial agranular cortex ablation. In the same animals, Eticlopride-induced Fos in globus pallidus was also examined. Five days after unilateral cortex injury, in rats showing neglect, the numbers of Fos immunoreactive nuclei induced by Eticlopride were reduced by 50% in caudate-putamen and 25% in globus pallidus of the ipsilateral hemisphere. These lesion effects were restricted to dorsolateral caudate-putamen and dorsal pallidum. Three or more weeks after cortical injury, in rats recovered from neglect, Eticlopride-induced Fos was normalized in caudate-putamen, but still decreased by 20% in globus pallidus. Along with previous findings, these results suggest that behavioral recovery from neglect produced by cortical injury may be at least partially mediated by normalizations of function of both striatopallidal and striatonigral neurons. In addition, the present findings suggest that normalization of function of pallidal cells activated by Eticlopride is not necessary for behavioral recovery from frontal cortex ablation. Lingering reductions in excitatory cortico-subthalamo-pallidal input may be responsible for the longer-lasting dysfunctions of these pallidal cells.
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Reduced Eticlopride-induced fos expression in caudate–putamen and globus pallidus after unilateral frontal cortex injury: relation to neglect
Neuroscience, 1997Co-Authors: J.m Vargo, J F MarshallAbstract:Unilateral ablation of medial agranular cortex in rats results in neglect of contralateral stimuli and reductions in amphetamine-induced expression of the immediate early gene, c-fos, in both caudate-putamen and globus pallidus. Both unilateral neglect and the reductions in dopamine agonist induction of subcortical Fos immunoreactivity dissipate over a matter of weeks. Dopamine agonism induces Fos predominantly in striatonigral cells and in globus pallidus via striatopallidal disinhibition, whereas Fos is induced in striatopallidal cells by administration of antagonists of the D2 dopamine receptor subfamily. To examine more directly effects of cortical injury on striatopallidal function, induction of striatal Fos by the D2 antagonist Eticlopride (0.1 mg/kg, s.c.) was examined in rats with medial agranular cortex ablation. In the same animals, Eticlopride-induced Fos in globus pallidus was also examined. Five days after unilateral cortex injury, in rats showing neglect, the numbers of Fos immunoreactive nuclei induced by Eticlopride were reduced by 50% in caudate-putamen and 25% in globus pallidus of the ipsilateral hemisphere. These lesion effects were restricted to dorsolateral caudate-putamen and dorsal pallidum. Three or more weeks after cortical injury, in rats recovered from neglect, Eticlopride-induced Fos was normalized in caudate-putamen, but still decreased by 20% in globus pallidus. Along with previous findings, these results suggest that behavioral recovery from neglect produced by cortical injury may be at least partially mediated by normalizations of function of both striatopallidal and striatonigral neurons. In addition, the present findings suggest that normalization of function of pallidal cells activated by Eticlopride is not necessary for behavioral recovery from frontal cortex ablation. Lingering reductions in excitatory cortico-subthalamo-pallidal input may be responsible for the longer-lasting dysfunctions of these pallidal cells.
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Amphetamine- and cocaine-induced fos in the rat striatum depends on D2 dopamine receptor activation.
Synapse, 1994Co-Authors: David N. Ruskin, J F MarshallAbstract:Amphetamine or cocaine injection causes expression of the immediateearly gene c-fos in the striatum. Previous studies have shown that dopamine D1 receptor activation is necessary for this effect, but have not established a consistent role for D2 receptors. We have investigated the involvement of D2 receptors in indirect dopamine agonist-induced striatal Fos-like immunoreactivity using the selective D2 antagonist Eticlopride. Eticlopride treatment (0.5 mg/kg) caused Fos expression by itself, but also decreased Fos expression in the central striatum due to amphetamine (5.0 mg/kg) or cocaine (40 mg/kg) by 90% and 85%, respectively. In striatonigral neurons, identified by labeling with the retrograde tracer Fluorogold iontophoresed into the substantia nigra pars reticulata, the blockade of stimulant-induced Fos-like immunofluorescence by Eticlopride was nearly complete, with decreases of 98% for amphetamine and 94% for cocaine. In striatonigral neurons, the D2 antagonist alone had minimal effect. We conclude that activation of both D1 and D2 receptor classes by dopamine agonists is necessary for induction of Fos in the striatonigral cells of normal rats. These results provide an important parallel to behavioral and electrophysiological work that also demonstrates D1/D2 interdependence in the control of normal basal ganglia functions. © 1994 Wiley-Liss, Inc.
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Chronic Eticlopride and dopamine denervation induce equal nonadditive increases in striatal D2 receptor density: autoradiographic evidence against the dual mechanism hypothesis.
Neuroscience, 1991Co-Authors: G J Lahoste, J F MarshallAbstract:In an attempt to resolve experimental discrepancies regarding the mode of action of D2 receptor regulation following denervation or chronic receptor blockade, rats with extensive unilateral destruction of the mesotelencephalic dopaminergic projections induced by intracerebral 6-hydroxydopamine were injected daily for 21 days with either saline or the potent, selective D2 antagonist Eticlopride (0.5 mg/kg, i.p.). Four days after the last injection of Eticlopride or saline, rats were killed, and brain sections through the caudate-putamen and nucleus accumbens septi were incubated with [3H]spiroperidol or (R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5- phenyl-1H-3-benzazepin-7-ol ([3H]SCH 23390) to assay D2 and D1 receptors, respectively. Autoradiographic analysis revealed that chronic Eticlopride treatment increased the density of D2 sites in the intact hemisphere for all regions examined without further augmenting the already increased density of D2 receptors seen in the dopamine-denervated hemisphere. D2 receptor density was independent of functional sensitivity as evidenced by the fact that rats treated chronically with Eticlopride rotated contralateral to the 6-hydroxydopamine lesion following systemic administration of the selective D2 agonist quinpirole during the neuroleptic wash-out period, despite the fact that D2 receptor binding was not significantly different in the left and right hemispheres of these subjects. D1 receptor density was not affected by Eticlopride treatment but was significantly reduced reduced in the dopamine-denervated hemisphere. [3H]Mazindol labeling of high-affinity DA uptake sites indicated that the extent of dopamine denervation was greater than 97% in both saline- and Eticlopride-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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Chronic Eticlopride and dopamine denervation induce equal nonadditive increases in striatal D2 receptor density: autoradiographic evidence against the dual mechanism hypothesis.
Neuroscience, 1991Co-Authors: G J Lahoste, J F MarshallAbstract:Abstract In an attempt to resolve experimental discrepancies regarding the mode of action of D 2 receptor regulation following denervation or chronic receptor blockade, rats with extensive unilateral destruction of the mesotelencephalic dopaminergic projections induced by intracerebral 6-hydroxydopamine were injected daily for 21 days with either saline or the potent, selective D 2 antagonist Eticlopride (0.5 mg/kg, i.p.). Four days after the last injection of Eticlopride or saline, rats were killed, and brain sections through the caudate-putamen and nucleus accumbens septi were incubated with [ 3 H]spiroperidol or (R)-(+)-8-chloro-2, 3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol ([ 3 H]SCH 23390) to assay D 2 and D 1 receptors, respectively. Autoradiographic analysis revealed that chronic Eticlopride treatment increased the density of D 2 sites in the intact hemisphere for all regions examined without further augmenting the already increased density of D 2 receptors seen in the dopamine-denervated hemisphere. D 2 receptor density was independent of functional sensitivity as evidenced by the fact that rats treated chronically with Eticlopride rotated contralateral to the 6-hydroxydopamine lesion following systemic administration of the selective D 2 agonist quinpirole during the neuroleptic wash-out period, despite the fact that D 2 receptor binding was not significantly different in the left and right hemispheres of these subjects. D 1 receptor density was not affected by Eticlopride treatment but was significantly reduced in the dopamine-denervated hemisphere. [ 3 H]Mazindol labeling of high-affinity DA uptake sites indicated that the extent of dopamine denervation was greater than 97% in both saline- and Eticlopride-treated rats. These findings are consistent with the view that chronic D 2 receptor blockade and dopamine denervation increase D 2 receptor density via a single, common mechanism. Data from other laboratories, in which additive effects of denervation and chronic antagonist treatment have been reported, may have resulted from incomplete denervation. Experimental discrepancies may also be due to differing means by which the mesotelencephalic dopaminergic neurons are injured.
Michael T. Bardo - One of the best experts on this subject based on the ideXlab platform.
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Renewal of sucrose-seeking behavior in rats: Role of D2 dopamine receptors
Pharmacology Biochemistry and Behavior, 2010Co-Authors: Anthony S. Rauhut, Laura Fenton, Michael T. BardoAbstract:Abstract The present study characterized renewal of sucrose-seeking behavior in rats (Experiment 1). The role of the dopamine subtype-2 (D 2 ) receptors in mediating renewal of sucrose-seeking behavior also was examined (Experiment 2). Rats were trained to respond for sucrose pellets (45 mg each) on a fixed-ratio 25 (Experiments 1 and 2) schedule of reinforcement in Context A. Following acquisition, rats underwent extinction and 4 renewal tests in Contexts B and A, respectively. In Experiment 2, rats were pretreated with vehicle or the D 2 dopamine receptor antagonist Eticlopride (5, 10, 20, or 40 μg/kg) 30 min prior to the first renewal test session. A follow-up experiment (Experiment 3) examined the effect of a high Eticlopride dose (40 μg/kg) on locomotor activity. Renewal of sucrose-seeking behavior persisted for 3 sessions. Eticlopride dose-dependently blocked renewal of sucrose-seeking behavior without suppressing locomotor activity, implicating a role of D 2 dopamine receptors in mediating renewal of sucrose-seeking behavior.
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7-OH-DPAT has d-amphetamine-like discriminative stimulus properties.
Pharmacology Biochemistry and Behavior, 1997Co-Authors: Rick A. Bevins, Jennifer E. Klebaur, Michael T. BardoAbstract:Rats were trained on a d-amphetamine (1 mg/kg) vs. saline discrimination task using food-maintained responding (fixed ratio = 25). In extinction tests, drug-appropriate responding decreased as the dose of amphetamine was substituted for the training dose decreased. The dopamine D2/D3 receptor agonist (±)7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OH-DPAT) substituted fully for the amphetamine discriminative stimulus at the higher doses examined (0.1, 0.3, 1.0 mg/kg). This substitution was accompanied by a substantial decrease in overall response rates. Eticlopride, a dopamine D2/D3 receptor antagonist, partially blocked 7-OH-DPAT substitution. Thus, at the higher doses, 7-OH-DPAT shared sufficient discriminative stimulus properties with the amphetamine to prompt full substitution. Eticlopride antagonism suggests a role for the D2/D3 dopamine receptor in this substitution.
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Repeated quinpirole treatment: locomotor activity, dopamine synthesis, and effects of selective dopamine antagonists.
Synapse, 1995Co-Authors: James K. Rowlett, Bruce A. Mattingly, Michael T. BardoAbstract:Repeated treatment with the non-selective dopamine agonist apomorphine results in behavioral sensitization and enhanced dopamine synthesis in dopamine projection fields. To examine the role of D2-type dopamine receptors in modulating these effects, the present experiment assessed the effects of repeated treatment with the D2-type agonist quinpirole on locomotor activity and dopamine synthesis. In the first experiment, rats were treated with vehicle or one of two doses (0.3 or 3.0 mg/kg) of quinpirole for 8 days. Daily measures of locomotor activity revealed an initial suppression of activity produced by quinpirole which dissipated over the 8 days of treatment. A trend for an increase in activity for 3.0 mg/kg quinpirole compared to vehicle was obtained on day 8. Twenty-four hours after cessation of treatment, dopamine synthesis, measured as accumulation of 3,4-dihydroxyphenylalanine (DOPA) after treatment with the DOPA decarboxylase inhibitor NSD-1015, was enhanced in the striatum, but not nucleus accumbensolfactory tubercle (NAOT) or ventral mesencephalon (VM). In Experiment 2, rats were treated for 8 days with vehicle, 3.0 mg/kg quinpirole or the D1 antagonist SCH 23390 (0.5 mg/kg) in a two (vehicle or quinpirole) × two (vehicle or SCH 23390) design. Quinpirolealone treatment resulted in a reduction of the locomotor suppressant effects of the drug. SCH 23390-alone and quinpirole-SCH 23390 combined treatment resulted in decreased activity compared to the vehicle control group that did not change across days. DOPA accumulation was enhanced in the striatum and NAOT after quinpirole treatment; however, SCH 23390 had no effect. In Experiment 3, rats were treated for 10 days with vehicle, 3.0 mg/kg quinpirole or the D2 antagonist Eticlopride (1.0 mg/kg) in a two (vehicle or quinpirole) × two (vehicle or Eticlopride) design. As in the first two experiments, repeated quinpirolealone treatment resulted in a reduction of the locomotor suppressant effects of the drug; however, locomotor activity in this group was enhanced compared to vehicle controls on day 10. Eticlopridealone and Eticlopride-quinpirole treated rats had suppressed locomotor activity across the 10 days. DOPA accumulation was enhanced by both repeated quinpirole and repeated Eticlopride treatment in the striatum and NAOT. DOPA accumulation in Eticlopride-quinpirole treated rats was not different from vehicle control levels in the NAOT, while no significant difference was obtained between the Eticlopridealone and Eticlopride-quinpirole groups in the striatum. The locomotor activity data suggest that repeated quinpirole treatment results in tolerance to the locomotor suppressant effect of the drug. Evidence for sensitization was obtained in two out of three of the experiments. These results suggest that enhanced dopamine synthesis after repeated non-selective dopamine agonist treatment is modulated by D2-type dopamine receptors. © 1995 Wiley-Liss, Inc.
Marla K. Perna - One of the best experts on this subject based on the ideXlab platform.
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The effects of Eticlopride on Morris water task performance in male and female rats neonatally treated with quinpirole
Psychopharmacology, 2005Co-Authors: Russell W. Brown, Kimberly N. Thompson, Ivy A. Click, Razaria A. C. Best, Stephanie K. Thacker, Marla K. PernaAbstract:Rationale Previous studies have shown that neonatal quinpirole treatment which results in long-term dopamine D2 receptor supersensitization (D2 receptor priming) produces cognitive deficits in preweanling and adult rats behaviorally tested on the Morris water task (MWT). Objective This study was designed to analyze whether pretraining administration of the D2 antagonist Eticlopride alleviates cognitive deficits produced by neonatal quinpirole treatment. Methods Both male and female Sprague–Dawley rats were treated with quinpirole HCl (1 mg/kg) or saline from postnatal days 1 to 21. From P22 to P24, rats were tested on the place version of the MWT in which a hidden platform remains stationary throughout training. From P25 to P28, rats were tested on the match-to-place version of the MWT, and rats are given a pair of daily training trials to locate the hidden platform that was moved to a new location each day. Fifteen minutes before each training session, rats were intraperitoneally administered with Eticlopride (0.01 or 0.02 mg/kg) or saline. Results Pretraining Eticlopride treatment alleviated cognitive deficits produced by neonatal quinpirole treatment in both male and female rats on the place version of the MWT, as well as in males tested on the match-to-place version of the MWT. However, there were no significant deficits produced by neonatal quinpirole treatment in females tested on the match-to-place version of the MWT, and control males demonstrated superiority over control females on this version of the task. Conclusions Pretraining administration of the dopamine D2 antagonist Eticlopride alleviated cognitive deficits produced by neonatal quinpirole treatment. However, it appears that the dopamine D2 receptor may have a more important influence on cognitive performance in males than in females, which may be related to increased sensitivity of the D2 receptor in males.
Russell W. Brown - One of the best experts on this subject based on the ideXlab platform.
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The Role of Dopamine D1 and D2 Receptors in Adolescent Methylphenidate Conditioned Place Preference: Sex Differences and Brain-Derived Neurotrophic Factor
Developmental Neuroscience, 2014Co-Authors: Elizabeth D. Cummins, Stephen B. Griffin, Chase M. Duty, Daniel J. Peterson, Katherine C. Burgess, Russell W. BrownAbstract:This study analyzed the role of dopamine D1 and D2 receptors in methylphenidate (MPH) conditioned place preference (CPP) in adolescent male and female rats, in addition to the role of these receptors in the effects of MPH on brain-derived neurotrophic factor (BDNF) in the dorsal striatum and nucleus accumbens. Using a nonbiased CPP procedure, the animals were conditioned from postnatal day (PD) 33 to 37. On conditioning trials, animals were first administered saline or their respective antagonist (0.1 or 0.2 mg/kg SCH-23390; 0.01 or 0.03 mg/kg Eticlopride HCl), followed by MPH (5 mg/kg). Approximately 10 min after MPH administration, the rats were placed into the paired context for a 10-min trial. One day after conditioning on PD38, a preference test was administered with dividers removed. One day following the preference test on PD39, brain tissue was removed, and the nucleus accumbens and striatum were analyzed for BDNF. Results revealed that MPH conditioning resulted in an increased preference that was blocked by either dose of SCH-23390, but generally not affected by either dose of Eticlopride. Further, the higher dose of SCH-23390 resulted in a conditioned place aversion in males, presumably due to an increased number of dopamine D1 receptors in adolescent males. MPH produced a significant increase of striatal and accumbal BDNF alleviated by SCH-23390 or Eticlopride. These results show that MPH results in CPP in adolescent male and female rats and these effects appear to be mediated by the dopamine D1 receptor, but the effects of MPH on BDNF appear to be mediated by both dopamine receptor families.
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Sex differences in nicotine sensitization and conditioned hyperactivity in adolescent rats neonatally treated with quinpirole: role of D2 and D3 receptor subtypes.
Behavioral Neuroscience, 2009Co-Authors: Brianna Sheppard, Julia Lehmann, Zackary A. Cope, Russell W. BrownAbstract:Neonatal quinpirole treatment in rats produces increased sensitivity of dopamine D2-like receptors throughout the animal's lifetime, referred to as D2 priming. There is little information on the effects of nicotine in adolescent rats, especially in a model that has clinical relevance to psychosis where increased D2 receptor sensitivity is common. Male and female rats were treated with quinpirole (1 mg/kg) or saline from postnatal (P) day 1-P21, given nicotine (0.5 mg/kg) or saline from P33 through P49, and placed into a locomotor arena for behavioral testing. Nicotine or saline treatment was preceded by the D2-like receptor antagonist Eticlopride, D3 antagonist nafadotride, or saline. Conditioned hyperactivity was analyzed on P50 in the same context in a drug-free test. In females, D2 priming increased the locomotor response to acute nicotine, but did not affect subsequent nicotine sensitization, and only non-D2-primed females demonstrated conditioned hyperactivity. Eticlopride and nafadotride blocked behavioral sensitization, although nafadotride was more effective at blocking nicotine-conditioned hyperactivity in females. In males, D 2 priming enhanced sensitization to nicotine and produced conditioned hyperactivity, which were blocked by Eticlopride and nafadotride. These results have implications for psychosis and comorbidity of nicotine abuse in adolescence.
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The effects of Eticlopride on Morris water task performance in male and female rats neonatally treated with quinpirole
Psychopharmacology, 2005Co-Authors: Russell W. Brown, Kimberly N. Thompson, Ivy A. Click, Razaria A. C. Best, Stephanie K. Thacker, Marla K. PernaAbstract:Rationale Previous studies have shown that neonatal quinpirole treatment which results in long-term dopamine D2 receptor supersensitization (D2 receptor priming) produces cognitive deficits in preweanling and adult rats behaviorally tested on the Morris water task (MWT). Objective This study was designed to analyze whether pretraining administration of the D2 antagonist Eticlopride alleviates cognitive deficits produced by neonatal quinpirole treatment. Methods Both male and female Sprague–Dawley rats were treated with quinpirole HCl (1 mg/kg) or saline from postnatal days 1 to 21. From P22 to P24, rats were tested on the place version of the MWT in which a hidden platform remains stationary throughout training. From P25 to P28, rats were tested on the match-to-place version of the MWT, and rats are given a pair of daily training trials to locate the hidden platform that was moved to a new location each day. Fifteen minutes before each training session, rats were intraperitoneally administered with Eticlopride (0.01 or 0.02 mg/kg) or saline. Results Pretraining Eticlopride treatment alleviated cognitive deficits produced by neonatal quinpirole treatment in both male and female rats on the place version of the MWT, as well as in males tested on the match-to-place version of the MWT. However, there were no significant deficits produced by neonatal quinpirole treatment in females tested on the match-to-place version of the MWT, and control males demonstrated superiority over control females on this version of the task. Conclusions Pretraining administration of the dopamine D2 antagonist Eticlopride alleviated cognitive deficits produced by neonatal quinpirole treatment. However, it appears that the dopamine D2 receptor may have a more important influence on cognitive performance in males than in females, which may be related to increased sensitivity of the D2 receptor in males.
J.m Vargo - One of the best experts on this subject based on the ideXlab platform.
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reduced Eticlopride induced fos expression in caudate putamen and globus pallidus after unilateral frontal cortex injury relation to neglect
Neuroscience, 1997Co-Authors: J.m Vargo, J F MarshallAbstract:Unilateral ablation of medial agranular cortex in rats results in neglect of contralateral stimuli and reductions in amphetamine-induced expression of the immediate early gene, c-fos, in both caudate-putamen and globus pallidus. Both unilateral neglect and the reductions in dopamine agonist induction of subcortical Fos immunoreactivity dissipate over a matter of weeks. Dopamine agonism induces Fos predominantly in striatonigral cells and in globus pallidus via striatopallidal disinhibition, whereas Fos is induced in striatopallidal cells by administration of antagonists of the D2 dopamine receptor subfamily. To examine more directly effects of cortical injury on striatopallidal function, induction of striatal Fos by the D2 antagonist Eticlopride (0.1 mg/kg, s.c.) was examined in rats with medial agranular cortex ablation. In the same animals, Eticlopride-induced Fos in globus pallidus was also examined. Five days after unilateral cortex injury, in rats showing neglect, the numbers of Fos immunoreactive nuclei induced by Eticlopride were reduced by 50% in caudate-putamen and 25% in globus pallidus of the ipsilateral hemisphere. These lesion effects were restricted to dorsolateral caudate-putamen and dorsal pallidum. Three or more weeks after cortical injury, in rats recovered from neglect, Eticlopride-induced Fos was normalized in caudate-putamen, but still decreased by 20% in globus pallidus. Along with previous findings, these results suggest that behavioral recovery from neglect produced by cortical injury may be at least partially mediated by normalizations of function of both striatopallidal and striatonigral neurons. In addition, the present findings suggest that normalization of function of pallidal cells activated by Eticlopride is not necessary for behavioral recovery from frontal cortex ablation. Lingering reductions in excitatory cortico-subthalamo-pallidal input may be responsible for the longer-lasting dysfunctions of these pallidal cells.
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Reduced Eticlopride-induced fos expression in caudate–putamen and globus pallidus after unilateral frontal cortex injury: relation to neglect
Neuroscience, 1997Co-Authors: J.m Vargo, J F MarshallAbstract:Unilateral ablation of medial agranular cortex in rats results in neglect of contralateral stimuli and reductions in amphetamine-induced expression of the immediate early gene, c-fos, in both caudate-putamen and globus pallidus. Both unilateral neglect and the reductions in dopamine agonist induction of subcortical Fos immunoreactivity dissipate over a matter of weeks. Dopamine agonism induces Fos predominantly in striatonigral cells and in globus pallidus via striatopallidal disinhibition, whereas Fos is induced in striatopallidal cells by administration of antagonists of the D2 dopamine receptor subfamily. To examine more directly effects of cortical injury on striatopallidal function, induction of striatal Fos by the D2 antagonist Eticlopride (0.1 mg/kg, s.c.) was examined in rats with medial agranular cortex ablation. In the same animals, Eticlopride-induced Fos in globus pallidus was also examined. Five days after unilateral cortex injury, in rats showing neglect, the numbers of Fos immunoreactive nuclei induced by Eticlopride were reduced by 50% in caudate-putamen and 25% in globus pallidus of the ipsilateral hemisphere. These lesion effects were restricted to dorsolateral caudate-putamen and dorsal pallidum. Three or more weeks after cortical injury, in rats recovered from neglect, Eticlopride-induced Fos was normalized in caudate-putamen, but still decreased by 20% in globus pallidus. Along with previous findings, these results suggest that behavioral recovery from neglect produced by cortical injury may be at least partially mediated by normalizations of function of both striatopallidal and striatonigral neurons. In addition, the present findings suggest that normalization of function of pallidal cells activated by Eticlopride is not necessary for behavioral recovery from frontal cortex ablation. Lingering reductions in excitatory cortico-subthalamo-pallidal input may be responsible for the longer-lasting dysfunctions of these pallidal cells.