15 Fakultätsübergreifend / Sonstige Einrichtung
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Item Open Access Differential effects of lesions of the dorsomedial and dorsolateral caudate putamen on reaction time performance in rats(1994) Hauber, Wolfgang; Schmidt, Werner J.In order to investigate the role of the dorsomedial and dorsolateral caudate-putamen (CPu) in movement initiation of rats, we examined the effects of quinolinic acid lesions (30 nmol in 1 μl) in these striatal subregions in a simple reaction time task. Results show that lesions of the dorsomedial, but not of the dorsolateral CPu increased reaction times. These findings provide further evidence for a functional heterogenity of the CPu and demonstrate an involvement of the dorsomedial CPu in processes related to rapid initiation of responsesItem Open Access Excitatory amino acid antagonists and Parkinson's disease [Reply to letter to the editor](1990) Schmidt, Werner J.; Bubser, Michael; Hauber, WolfgangGirault et al. draw similar conclusions from their studies of the regulation of protein phosphorylation by dopamine and glutamate in striatonigral neurones as we did on the basis of behavioural findings, i.e. that dopamine and glutamate may exert opposite effects within the neostriatum. Admittedly, this view is oversimplified, but this transmitter balance does seem to be relevant to the parkinsonian symptoms akinesia and rigidity.Item Open Access Role of the medial orbitofrontal cortex and ventral tegmental area in effort-related responding(2020) Münster, Alexandra; Votteler, Angeline; Sommer, Susanne; Hauber, WolfgangDie Arbeit untersucht die Interaktion von zwei Gehirnarealen, dem medialen Orbitofrontalcortex und dem Ventralen Tegmentalen Areal, bei der Handlungssteuerung.Item Open Access Anticataleptic potencies of glutamate antagonists(1991) Schmidt, Werner J.; Zadow, Beate; Kretschmer, Beate D.; Hauber, WolfgangThe anticataleptic effects of non-competitive and competitive NMDA antagonists as well as those of an agonist at the allosteric glycine binding site of the NMDA receptor were tested in the catalepsy model. Some of these drugs were further tested in a reaction time task demanding rapid locomotor initiation. The results show that the non-competitive NMDA antagonists dizocilpine and memantine as well as the competitive antagonists CGP 39551, CGP 37849 and CPPene antagonized dopamine D2 receptor mediated catalepsy induced by haloperidol. D-cycloserine, a partial glycine agonist per se had no effects, but it enhanced the anticataleptic effects of dizocilpine when coadministered. However, the effects of CGP 37849 were abolished. Dopamine D1 receptor mediated catalepsy induced by SCH 23390 was antagonized by dizocilpine, memantine, CPPene, but not by CGP 37849. In the reaction time task dizocilpine, memantine and CGP 37849 were tested for their anti-akinetic and anti-bradykinetic potencies. All these compounds improved haloperidolinduced slowing of reaction time. However, they acted differentially on haloperidol-induced slowing of movement execution and decreased initial acceleration. Thus, antagonists at the NMDA receptor may have a therapeutic potential in the treatment of Parkinson''s disease. Their potency can be manipulated specifically at the glycine binding siteItem Open Access Excitatory amino acids and Parkinson's disease [Letter to the editor](1990) Schmidt, Werner J.; Bubser, Michael; Hauber, Wolfgang-Item Open Access The NMDA antagonist dizocilpine (MK-801) reverses haloperidol-induced movement initiation deficits(1990) Hauber, Wolfgang; Schmidt, Werner J.The present study shows that systemic dopamine receptor blockade impaired movement initiation of rats, trained in a simple reaction time task for rapid initiation of locomotion in response to a combined optic/acoustic cue. Reaction time, movement time and the accelerative force were recorded for each initiation of locomotion. Results indicate a dose-related increase of reaction time following systemic administration of haloperidol (0.1, 0.15, 0.3 mg/kg i.p.). Measures derived from resulting force-time patterns showed a haloperidol-induced decrease (0.15 mg/kg i.p.) of the mean rate of force development, indicating a decreased initial acceleration. These effects were reversed by systemic co-administration of dizocilpine (MK-801) (0.08 mg/kg i.p.), a selective non-competitive N-methyl-d-aspartate (NMDA) antagonist. The haloperidol-induced movement initiation deficits in this task are in part comparable to akinesia seen in Parkinson's disease and their reversal by dizocilpine has implications for the treatment of this disease.Item Open Access Behavioural pharmacology of glutamate in the basal ganglia(1992) Schmidt, Werner J.; Bubser, Michael; Hauber, WolfgangIn Parkinson's disease the dopaminergic inhibition - mediated by DA2 receptors in the triatum - is reduced. Therefore glutamatergic excitation predominates in the antero-dorsal striatum. In turn the glutamatergic neurons of the subthalamic nucleus become disinhibited. Antagonists of the NMDAsubtype of glutamate receptor injected locally into the glutamatergically innervated nuclei or competitive and non-competitive NMDA-antagonista administered systemically, counteract parkinsonian symptom in animals.Item Open Access A novel reaction time task for investigating force and time parameters of locomotor initiation in rats(1990) Hauber, WolfgangA novel simple reaction-time task for rats is described in the present study. Food-deprived rats were trained in a modified runway for rapid locomotor initiation, in response to a combined optical/acoustic stimulus, to receive a food reward. Rats rapidly learned this task with small variability, and movement patterns of locomotor initiation are congruent under these conditions. Reaction time, movement time and accelerative forces were recorded from each initiation of locomotion by means of video equipment and a force platform. The quantification modes yielded consistent results and a quantitative description of measured force and time parameters is given. The task may be especially appropriate for investigating basal ganglia functions. The present results will be the basis for investigating initiation of locomotion in animal models of neurological diseases.