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  • 1
    Electronic Resource
    Electronic Resource
    The contribution of the different binding sites of the N-methyl-D-aspartate (NMDA) receptor to the expression of behavior (1992)
    Springer
    Journal of neural transmission 87 (1992), S. 23-35 
    Details
    ISSN: 1435-1463
    Keywords: NMDA receptor ; locomotion ; catalepsy ; stereotypy ; rat ; CGP 37849 ; dizocilpine (MK-801) ; glycine ; D-cycloserine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of competitive (CGP 37849 and CGP 39551) and noncompetitive (dizocilpine) N-methyl-D-aspartate (NMDA) antagonists were tested in three animal models (catalepsy, sniffing, locomotion) and, in addition, the modulation of these effects by an agonist of the strychnine-insensitive glycine binding site was investigated. Both competitive and non-competitive NMDA antagonists reduced neuroleptic-induced catalepsy. Weak sniffing was induced by the competitive antagonist but strong sniffing by the non-competitive NMDA antagonist. Due to muscle relaxation the competitive antagonist reduced locomotion, in contrast to stimulation of locomotor activity induced by the noncompetitive NMDA antagonist. The glycine agonist (D-cycloserine) potentiated the effects of the non-competitive but antagonized those of the competitive NMDA antagonist.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01253108
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  • 2
    Electronic Resource
    Electronic Resource
    Anticataleptic potencies of glutamate-antagonists (1991)
    Springer
    Amino acids 1 (1991), S. 225-237 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Catalepsy ; Movement initiation ; NMDA antagonists ; Glycine ; Parkinson's disease ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The 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 site.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00806920
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  • 3
    Electronic Resource
    Electronic Resource
    Dopamine-glutamate interactions in the basal ganglia (1998)
    Springer
    Amino acids 14 (1998), S. 5-10 
    Details
    ISSN: 1438-2199
    Keywords: Basal ganglia loops ; Reward ; Sensitization ; NMDA receptor ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In an attempt to formulate a working hypothesis of basal-ganglia functions, arguments are considered suggesting that the basal ganglia are involved in a process of response selection i.e. in the facilitation of “wanted” and in the suppression of “unwanted” behaviour. The meso-accumbal dopamine-system is considered to mediate natural and drug-induced reward and sensitization. The meso-striatal dopamine-system seems to fulfill similar funcions: It may mediate reinforcement which strengthens a given behaviour when elicited subsequently, but which is not experienced as reward or hedonia. Glutamate as the transmitter of the corticofugal projections to the basal ganglia nuclei and of the subthalamic neurons is critically involved in basal ganglia funcions and dysfunctions; for example Parkinson's disease can be considered to be a secondary hyperglutamatergic disease. Additionally, glutamate is an essential factor in the plasticity response of the basal-ganglia. However, opposite to previous suggestions, the NMDA-receptor blocker MK-801 does not prevent psychostimulant- nor morphine-induced day to day increase (sensitization) of locomotion. Also the day to day increase of haloperidol-induced catalepsy was not prevented by MK-801.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01345235
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  • 4
    Electronic Resource
    Electronic Resource
    The role of NMDA receptors in the slow neuronal degeneration of Parkinson's disease (1998)
    Springer
    Amino acids 14 (1998), S. 17-23 
    Details
    ISSN: 1438-2199
    Keywords: NMDA receptors ; Excitotoxicity ; Chronic neuronal degeneration ; Nigrostriatal neurons ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Parkinson's disease is a disorder, in which neurons of various neuronal systems degenerate. Furthermore, in such degenerating neurons, the cytoskeleton seems to be affected. In this respect, Parkinson's disease resembles Alzheimer's disease. Since it has been shown, that elevated levels of intracellular calcium can disrupt the cytoskeleton and that the stimulation of glutamate (NMDA) receptors can cause high intracellular concentrations of calcium, it has been suggested, that the stimulation of glutamate receptors plays a role in the slow degeneration in Alzheimer's and Parkinson's disease. In case of the degeneration of the dopaminergic nigrostriatal system in Parkinson's disease, neurons that contain calcium binding protein appear to be less vulnerable than the neurons that lack it, suggesting that calcium binding protein might protect these neurons from degeneration by preventing that cytosolic calcium concentrations increase excessively. And, since there is in the nigrostriatal system a glutamatergic afferent pathway (the prefrontonigral projection) and since dopaminergic nigrostriatal neurons contain postsynaptic NMDA receptors, glutamatergic excitation may play a role in the degeneration of the nigrostriatal system in Parkinson's disease. If so, it may be possible to protect the neurodegeneration of these dopaminergic neurons by NMDA receptor antagonists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01345237
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  • 5
    Electronic Resource
    Electronic Resource
    6-Hydroxydopamine lesion of locus coeruleus and the antiparkinsonian potential of NMDA-receptor antagonists in rats (1997)
    Springer
    Journal of neural transmission 104 (1997), S. 363-377 
    Details
    ISSN: 1435-1463
    Keywords: Noradrenaline ; locus coeruleus ; 6-OHDA lesion ; NMDA receptor-antagonists ; L-DOPA ; Parkinson's disease ; open field ; locomotion ; exploration ; behavior ; rat ; HPLC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Behavioral and neurochemical effects after bilateral 6-hydroxy-dopamine locus coeruleus- (LC) lesion were examined in rats and compared to sham-lesioned controls. Behavior after treatment with the antiakinetic drugs dizocilpine, amantadine, memantine or L-DOPA as well as joint treatment of these drugs with haloperidol were tested in an open field with holeboard and in an experimental chamber. Under saline spontaneous activity (open field with holeboard) and sniffing (experimental chamber) were reduced after lesion. Injection of the proparkinsonian drug haloperidol decreased sniffing in all rats but to a greater extent in LC-lesioned rats. In combination with haloperidol none of the tested drugs could completely compensate for the motor deficits induced by the lesion. Neurochemical data revealed a reduced content of noradrenaline in the prefrontal cortex and in the posterior striatum of LC-lesioned rats. These results indicate that loss of LC neurons intensifies parkinsonian symptoms induced by blockade of dopamine D2-receptors, and lowers the antiakinetic potential of dizocilpine, amantadine, memantine or L-DOPA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01277657
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  • 6
    Electronic Resource
    Electronic Resource
    MK-801-induced stereotypy and its antagonism by neuroleptic drugs (1990)
    Springer
    Journal of neural transmission 81 (1990), S. 173-182 
    Details
    ISSN: 1435-1463
    Keywords: NMDA-receptor ; MK-801 ; haloperidol ; clozapine ; stereotypy ; sniffing ; locomotion ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary MK-801 [(+)-5-methyl-10,11-dihydroxy-5H-dibenzo-(a,d)cyclo-hepten-5, 10-imine hydrogen maleate], which blocks glutamatergic transmission at the NMDA-receptor-gated ion chanel, induced stereotypies which are similar to those found after intrastriatal injections of AP-5, e.g. sniffing and locomotion. Tests in familiar or unfamiliar environment (non-stressful or stressful situation) did not qualitatively change MK-801-induced effects. Haloperidol (0.1mg/kg, IP) delayed the onset and shortened the duration of MK-801 (0.16; 0.33mg/ kg, IP)-induced stereotypy whereas clozapine (5 mg/kg, SC) potently antagonized it. However, exact quantification of sniffing, measured in an experimental chamber designed for this purpose, revealed an antagonism by both drugs, haloperidol as well as clozapine. Stereotypy is considered to represent an animal model of schizophrenia, and the antagonism of stereotypy with classical (haloperidol) as well as with atypical (clozapine) antipsychotic drugs is in accordance with the glutamate hypothesis of schizophrenia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01245040
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  • 7
    Electronic Resource
    Electronic Resource
    Glycine site antagonists abolish dopamine D 2 but not D 1 receptor mediated catalepsy in rats (1994)
    Springer
    Journal of neural transmission 95 (1994), S. 123-136 
    Details
    ISSN: 1435-1463
    Keywords: Glycine ; NMDA ; 7-chlorokynurenate ; (R)-HA-966 ; haloperidol ; SCH 23390 ; dopamine ; D 1, D 2, catalepsy ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Catalepsy—a state of postural immobility (akinesia) with muscular rigidity (rigor)—and reduced locomotion in animals are behavioral deficits showing similarities with symptoms of Parkinson's disease (PD). The effects of the glycine site antagonists 7-chlorokynurenate and (R)-HA-966 on haloperidol-(D2 antagonist) and SCH 23390-(D 1 antagonist) induced catalepsy and reduced locomotion are investigated in rats. Both antagonists dose-dependently counteract dopamine D 2 receptor mediated catalepsy but they have no influence on locomotion. Neither 7-chlorokynurenate nor (R)-HA-966 has any effect on dopamine D 1 receptor mediated catalepsy. This finding is surprising, since NMDA receptor antagonists counteract both, dopamine D 1 and D 2 receptor mediated catalepsy. D 1 and D 2 receptors are located on different populations of neurons. Thus, the present findings suggest that these different neuronal populations have different sensitivity for ligands binding at the glycine binding site of the NMDA receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01276431
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