M. C. Ritz

Publications43
h-index23
Citations4,892
Highly Influential Citations176
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Cocaine receptors on dopamine transporters are related to self-administration of cocaine.
TLDR
It is shown here that the potencies of cocaine-like drugs in self-administration studies correlate with their potencies in inhibiting [3H]mazindol binding to the dopamine transporters in the rat striatum, but not with theirPotencies in binding to a large number of other presynaptic and postsynaptic binding sites.
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The dopamine hypothesis of the reinforcing properties of cocaine
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Cocaine inhibition of ligand binding at dopamine, norepinephrine and serotonin transporters: a structure-activity study.
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Relationship between self-administration of amphetamine and monoamine receptors in brain: comparison with cocaine.
  • M. C. Ritz, M. Kuhar
  • Biology, Psychology
    The Journal of pharmacology and experimental…
  • 1 March 1989
TLDR
Comparisons of the potencies of these compounds in studies of drug reinforced behavior with their binding potencies at monoaminergic uptake sites and neurotransmitter receptor sites indicate that d-amphetamine exhibits a pharmacologically relevant micromolar affinity for dopamine, norepinephrine and serotonin uptake sites as well as for alpha-2 adrenergic receptor sites.
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Cocaine-induced seizures and lethality appear to be associated with distinct central nervous system binding sites.
  • M. C. Ritz, F. George
  • Biology, Psychology
    The Journal of pharmacology and experimental…
  • 1 March 1993
TLDR
The findings suggest that, although seizure initiation may depend primarily on affinity of cocaine and related compounds for binding sites associated with the serotonin transporter, the seizure-inducing properties of cocaine may ultimately depend on a final summation of its effects not only on serotonergic systems, but on muscarinic and sigma neuronal systems as well.
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Cocaine inhibits muscarinic cholinergic receptors in heart and brain.
TLDR
Results indicate that cocaine can act as an antimuscarinic agent, particularly at higher, toxic doses.
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Cocaine-induced convulsions: pharmacological antagonism at serotonergic, muscarinic and sigma receptors
TLDR
Of the CNS binding sites with which cocaine is known to interact, the results are consistent with the conclusion that 5-HT transporters and5-HT2 receptor sites appear to be direct and primary sites related to cocaine-induced convulsions, while M1 and sigma binding sites seem to play important but secondary and modulatory roles in this response.
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Ethanol-reinforced behavior in P, NP, HAD and LAD rats: differential genetic regulation of reinforcement and motivation.
TLDR
The results suggest that the phenomenon of ethanol drinking is a composite of at least three genetically independent factors governing different aspects of ethanol-seeking behavior: a permissive factor allowing animals to readily overcome the aversive sensory effects of ethanol, a reinforcement factor that determines whether a substance can come to serve as a positive reinforcer, and a motivational factor related to the subjects' drive state with regard to drug seeking.
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Differential effects of the pharmacological manipulation of serotonin systems on cocaine and amphetamine self-administration in rats.
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Cocaine toxicity: concurrent influence of dopaminergic, muscarinic and sigma receptors in mediating cocaine-induced lethality
TLDR
The present results demonstrate that pharmacological manipulations of these predicted neurotransmitter systems alter the occurrence of cocaine-induced lethality in C57BL/6J mice, and provide converging supportive evidence that the lethal effects of cocaine depend upon concurrent interactions with dopaminergic, muscarinic M1 and sigma receptor sites.
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