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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.
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.
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.
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.
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.
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.
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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