Cocaine Action
Cocaine Action - Related Videos
07:51
A Protocol for Measuring Cue Reactivity in a Rat Model of Cocaine Use Disorder
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Cited by 6 •
2018
Cue reactivity is conceptualized as sensitivity to cues linked with drug-taking experiences that contribute to craving and relapse in abstinent humans. Cue reactivity is modeled in rats by measuring attentional orientation toward drug-associated cues that results in appetitive approach behavior in a cue reactivity test following self-administration and forced abstinence.
08:54
A Procedure for Studying the Footshock-Induced Reinstatement of Cocaine Seeking in Laboratory Rats
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Cited by 14 •
2011
Animal models of relapse, known as reinstatement procedures, have been used extensively to study the role of stress in relapse to drug seeking. Here, we report on a method for inducing the reinstatement of cocaine seeking in laboratory rats via acute exposures to mild, intermittent electric footshock.
10:28
Assessment of Cocaine-induced Behavioral Sensitization and Conditioned Place Preference in Mice
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Cited by 19 •
2016
This protocol is intended to enable researchers to conduct experiments designed to test these aspects of addiction using the conditioned place preference and locomotor behavioral sensitization assays.
08:22
Stereotaxic Microinjection of Viral Vectors Expressing Cre Recombinase to Study the Role of Target Genes in Cocaine Conditioned Place Preference
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Cited by 2 •
2013
This article describes how to microinject viral vectors into mouse brain and then test in a conditioned place preference paradigm that includes an acquisition, extinction and reinstatement phase.
01:24
CNS Stimulants: Cocaine, Amphetamines and Cannabinoids
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2024
CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its effects by...
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Blocking dopamine transporters leaves more dopamine in synapses, strengthening signaling in neural circuits associated with reward. This persistent increase helps explain cocaine’s intense reinforcement and relevance to dependence research. In pharmacology, transporter effects are therefore examined not only as molecular events but also as mechanisms that connect drug exposure with repeated use and substance-use behaviors.
Reduced norepinephrine reuptake increases this neurotransmitter in synapses and helps account for heightened alertness and sympathetic cardiovascular effects. The same mechanism contributes to vasoconstriction and tachycardia, linking a change in neuronal signaling to measurable cardiovascular responses. These relationships make norepinephrine transporter activity important when interpreting cocaine intoxication and toxicity.
Transporter blockade changes neurotransmitter concentrations by reducing reuptake, whereas sodium-channel blockade directly influences electrical signaling in excitable cells. The latter produces local anesthetic effects and can affect electrical conduction. Considering both mechanisms prevents cocaine action from being viewed only through reward pathways and helps explain why nervous-system and cardiovascular consequences can occur together.
Cocaine also blocks serotonin transporters, increasing serotonin in synapses alongside dopamine and norepinephrine. The combined transporter effects produce a broader alteration of chemical communication than would result from changing a single neurotransmitter system. This multi-transmitter profile is important in pharmacology because it links cocaine exposure to complex behavioral and physiological outcomes rather than one isolated response.
Studies commonly connect molecular mechanisms with reinforcement, dependence, intoxication, overdose, and cardiovascular toxicity. Researchers can ask how transporter blockade, sodium-channel effects, and resulting physiological changes relate to these outcomes. This framework supports pharmacology and neurobiology research by organizing observations across synaptic signaling, electrical conduction, cardiovascular function, and substance-use behavior.
Understanding the separate and combined effects on dopamine, norepinephrine, serotonin transporters, and voltage-gated sodium channels identifies the mechanisms that underlie cocaine-related outcomes. That knowledge supports research into pharmacological strategies for treatment, while also helping investigators interpret intoxication and overdose. The topic therefore connects basic drug action with clinically relevant substance-use research without reducing the problem to one target.