Cocaine Mechanism
Cocaine Mechanism - 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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Dopamine signaling is central to cocaine’s reinforcing effects. When dopamine reuptake is blocked, dopamine remains elevated in synaptic spaces, strengthening signaling associated with euphoria and reinforcement. In pharmacology, this link helps explain why repeated exposure can become clinically important and why cocaine use disorder research focuses on reward-related consequences rather than treating stimulation as only a cardiovascular event.
Norepinephrine accumulation connects transporter blockade to cardiovascular strain. By preventing norepinephrine reuptake, cocaine can increase signaling that raises heart rate and blood pressure. This pathway gives pharmacologists a mechanism for studying acute cardiovascular effects and for distinguishing them from dopamine-associated euphoria or serotonin-related signaling, even though all three transporter systems are affected at once.
Voltage-gated sodium-channel inhibition produces a different pharmacological consequence from monoamine transporter blockade. Rather than increasing a neurotransmitter in synaptic spaces, it reduces nerve impulse transmission, accounting for cocaine’s local anesthetic effect. This distinction matters when interpreting the drug’s combined actions: one mechanism changes chemical signaling, while the other directly limits propagation of neural impulses.
Acute toxicity research must account for the simultaneous elevation of norepinephrine, dopamine, and serotonin signaling and the inhibition of sodium channels. The combined profile can be considered alongside increased heart rate, higher blood pressure, and cardiovascular strain. A mechanistic framework helps investigators connect observed harmful effects with multiple pharmacological targets instead of attributing toxicity to a single pathway.
Transporter blockade provides a basis for examining drug interactions because it changes the amount of several neurotransmitters remaining in synaptic spaces. Sodium-channel inhibition adds a separate effect on nerve impulse transmission. Pharmacology studies can use these distinct targets to ask whether another substance or treatment modifies cocaine-associated signaling, cardiovascular strain, or local anesthetic action, without assuming all effects share one mechanism.
Mechanism-guided treatment research focuses on reducing harmful consequences rather than reproducing cocaine’s effects. Relevant targets include excessive dopamine, norepinephrine, and serotonin signaling, along with sodium-channel inhibition. Understanding which pathway contributes to reinforcement, cardiovascular strain, or reduced impulse transmission helps researchers evaluate treatments designed to lessen specific effects and address cocaine use disorder.