Related Experiment Video
Updated: Aug 14, 2025
09:16
A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
Published on: January 22, 2016
15.3K
Adenosine receptor stimulation inhibits methamphetamine-associated cue seeking
Ryan K Bachtell1,2, Tracey A Larson1, Madeline C Winkler1
1Department of Psychology and Neuroscience and Center for Neuroscience, University of Colorado Boulder, Boulder, CO, USA.
Journal of Psychopharmacology (Oxford, England)
|January 11, 2023
Summary
Stimulating adenosine A1 or A2A receptors significantly reduced methamphetamine seeking behaviors in rats. This finding offers a potential new therapeutic target for treating methamphetamine dependence.
Area of Science:
- Neuroscience
- Pharmacology
- Addiction Research
Background:
- Methamphetamine (METH) is a dangerous psychostimulant with high abuse potential.
- No effective pharmacotherapy currently exists for METH dependence.
- Adenosine receptors are emerging as potential targets for METH dependence treatment.
Purpose of the Study:
- To investigate the effects of stimulating adenosine A1 receptor (A1R) and adenosine A2A receptor (A2AR) subtypes on METH seeking.
- To evaluate these effects in both cue-induced reinstatement and cue-craving models of relapse.
Main Methods:
- Rats were trained to self-administer METH.
- Cue-induced reinstatement of METH seeking was assessed after extinction training.
- A1R or A2AR agonists were administered to evaluate effects on METH seeking and cue-craving.
Main Results:
- Pretreatment with A1R or A2AR agonists reduced cue-induced reinstatement of METH seeking in both male and female rats.
- A1R or A2AR agonist pretreatment also inhibited cue craving in both sexes.
Conclusions:
- Stimulation of A1R or A2AR effectively inhibits METH-seeking behavior triggered by METH-associated cues.
- This inhibition may result from disrupted cue-induced dopamine and glutamate signaling.
Related Concept Videos
01:25Adrenergic Agonists: Indirect-Acting Agents
1.8K
Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
1.8K
01:21Drugs Affecting Neurotransmitter Release or Uptake
1.2K
Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
1.2K
01:20Desensitization and Tachyphylaxis
2.0K
Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
2.0K
01:29Drugs Affecting Neurotransmitter Synthesis
1.5K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
1.5K
01:28Adrenergic Agonists: Mixed-Action Agents
809
Mixed-action adrenergic agonists, like ephedrine and pseudoephedrine, directly and indirectly affect adrenergic receptors. These agents stimulate adrenoceptors and indirectly release stored neurotransmitters, amplifying the adrenergic response.
Ephedrine and pseudoephedrine lack a catecholamine group, making them less susceptible to degradation by metabolic enzymes. They have increased oral bioavailability and lipophilicity, resulting in a longer duration of action. Their response is reduced by...
Ephedrine and pseudoephedrine lack a catecholamine group, making them less susceptible to degradation by metabolic enzymes. They have increased oral bioavailability and lipophilicity, resulting in a longer duration of action. Their response is reduced by...
809
01:30Adrenergic Agonists: Direct-Acting Agents
1.6K
Drugs that mimic the action of endogenous catecholamines like noradrenaline and adrenaline are called adrenergic agonists or sympathomimetics. Based on their mechanism of action, sympathomimetics can be classified as direct-, indirect-, or mixed-acting sympathomimetics. Direct-acting adrenergic agonists activate adrenoceptors without affecting presynaptic neurons, making them independent of neuronal catecholamine-depleting agents like reserpine and guanethidine.
These agents can be classified...
These agents can be classified...
1.6K