Related Experiment Video
Updated: Jun 11, 2026
04:11
A Conditioned Place Preference Protocol for Measuring Incubation of Craving in Rats
Published on: November 6, 2018
Contribution of limbic norepinephrine to cannabinoid-induced aversion
Ana Franky Carvalho1, Arith-Ruth S Reyes, Robert C Sterling
1Neuroscience, Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA. arfranky@gmail.com
Psychopharmacology
|July 6, 2010
Summary
Norepinephrine (NE) in the nucleus accumbens is crucial for cannabinoid-induced aversion but not anxiety. This finding helps understand cannabinoid side effects by pinpointing specific neural pathways involved in aversion responses.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- The endocannabinoid system is a target for novel therapeutics.
- Cannabinoid-based agents cause side effects, limiting clinical use.
- Understanding cannabinoid neurocircuitry is key to mitigating adverse effects.
Purpose of the Study:
- Investigate norepinephrine's role in cannabinoid aversion and anxiety.
- Determine if limbic forebrain norepinephrine is critical for these effects.
Main Methods:
- Used immunotoxin lesions to deplete norepinephrine.
- Employed place conditioning and elevated zero maze for behavioral analysis in rats.
Main Results:
- WIN 55,212-2 (a CB1/CB2 agonist) induced significant place aversion.
- Norepinephrine depletion in the nucleus accumbens blocked aversion.
- Norepinephrine depletion in the bed nucleus of the stria terminalis did not affect aversion or anxiety.
Conclusions:
- Limbic norepinephrine, specifically in the nucleus accumbens, is essential for cannabinoid-induced aversion.
- Norepinephrine is not essential for cannabinoid-induced anxiety-like behaviors.
Related Concept Videos
01:21Chemotherapy-Induced Nausea and Vomiting: Cannabinoids
Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
Two synthetic agonists of THC,...
Two synthetic agonists of THC,...
01:25Analgesia and Pain Management
Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
01:24CNS Stimulants: Cocaine, Amphetamines and Cannabinoids
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...
01:15Functional Brain Systems: Limbic System
The limbic system, often called the "emotional brain," is a complex set of structures located deep within the brain. The intricate network of the limbic system supports a wide range of psychological functions, from emotional regulation to memory formation and sensory processing. This functional brain region encompasses specific parts of the diencephalon and the cerebrum, integrating the higher mental functions of the cerebral cortex with the primitive emotional responses of the deep brain...
01:25Adrenergic Agonists: Indirect-Acting Agents
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 bioavailability, and...
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 bioavailability, and...