Source Paper
Cannabinoids Enhance Subsecond Dopamine Release in the Nucleus Accumbens of Awake Rats
Joseph F. Cheer, Kate M. Wassum, Michael L. A. V. Heien, Paul E. M. Phillips, R. Mark Wightman
Journal of Neuroscience • 2004
Cannabinoid Agonist Administration and Behavioral Assessment
Objective: To assess the effects of CB1 receptor agonist administration on catalepsy, locomotion, and dopamine release dynamics in the nucleus accumbens of awake rats using fast-scan cyclic voltammetry
Gather these items before starting the experiment. Check off items as you prepare.
Equipment2
Materials2
Not specified • Not specified • Not specified • Not specified
Not specified • Not specified • Not specified • Not specified
Software1
Not specified • Not specified
As an Amazon Associate, we earn from qualifying purchases. Product links help support this free resource.
Protocol Steps
Surgical implantation and electrode placement
Implant electrodes in the nucleus accumbens of freely moving rats for fast-scan cyclic voltammetry monitoring
Note: Rats must be freely moving to allow behavioral assessment
View evidence from paper
“monitor extracellular dopamine in the nucleus accumbens of freely moving rats with subsecond timescale resolution”
Baseline dopamine monitoring
Establish baseline extracellular dopamine levels and spontaneous dopamine transient frequency in nucleus accumbens
Note: Measure nonstimulated dopamine concentration transients
View evidence from paper
“monitor extracellular dopamine in the nucleus accumbens of freely moving rats with subsecond timescale resolution”
Intravenous administration of CB1 agonist
Administer CB1 receptor agonist intravenously in dose-dependent manner while monitoring behavioral and neurochemical responses
Note: Dose-dependent administration to assess dose-response relationship
View evidence from paper
“Intravenous administration of the central cannabinoid (CB1) receptor agonist, R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-(1-naphthalenyl) methanone mesylate, dose-dependently produced catalepsy”
Assessment of catalepsy
Measure cataleptic responses following CB1 agonist administration
Note: Catalepsy is a primary behavioral outcome measure
View evidence from paper
“dose-dependently produced catalepsy, decreased locomotion”
Assessment of locomotion
Monitor locomotor activity in freely moving rats following CB1 agonist administration
Note: Decreased locomotion is expected outcome
View evidence from paper
“decreased locomotion, and reduced the amplitude of electrically evoked dopamine release”
Measurement of electrically evoked dopamine release
Apply electrical stimulation and measure amplitude of evoked dopamine release using fast-scan cyclic voltammetry
Note: Amplitude is expected to be reduced by CB1 agonist
View evidence from paper
“reduced the amplitude of electrically evoked dopamine release while markedly increasing the frequency of detected (nonstimulated) dopamine concentration transients”
Measurement of spontaneous dopamine transients
Monitor frequency of nonstimulated dopamine concentration transients in nucleus accumbens during CB1 agonist effects
Note: Frequency is expected to increase markedly with CB1 agonist
View evidence from paper
“markedly increasing the frequency of detected (nonstimulated) dopamine concentration transients”
Administration of CB1 antagonist
Administer CB1 receptor antagonist to reverse and prevent agonist-induced effects
Note: Antagonist alone does not affect dopamine release
View evidence from paper
“The CB1 receptor antagonist [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide] reversed and prevented all agonist-induced effects but did not show effects on dopamine release when injected alone”
Post-antagonist monitoring
Continue monitoring dopamine release, catalepsy, and locomotion following CB1 antagonist administration to confirm reversal of agonist effects
Note: Verify complete reversal of all agonist-induced behavioral and neurochemical effects
View evidence from paper
“reversed and prevented all agonist-induced effects”