Behavioral effects of CB2-R activation and blockade.

<p><i>A</i>, Mouse spontaneous locomotor activity following acute treatment with CB2 agonist JWH015 (1–20 mg/kg), in mouse strain, C57Bl/6 (a and b); BALBc, (c and d) and DBA/2 (e and f). <i>B</i>, Effect of JWH015 in C57Bl/6 mice in the two compartment black and white box, showing time spent in the black and white chamber. <i>C</i>, Acute effects of SR144528 – a CB2-R antagonist on DBA/2 mouse spontaneous locomotor activity and stereotype behavior. <i>D</i>, Acute effects of SR144528, in DBA/2 male and female mice in the two chamber black and white test box, showing time spent in the black and white chamber.</p

CB2-R- activation and blockade on anhedonia induced by chronic mild stress (CMS).

<p><i>A</i>, Weekly sucrose consumption in stress and control mice. <i>B</i>, Effect of JWH015 (20 mg/kg) on mouse weekly sucrose consumption test. C, Effect of AM630 (1 and 3 mg/kg) on mouse weekly sucrose consumption test.</p

CB2-R gene targeting modifies behavior.

<p><i>A</i>, Behavioral effects of CB2 intracerebral gene targeting by antisense oligonucleotide microinjected into the mouse brain and performance of mice in plus-maze test was assessed before and after 3 days of twice daily microinjection. AS1 and AS2 were before and after CB2 antisense oligo microinjection. V1 and V2 are controls. <i>B</i>, performance in plus-maze test following CMS or mice exposed prenatally to capsaicin and the effect of JWH015 (20 mg/kg).</p

Allelic and genotype distribution of R63Q polymorphism in the <i>CB2 gene</i>.

<p>Comparisons were made between patients with major depression and the healthy controls. Significant differences are observed in allelic frequency and genotype distribution in the R recessive model. OR is odd ratio.</p

Subcellular localization of rat hippocampal CB2-Rs.

<p><i>A</i>, a CB2-IR dendrite [CB2(+) D] receiving multiple synaptic contacts from axon terminals lacking CB2-R immunolabeling [CB2(−) AT]. B, a CB2-IR dendrite [CB2(+) D] was contacted by a non-immunoreactive axon terminal [CB2(−) AT]. Scale bar represents 0.3 µm.</p

Brain CB2-Rs: Immunohistochemistry in mouse and rat brain.

<p><i>A</i>, CB2-IR in apical dendrites and cell bodies of pyramidal neurons of rat cerebral cortex. <i>B</i>, CB2-IR in mouse cerebral cortex. <i>C</i>, CB2-IR in rat corpus callosum and <i>D</i>, CB2-IR in mouse hippocampal allocortex and some interneurons in the striatum oriens and stratum radiatum.</p

Brain CB2-Rs: Immunoractivity (IR) and pre-adsorption with immunizing peptide.

<p><i>A</i>, CB2-IR in the left panel and lack of CB2-IR in the right panel, <i>B</i>, when the CB2 antibody was pre-adsorped with the peptide.</p

Presence of <i>CB2</i> gene in the brain.

<p>A, Relative brain expression of <i>CB2</i> gene in C57BL/6J and BALBc strains subjected to stress. <i>B</i>, Relative <i>CB2</i> gene expression levels in the striatum, midbrain, and hippocampus of C57Bl/6J mice. <i>C</i>, Mouse whole brain relative <i>CB2</i> gene expression levels following chronic treatment with heroin and cocaine. <i>D</i>, relative <i>CB2</i> gene expression levels in striatum and midbrain of mice that developed alcohol preference. <i>CB2</i> gene expression was relative to the standard laboratory brain obtained from C57BL/6J that was set to 1.0. The positive control was from the spleen and no cDNA in TaqMan PCR reaction served as negative controls.</p

Brain CB2-Rs: Immunoblots, genotyping and <i>in-situ</i> hybridization.

<p><i>A</i>, <i>In-situ</i> hybridization indicating <i>CB2</i> gene is expressed in the cerebellum of wild type and not in the cerebellum of the CB2-R deficient mice and also in sense controls in the wild type mice. <i>B</i>, RFLP genotyping discrimination on agarose gel for <i>CB2</i> Q63R polymorphism in depressed subjects (Ba) and, Resequences of <i>CB2</i> Q63R polymorphism (Bb). <i>C</i>, Western blotting of CB2-Rs in CMS and control mice (left panel) and in right panel in mice exposed to 4 mg/kg capsaicin in utero.</p