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  • 1
    Electronic Resource
    Electronic Resource
    Adenosine A2A receptors are involved in physical dependence and place conditioning induced by THC (2004)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 20 (2004), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A2A adenosine and CB1 cannabinoid receptors are highly expressed in the central nervous system, where they modulate numerous physiological processes including adaptive responses to drugs of abuse. Both purinergic and cannabinoid systems interact with dopamine neurotransmission (through A2A and CB1 receptors, respectively). Changes in dopamine neurotransmission play an important role in addictive-related behaviours. In this study, we investigated the contribution of A2A adenosine receptors in several behavioural responses of Δ9-tetrahydrocannabinol (THC) related to its addictive properties, including tolerance, physical dependence and motivational effects. For this purpose, we first investigated acute THC responses in mice lacking A2A adenosine receptors. Antinociception, hypolocomotion and hypothermia induced by acute THC administration remained unaffected in mutant mice. Chronic THC treatment developed similar tolerance to these acute effects in wild-type and A2A-knockout mice. However, differences in the body weight pattern were found between genotypes during such chronic treatment. Interestingly, the somatic manifestations of SR141716A-precipitated THC withdrawal were significantly attenuated in mutant mice. The motivational responses of THC were also evaluated by using the place-conditioning paradigm. A significant reduction of THC-induced rewarding and aversive effects was found in mice lacking A2A adenosine receptors in comparison with wild-type littermates. Binding studies revealed that these behavioural changes were not associated with any modification in the distribution and/or functional activity of CB1 receptors in knockout mice. Therefore, this study shows, for the first time, a specific involvement of A2A receptors in the addictive-related properties of cannabinoids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2004.03682.x
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  • 2
    Electronic Resource
    Electronic Resource
    Cannabinoid receptor and WIN 55 212-2-stimulated [35S]-GTPγS binding in the brain of mu-, delta- and kappa-opioid receptor knockout mice (2003)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 18 (2003), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Numerous studies have shown the existence of functional links between the endogenous cannabinoid and opioid systems. However, extensive research is still needed to elucidate the biochemical mechanisms involved in this cannabinoid–opioid interaction. Mice lacking mu- (MOR), delta- (DOR) and kappa- (KOR) opioid receptors have been generated and some specific pharmacological effects induced by cannabinoids have been reported to be modified in these animals. In order to clarify further the possible mechanisms involved in this modification of cannabinoid responses we have now evaluated the expression and functional activity of cannabinoid receptors in different brain structures in these mutant animals. For this purpose, we have performed quantitative receptor autoradiography of CB1 cannabinoid receptors and activation of GTP-binding proteins by CB1 agonists in the brain of wild-type and homozygous MOR, DOR and KOR knockout mice. There were no significant differences in the levels of CB1 receptors in the brain of MOR mutant mice. In contrast, the efficacy of CB1 receptor activation by the cannabinoid agonist WIN 55 212-2 was dramatically reduced in the caudate-putamen of MOR knockout animals. The density of CB1 receptors as well as the stimulation of GTP-binding proteins by WIN 55 212-2 were significantly increased in the substantia nigra of mice deficient in DOR. Finally, there were no major changes in the levels and functional activity of CB1 cannabinoid receptors in any brain region in KOR knockout mice. Taken together, these results indicate that deletion of MOR and DOR causes alterations in cannabinoid receptor levels and functional activity in specific brain structures, which could explain some of the functional interactions observed between these two neuronal systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2003.02951.x
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  • 3
    Electronic Resource
    Electronic Resource
    Increase of morphine withdrawal in mice lacking A2a receptors and no changes in CB1/A2a double knockout mice (2003)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 17 (2003), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: CB1 cannabinoid and A2a adenosine receptors are highly expressed in the central nervous system where they modulate numerous physiological processes including emotional behaviour and the responses of several drugs of abuse. To investigate the contribution of these receptors in emotional-like responses and opioid dependence we have generated CB1/A2a double deficient mice (\mathrm{CB}^{-/-}_{1}/\mathrm{A}^{-/-}_{2\mathrm{a}}). The spontaneous locomotor activity was reduced in double knockout as compared to wild-type animals. Emotional-like responses of \mathrm{CB}^{-/-}_{1}/\mathrm{A}^{-/-}_{2\mathrm{a}} mice were investigated using the elevated plus-maze and the lit-dark box. Mutant mice exhibited an increased level of anxiety in both behavioural models. The specific involvement of CB1 and A2a receptors in morphine dependence was evaluated by using A2a knockout mice and CB1/A2a double mutant mice. The severity of naloxone-precipitated morphine withdrawal syndrome was significantly increased in the absence of A2a adenosine receptors whereas no modifications were observed in the double knockout mice. These results suggest that both receptors participate in the control of emotional behaviour and seem to play an opposite role in the expression of opioid physical dependence.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2003.02439.x
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  • 4
    Electronic Resource
    Electronic Resource
    κ- and δ-opioid receptor functional activities are increased in the caudate putamen of cannabinoid CB1 receptor knockout mice (2005)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 22 (2005), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The purpose of this study was to examine the functional interaction between endogenous opioid and cannabinoid receptor systems in the caudate putamen and nucleus accumbens. We therefore examined by autoradiography the functional activity and density of µ-, κ- and δ-opioid receptors in both brain regions of cannabinoid CB1 receptor knockout mice. Functional activity was estimated by measuring agonist-stimulated [35S]GTPγS binding. Results showed that deletion of the CB1 cannabinoid receptor markedly increased κ-opioid (50%) and δ-opioid (42%) receptor activities whereas no differences were found in µ-opioid receptor in the caudate putamen. In contrast, binding autoradiography showed a similar density of µ-, κ- and δ-opioid receptors between mutant and wild-type mice. No differences were found in densities or activities of µ-, κ- and δ-opioid receptors between mutant and wild-type mice in the nucleus accumbens. Taken together, our results revealed that deletion of CB1 cannabinoid receptors produced a pronounced increase in the activity of κ- and δ-opioid receptors in the caudate putamen. This endogenous interaction between opioid and cannabinoid receptors may be relevant to further understand a variety of neuroadaptative processes involving the participation of opioid receptors, such as motor behaviour, emotional responses and drug dependence.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2005.04372.x
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  • 5
    Electronic Resource
    Electronic Resource
    Δ9-tetrahydrocannabinol decreases somatic and motivational manifestations of nicotine withdrawal in mice (2004)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 20 (2004), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The possible interactions between Δ9-tetrahydrocannabinol (Δ9-THC) and nicotine remain unclear in spite of the current association of cannabis and tobacco in humans. The aim of the present study was to explore the interactions between these two drugs of abuse by evaluating the consequences of Δ9-THC administration on the somatic manifestations and the aversive motivational state associated with nicotine withdrawal in mice. Acute Δ9-THC administration significantly decreased the incidence of several nicotine withdrawal signs precipitated by mecamylamine or naloxone, such as wet-dog-shakes, paw tremor and scratches. In both experimental conditions, the global withdrawal score was also significantly attenuated by acute Δ9-THC administration. This effect of Δ9-THC was not due to possible adaptive changes induced by chronic nicotine on CB1 cannabinoid receptors, as the density and functional activity of these receptors were not modified by chronic nicotine administration in the different brain structures investigated. We also evaluated the consequences of Δ9-THC administration on c-Fos expression in several brain structures after chronic nicotine administration and withdrawal. c-Fos was decreased in the caudate putamen and the dentate gyrus after mecamylamine precipitated nicotine withdrawal. However, acute Δ9-THC administration did not modify c-Fos expression under these experimental conditions. Finally, Δ9-THC also reversed conditioned place aversion associated to naloxone precipitated nicotine withdrawal. Taken together, these results indicate that Δ9-THC administration attenuated somatic signs of nicotine withdrawal and this effect was not associated with compensatory changes on CB1 cannabinoid receptors during chronic nicotine administration. In addition, Δ9-THC also ameliorated the aversive motivational consequences of nicotine withdrawal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2004.03714.x
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  • 6
    Electronic Resource
    Electronic Resource
    Anandamide, but not 2-arachidonoylglycerol, accumulates during in vivo neurodegeneration (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Endogenous cannabinoid receptor ligands (endocannabinoids) may rescue neurons from glutamate excitotoxicity. As these substances also accumulate in cultured immature neurons following neuronal damage, elevated endocannabinoid concentrations may be interpreted as a putative neuroprotective response. However, it is not known how glutamatergic insults affect in vivo endocannabinoid homeostasis, i.e. N-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG), as well as other constituents of their lipid families, N-acylethanolamines (NAEs) and 2-monoacylglycerols (2-MAGs), respectively. Here we employed three in vivo neonatal rat models characterized by widespread neurodegeneration as a consequence of altered glutamatergic neurotransmission and assessed changes in endocannabinoid homeostasis. A 46-fold increase of cortical NAE concentrations (anandamide, 13-fold) was noted 24 h after intracerebral NMDA injection, while less severe insults triggered by mild concussive head trauma or NMDA receptor blockade produced a less pronounced NAE accumulation. By contrast, levels of 2-AG and other 2-MAGs were virtually unaffected by the insults employed, rendering it likely that key enzymes in biosynthetic pathways of the two different endocannabinoid structures are not equally associated to intracellular events that cause neuronal damage in vivo. Analysis of cannabinoid CB1 receptor mRNA expression and binding capacity revealed that cortical subfields exhibited an up-regulation of these parameters following mild concussive head trauma and exposure to NMDA receptor blockade. This may suggest that mild to moderate brain injury may trigger elevated endocannabinoid activity via concomitant increase of anandamide levels, but not 2-AG, and CB1 receptor density.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00542.x
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  • 7
    Electronic Resource
    Electronic Resource
    Decreased Cannabinoid CB1 Receptor mRNA Levels and Immunoreactivity in Pituitary Tumors Induced by Prolonged Exposure to Estrogens (2000)
    Springer
    Pituitary 3 (2000), S. 221-227 
    Details
    ISSN: 1573-7403
    Keywords: CB1 receptors ; cannabinoid ; anterior pituitary gland ; pituitary tumors ; DES ; prolactin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies have demonstrated the occurrence of endocannabinoids and their CB1 receptor subtype in the anterior pituitary gland, despite previous evidence suggesting their exclusive presence and action in the neuroendocrine hypothalamus. The present study was designed to examine the potential changes in these CB1 receptors located in the anterior pituitary gland in three different experimental situations, which are known to affect anterior pituitary function: (i) estrogen-induced pituitary tumorization, (ii) presence of ectopic pituitaries, and (iii) chronic treatment with D1 or D2 dopaminergic receptor agonists or antagonists. Results were as follows. Induction of pituitary tumorization by implantation of silastic capsules containing diethylstilbestrol, a synthetic estrogen, produced the expected body weight loss and increase in pituitary weight and plasma prolactin (PRL) levels. In hyperplastic pituitaries, both CB1 receptor mRNA levels and immunoreactivity decreased significantly. Double labelling studies demonstrated that CB1 receptors colocalized, in pituitary tumors, with PRL- or luteinizing hormone-containing cells, as they did in normal pituitaries. Plasma PRL levels were also increased in rats bearing ectopic pituitaries implanted under the kidney capsule. As previously reported, this increase was originated by the hormone release from the ectopic gland, because the normotopic pituitary collaborated scarcely to elevate PRL levels since it was hypofunctional due to the activation of peripheral PRL-induced feedback mechanisms. However, in this hypofunctional anterior pituitary, there were not any changes in CB1 receptor mRNA levels and immunoreactivity. Finally, chronic treatment with SKF38393, a D1 receptor agonist, or bromocriptine, a D2 receptor agonist, or with their corresponding antagonists, SCH 23390 or sulpiride, respectively, did not alter CB1 receptor mRNA levels and immunoreactivity, although produced the expected changes in plasma PRL levels. In summary, estrogen-induced pituitary tumorization was associated with a marked reduction in CB1 receptors, despite the fact that these receptors were located, among others, on lactotroph cells which develop hyperplasia during tumor induction. Whether this decrease is associated with the ethiology of pituitary tumor induction and whether their pharmacological activation might affect tumorization process are presently unknown, but this will be subjected of further research.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1012874029689
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