Additive subthreshold dose effects of cannabinoid CB1 receptor antagonist and selective serotonin reuptake inhibitor in antidepressant behavioral tests

Takahashi, Eiki; Katayama, Megumi; Niimi, Kimie; Itakura, Chitoshi

doi:10.1016/j.ejphar.2008.05.020

Cited by 34 publications

(18 citation statements)

References 32 publications

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“…For instance, in our experiments, unlike from that of Bambico et al, a single 6 min test period was applied instead of the traditional two-day paradigm, which may provide some explanation for the discrepancy. Moreover, CB 1 R-receptor antagonists also convey antidepressant effect in animal tests (Griebel et al, 2005;Shearman et al, 2003;Takahashi et al, 2008) and there are data supporting the association between cannabis use and later incidence of depression (Degenhardt et al, 2001). This suggests that the relationship between CB 1 R activation and mood regulation is not unidirectional.…”

Section: Discussionmentioning

confidence: 94%

Presynaptic α2-adrenoceptors control the inhibitory action of presynaptic CB1 cannabinoid receptors on prefrontocortical norepinephrine release in the rat

et al. 2012

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Section: Discussionmentioning

confidence: 94%

Presynaptic α2-adrenoceptors control the inhibitory action of presynaptic CB1 cannabinoid receptors on prefrontocortical norepinephrine release in the rat

et al. 2012

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“…As previously noted, CB 1 knockout mice display a heightened HPA axis response to stress (Uriguen et al ., 2004), in line with one of the most consistent findings in major depressive disorder. Although acute CB 1 receptor antagonist administration produces antidepressive-like responses in rodents (Griebel et al ., 2005; Shearman et al ., 2003; Takahashi et al ., 2008; Tzavara et al ., 2003), recent evidence suggests that a depression-like profile is evident following chronic antagonist administration (Beyer et al ., 2010). Long-lasting CB 1 receptor blockade induces a depressive behavioral phenotype in rats that is associated with well-known biochemical markers of depression along with diminished neuroplasticity and synaptic efficiency in the PFC (Rubino et al ., 2009; Rubino et al ., 2008).…”

Section: Endocannabinoids and Affective State Related To Drug Depementioning

confidence: 99%

Endocannabinoid influence in drug reinforcement, dependence and addiction-related behaviors

Serrano

Parsons

2011

Pharmacology & Therapeutics

156

136

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The endogenous cannabinoid system is an important regulatory system involved in physiological homeostasis. Endocannabinoid signaling is known to modulate neural development, immune function, metabolism, synaptic plasticity and emotional state. Accumulating evidence also implicates brain endocannabinoid signaling in the etiology of drug addiction which is characterized by compulsive drug seeking, loss of control in limiting drug intake, emergence of a negative emotional state in the absence of drug use and a persistent vulnerability toward relapse to drug use during protracted abstinence. In this review we discuss the effects of drug intake on brain endocannabinoid signaling, evidence implicating the endocannabinoid system in the motivation for drug consumption, and drug-induced alterations in endocannabinoid function that may contribute to various aspects of addiction including dysregulated synaptic plasticity, increased stress responsivity, negative affective states, drug craving and relapse to drug taking. Current knowledge of genetic variants in endocannabinoid signaling associated with addiction is also discussed.

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“…Since CPP and ω-conotoxin GVIA are thought to be effect on analgesia [19,20], cognitive tests without stimulations would be more appropriate for this study. The administration of different drugs at a lower dose induced the effects of phenotypes and identified functional signaling pathways [16], because the precise neuronal circuit systems play an important role in phenotypes at behavioral levels.…”

Section: Resultsmentioning

confidence: 99%

“…In previous study, subthreshold doses of cannabinoid CB1 receptor antagonist and selective serotonin reuptake inhibitors, which separately had no effect on antidepressant behavioral tests, showed a clear effect in combination without the side effects [16], suggesting that combinations of compounds with different molecular targets are useful tools to study the neuronal signaling mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Cav2.2-mediated NMDA receptor signaling in short-term memory

Takahashi

2015

Integr Mol Med

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It has been reported that Cav2.1-mediated N-methyl-D-aspartate (NMDA) receptor signaling is critical pathway in hippocampus and nucleus accumbens for spatial short-term memory. Neuronal voltage-dependent Cav2.1 and Cav2.2 have predominantly expressions at presynaptic neuronal terminals and mediate glutamate release in the central nervous systems. Recently, although Cav2.2 in the hippocampus and nucleus accumbens is also critical for spatial cognition, it remains unknown that functional Cav2.2-mediated NMDA receptor signaling in cognitive performance at the system level. This study examined whether Cav2.2-mediated NMDA receptor signaling mediates spatial short-term memory using the Y-maze test via a combined subthreshold doses of pharmacological approach. In previous our studies, Mice received systemic injection of NMDA receptor blocker (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP, 5mg/kg), mice received intrahippocampal injection of Cav2.2 blocker (ω-conotoxin GVIA, 1pg/side), or mice received intra-accumbens injection of Cav2.2 blocker (ω-conotoxin GVIA, 1pg/ side) were ineffective for the spatial short-term memory. However, a combination of subthreshold doses of 5mg/kg CPP systemic injection and 1pg/side ω-conotoxin GVIA intra-hippocampal injection triggered a spatial short-term memory deficit. Furthermore, a combination of subthreshold doses of 5mg/kg CPP systemic injection and 1pg/side ω-conotoxin GVIA intra-accumbens injection also showed impaired spontaneous alternation patterns. These results indicate that Cav2.2-mediated NMDA receptor signaling is critical in the hippocampus and nucleus accumbens for spatial short-term memory. These subthreshold pharmacological approach presented here is easily performed and can be used to study functional signaling pathways in various regions.

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Additive subthreshold dose effects of cannabinoid CB1 receptor antagonist and selective serotonin reuptake inhibitor in antidepressant behavioral tests

Cited by 34 publications

References 32 publications

Presynaptic α2-adrenoceptors control the inhibitory action of presynaptic CB1 cannabinoid receptors on prefrontocortical norepinephrine release in the rat

Presynaptic α2-adrenoceptors control the inhibitory action of presynaptic CB1 cannabinoid receptors on prefrontocortical norepinephrine release in the rat

Endocannabinoid influence in drug reinforcement, dependence and addiction-related behaviors

Cav2.2-mediated NMDA receptor signaling in short-term memory

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