Involvement of medial prefrontal cortex alpha-2 adrenoceptors on memory acquisition deficit induced by arachidonylcyclopropylamide, a cannabinoid CB₁ receptor agonist, in rats; possible involvement of Ca²⁺ channels

Abstract

Functional interactions between cannabinoid and alpha-2 adrenergic systems in cognitive control in the medial prefrontal cortex (mPFC) seem possible. The present study evaluated the possible role of alpha-2 adrenoceptors of the prefrontal cortex on effect of arachidonylcyclopropylamide (ACPA), a cannabinoid CB1 receptor (CB1R) agonist, in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulae in the mPFC, trained in a step-through task, and tested 24 h after training to measure step-through latency. Results indicate that pre-training microinjection of ACPA (0.05 and 0.5 μg/rat) and clonidine (alpha-2 adrenoceptor agonist; 1 and 2 μg/rat) reduce memory acquisition. Pre-training subthreshold dose of clonidine (0.5 µg/rat) restored memory-impairing effect of ACPA (0.05 and 0.5 µg/rat). On the other hand, pre-training administration of the alpha-2 adrenoceptor antagonist yohimbine in all doses used (0.5, 1, and 2 μg/rat) did not affect memory acquisition by itself, while a subthreshold dose of yohimbine (2 µg/rat) potentiated memory impairment induced by ACPA (0.005 µg/rat). Finally, a subthreshold dose of SKF96365 (a Ca(2+) channel blocker) blocked clonidine and yohimbine effect of memory responses induced by ACPA. In conclusion, these data indicate that mPFC alpha-2 adrenoceptors play an important role in ACPA-induced amnesia and Ca(2+) channels have a critical role this phenomenon.

In Vivo Availability of Cannabinoid 1 Receptor Levels in Patients With First-Episode Psychosis

“…Our finding that CB1R levels were lower in patient cohorts irrespective of antipsychotic medication use is consistent with preclinical literature indicating that antipsychotics do not alter CB1R density in rodents . Our finding that cortical CB1R availability is associated with poorer cognitive function is consistent with preclinical literature showing that CB1R agonists administered centrally to the medial prefrontal cortex impair cognition …”

“… 44 Our finding that cortical CB1R availability is associated with poorer cognitive function is consistent with preclinical literature showing that CB1R agonists administered centrally to the medial prefrontal cortex impair cognition. 45 , 46 , 47 …”

Investigating the effect of crocin on memory deficits induced by total sleep deprivation (TSD) with respect to the BDNF, TrkB and ERK levels in the hippocampus of male Wistar rats

“…The dark compartment had black Plexiglas walls and steel rods in its floor. The steel rods were at 1 cm intervals and were connected to a stimulator with a connection wire to induce foot shocks (50 Hz, 3 s, 1 mA intensity) to the grid floor of the dark compartment during the experiment (Beiranvand et al, 2016). Evaluation of passive avoidance performance consisted of two sessions: training and retrieval tests.…”

Cortical adrenoceptor expression, function and adaptation under conditions of cannabinoid receptor deletion

“…Considering that nabilone’s efficacy in the treatment of PTSD is attributed to the actions of cannabinoids on NE circuitry (Reyes et al, 2009; Villanueva et al, 2009; Carvalho et al, 2010a; Carvalho et al, 2010b) and that cortical NE neurotransmission is involved in cognitive and behavioral states including anxiety (Arnsten, 2007; Ramos and Arnsten, 2007; Arnsten and Pliszka, 2011), cannabinoid and adrenergic receptor interactions may underlie the regulation of cortical function by cannabinoids. Interestingly, recent studies have shown that CB1 and CB2 receptors also play a role in splenic contraction (Simkins et al, 2016), that both peripheral and central CB1 receptors control stress-induced impairment of memory consolidation (Busquets-Garcia et al, 2016) and that a memory acquisition deficit induced by CB1 receptor agonist, arachidonylcyclopropylamide, involved α2-adrenoceptors in the mPFC (Beiranvand et al, 2016). Thus, these findings may have implications for advancing our understanding of the circuitry underlying α2-adrenoceptor and CB1 receptor interactions that may be targeted in the development of pharmacological treatment for neuropsychiatric disorders.…”