ABSTRACT
Cannabinoids exert widespread effects on cognitive functions. An overlapped distribution of GABA receptors and cannabinoid receptors has been reported in some brain structures [e.g. dorsal hippocampus]. Thus, the present study was undertaken to examine the possible role of the dorsal hippocampus GABA[A] receptors on ACPA induced amnesia and ACPA state-dependent memory. This experimental study was conducted on 250 adult male NMRI mice. Muscimol and ACPA were used as agonists of GABA[A] and the cannabinoid CB1 receptors, respectively. Mice were anaesthetized and cannulae were implanted bilaterally into the CA1 regions of the dorsal hippocampus. Seven days after post-surgery recovery, the behavioral testing was performed using an inhibitory avoidance task and the step-down latency of the animals was used to assess memory retention. Post-training administration of ACPA [3ng/mouse] impaired the memory retrieval. The memory impairment induced by ACPA was fully reversed by pre-test administration of ACPA or muscimol. The results suggest that the GABA[A] receptors of the dorsal hippocampal may play an important role in ACPA-induced amnesia and ACPA state-dependent memory
ABSTRACT
Due to overlapping distribution of GABA receptors with nicotinic receptors in some parts of brain such as dorsal hippocampus, the functional interactions between nicotinic acetylcholine and GABA ergic systems in cognitive control seems possible. The present study evaluated the possible role of nicotinic receptors of the dorsal hippocampus in muscimol [the GABA[A] receptor agonist] induced amnesia and muscimol state-dependent memory in adult male mice. This experimental study included 185 adult male NMRI mice. The drugs used in this study were muscimol and nicotine. The mice were anaesthetized and placed into a stereotaxic apparatus. Cannulas were implanted bilaterally in the CA1 regions of the dorsal hippocampus. After a seven day recovery period, the behavioral testing was performed by using inhibitory avoidance task. Prolongation of the step-down latency was measured as a criterion for the assessment of memory retention. Post-training administration of muscimol [0.15 and 0.075 micro g/mouse] decreased the memory retrieval. The memory impairment induced by muscimol [0.15micro g/mouse] was completely reversed by administration of muscimol or nicotine [1.5 and 1 micro g/mouse] on the test day, which suggests muscimol, induced state-dependent memory. These results suggested that nicotinic receptors of the dorsal hippocampus may play an important role in muscimol -induced amnesia and muscimol state-dependent memory
Subject(s)
Animals, Laboratory , Muscimol , Memory , Avoidance Learning , Amnesia , Hippocampus , MiceABSTRACT
Both endogenous cannabinoids and opiate substances have high levels of expression in the brain and may have important neuromodulatory functions. The present study evaluated the possible role of cannabinoid system of the dorsal hippocampus in morphine induced amnesia and morphine state-dependent memory in adult male mice. In this experimental study 255 adult male NMRI mice were anaesthetized and put into a stereotaxic device and cannula were implanted bilaterally in the CA1 regions of their dorsal hippocampus. Seven days after recovery from surgery, the behavioral testing was started by use of inhibitory avoidance task. In this study morphine and WIN55, 212-2 was used as opioid receptor agonist and cannabinoid receptor agonist respectively. Intra peritoneal [i.p.] administration of morphine immediately after training, decreased memory formation in a dose-dependent way [P<0.01]. Amnesia induced by post-training morphine injection was reversed by pre-test administration of the same dose of morphine that is due to a state-dependent effect [P<0.001]. Pre-test intra-CA1 administration of WIN55 212-2 after training, reversed amnesia induced by morphine and restored normal memory state [P<0.001]. The results of this study suggested that cannabinoid receptors of the dorsal hippocampal CA1 regions might play an important role in morphine-induced amnesia and morphine state-dependent memory