Nitric oxide in the dorsal hippocampal area is involved on muscimol state-dependent memory in the step-down passive avoidance test

Psychosis is a complex mental illness, characterised by positive, negative and cognitive symptoms. NMDA receptor antagonists have been established to induce behavioural as well as biochemical changes in rodents similar to psychotic patients. The aim of the present study was to investigate the effective dose and treatment period of ketamine to induce some behavioural changes. The results suggest that acute treatment of ketamine (50 and 100 mg/kg, i.p.) induced hyperlocomotor activity and reduced step down latency time in passive avoidance test, whereas in effective in forced swim test. Further, with the chronic administration of ketamine (50 and 100 mg/kg, i.p.) effective to produced hyperlocomotor activity, reduced the step down latency time in passive avoidance test and enhanced the immobility duration in forced swim test. Moreover, these behavioural changes persisted for 7 days after the treatment period. Thus, our findings suggest that the chronic administration of Ketamine (50 and 100 mg/kg, i.p.) potential to produce behavioural changes, would serve as an effective tool to screen antipsychotic drugs.

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NMDA receptors in the dorsal hippocampal area are involved in tramadol state-dependent memory of passive avoidance learning in mice

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2017-0228 ◽

2018 ◽

Vol 96 (1) ◽

pp. 45-50 ◽

Cited By ~ 7

Author(s):

Majid Jafari-Sabet ◽

Hamed Mofidi ◽

Mohammad-Sadegh Attarian-Khosroshahi

Keyword(s):

Passive Avoidance ◽

Memory Retrieval ◽

Memory Impairment ◽

Avoidance Task ◽

Memory Retention ◽

State Dependent ◽

Dorsal Hippocampal ◽

Opioid Receptor Agonist ◽

Hippocampal Area ◽

Μ Opioid Receptor

The precise neurobiological mechanisms of tramadol abuse underlying the cognitive function are still unknown. The aim of the present study was to examine the possible effects of intra-CA1 injections of N-methyl-d-aspartate (NMDA), a glutamate NMDA receptor (NMDAR) agonist, and d,l-2-amino-5-phosphonopentanoic acid (DL-AP5), a competitive NMDAR antagonist, on tramadol state-dependent memory. A single-trial step-down passive avoidance task was used for the assessment of memory retrieval in adult male NMRI mice. Post-training i.p. administration of an atypical μ-opioid receptor agonist, tramadol (2.5 and 5 mg/kg), dose-dependently induced impairment of memory retention. Pre-test injection of tramadol (2.5 and 5 mg/kg) induced state-dependent retrieval of the memory acquired under post-training administration of tramadol (5 mg/kg) influence. Pre-test intra-CA1 injection of NMDA (10−5 and 10−4 μg/mouse) 5 min before the administration of tramadol (5 mg/kg, i.p.) dose-dependently inhibited tramadol state-dependent memory. Pre-test intra-CA1 injection of DL-AP5 (0.25 and 0.5 μg/mouse) reversed the memory impairment induced by post-training administration of tramadol (5 mg/kg). Pre-test administration of DL-AP5 (0.25 and 0.5 μg/mouse) with an ineffective dose of tramadol (1.25 mg/kg) restored the retrieval and induced tramadol state-dependent memory. It can be concluded that dorsal hippocampal NMDAR mechanisms play an important role in the modulation of tramadol state-dependent memory.

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