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

Abstract

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 and 10 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.

Cross state-dependency of learning between 5-HT1A and/or 5-HT7 receptor agonists and muscimol in the mouse dorsal hippocampus

“…On the other hand, our previous studies and those of other investigators have revealed that both consolidation and retrieval of one-trial avoidance are regulated by CA1 μ-opioid receptors, CA1 alpha-2 receptors, CA1 muscarinic ACh receptors, CA1 CB1 receptors, CA1 GABA-A receptors and 5HT1A receptors, and require both activity of CAMKII, ERK, PKA and CREB in the hippocampus and in other brain regions (Izquierdo et al, 2006;Jafari-Sabet, 2011;Jafari-Sabet and Karimi, 2017;Jafari-Sabet et al, 2013, 2018a, 2018bMahgoub et al, 2006;Phelps, 2004;Zarrindast et al, 2006).…”

“…It is well established that CA1 regions of the hippocampus are crucial for memory formation (Ranganath, 2019) and also memory consolidation and retrieval in one-trial inhibitory avoidance (Izquierdo et al, 2006; Jafari-Sabet, 2006; Jafari-Sabet et al, 2013, 2018a, 2018b).…”

The Role of NMDAR and BDNF in Cognitive Dysfunction Induced by Different Microwave Radiation Conditions in Rats

“…NMDARs present on the presynaptic and postsynaptic membrane bound with glutamate released from presynaptic terminals to regulate synaptic plasticity [6,13]. NMDARs are composed of NR1 and NR2 or NR3 subunits, among which NR2A and NR2B play key roles in activity-dependent synaptic plasticity [51]. Wang H [23] studied the effects of 2.856 GHz radiation with an average power density of 2.5, 5 or 10 mW/cm 2 for 6 min/day (5 d/week, up to 6 weeks) on NMDARs expressions and phosphorylation.…”

State-dependent memory and its modulation by different brain areas and neurotransmitters

“…Nonetheless, variations of this balance in each direction can potentiate state-dependent memory. For instance, cholinergic signalings of state-dependent memory involved both inhibiting cholinergic activity by scopolamine and growing cholinergic activity by physostigmine (Jafari-Sabet et al, 2018[ 31 ]). Additionally, opiates support state-dependent memory and of all types of opioid receptors, morphine stimulated µ-receptors to appear to be the maximum effective (Zarrindast et al, 2006[ 87 ]).…”