Abstract
Cognitive dysfunction is just one of the detrimental consequences associated with ketamine abuse. Increasing evidence indicates that ketamine abuse induces tau hyperphosphorylation and thus leads to memory impairment
Highlights
Cognitive dysfunction is just one of the detrimental consequences associated with ketamine abuse
We explored the time-dependent effects of ketamine with and without ethanol on the mRNA expression levels of the tau hyperphosphorylation related genes (GSK3β and phosphatase 2A (PP2A)) and Aβ deposition related gene (BACE1) in the hippocampus and striatum of the rats using qRT-PCR
As shown in (Figure 1), compared with the control group, treatment with ketamine (30 mg/kg; 3 months) significantly increased the levels of all three mRNA in rat hippocampus, increasing GSK3β mRNA by 48.12% (Figure 1A), p = 0.026 versus K30+E; 3 months), PP2A mRNA by 64.43% (Figure 1B), p = 0.0008 versus control, p = 0.0013 versus K30+E; 3 months), and BACE1 mRNA by 23.81% (Figure 1C), p = 0.0005 versus K30; 6 months)
Summary
Cognitive dysfunction is just one of the detrimental consequences associated with ketamine abuse. Increasing evidence indicates that ketamine abuse induces tau hyperphosphorylation and leads to memory impairment. Upon three consecutive days of the administration, recreational ketamine users display semantic memory impairment and dissociative and schizotypal symptomatology, associated with ketamine’s action through NMDA receptors [4,5]. Studies have shown that ketamine’s use at an anesthetic or sub-anesthetic dose could impair the cognitive processes involved in learning and memory, suggesting that nonassociative taste memories may be disrupted by NMDA receptor blockade [6,7]. Current animal research indicates that repeated ketamine exposure augmented NMDA receptor subunit gene expression, notably subunit 1 (NMDAR1 or GluN1). Full sequencing of NMDA receptor genes may help to understand the individual’s vulnerability to ketamine abuse [8]
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