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- Title
Mitragynine (Kratom) impairs spatial learning and hippocampal synaptic transmission in rats.
- Authors
Hassan, Zurina; Suhaimi, Farah W; Ramanathan, Surash; Ling, King-Hwa; Effendy, Mohamad A; Müller, Christian P; Dringenberg, Hans C
- Abstract
<bold>Background: </bold>Mitragynine is the major alkaloid of Mitragyna speciosa (Korth.) or Kratom, a psychoactive plant widely abused in Southeast Asia. While addictive effects of the substance are emerging, adverse cognitive effects of this drug and neuropharmacological actions are insufficiently understood.<bold>Aims: </bold>In the present study, we investigated the effects of mitragynine on spatial learning and synaptic transmission in the CA1 region of the hippocampus.<bold>Methods: </bold>Male Sprague Dawley rats received daily (for 12 days) training sessions in the Morris water maze, with each session followed by treatment either with mitragynine (1, 5, or 10 mg/kg; intraperitoneally), morphine (5 mg/kg; intraperitoneally) or a vehicle. In the second experiment, we recorded field excitatory postsynaptic potentials in the hippocampal CA1 area in anesthetized rats and assessed the effects of mitragynine on baseline synaptic transmission, paired-pulse facilitation, and long-term potentiation. Gene expression of major memory- and addiction-related genes was investigated and the effects of mitragynine on Ca2+ influx was also examined in cultured primary neurons from E16-E18 rats.<bold>Results/outcomes: </bold>Escape latency results indicate that animals treated with mitragynine displayed a slower rate of acquisition as compared to their control counterparts. Further, mitragynine treatment significantly reduced the amplitude of baseline (i.e. non-potentiated) field excitatory postsynaptic potentials and resulted in a minor suppression of long-term potentiation in CA1. Bdnf and αCaMKII mRNA expressions in the brain were not affected and Ca2+ influx elicited by glutamate application was inhibited in neurons pre-treated with mitragynine.<bold>Conclusions/interpretation: </bold>These data suggest that high doses of mitragynine (5 and 10 mg/kg) cause memory deficits, possibly via inhibition of Ca2+ influx and disruption of hippocampal synaptic transmission and long-term potentiation induction.
- Subjects
SOUTHEAST Asia; LONG-term potentiation; NEURAL transmission; EXCITATORY postsynaptic potential; SPRAGUE Dawley rats; KRATOM; DRUG side effects
- Publication
Journal of Psychopharmacology, 2019, Vol 33, Issue 7, p908
- ISSN
0269-8811
- Publication type
journal article
- DOI
10.1177/0269881119844186