AI Article Synopsis
- Mitragynine, derived from Kratom, has been shown to alter synaptic transmission in the hippocampus, but its specific effects on glutamatergic neurotransmission and synaptic plasticity remain unclear.
- Researchers investigated the involvement of AMPA and NMDA glutamate receptors in mitragynine's impact on synaptic changes by administering the substance to rats and assessing synaptic activity through recorded responses.
- The results indicated that mitragynine, along with the receptor antagonists (NBQX for AMPA and MK-801 for NMDA), disrupted baseline synaptic transmission and long-term potentiation (LTP), suggesting that mitragynine may act as a weak antagonist for both types of receptors without affecting paired-p
Article Abstract
Mitragynine, an indole alkaloid from the plant Mitragyna speciosa (Kratom), has been reported to modify hippocampal synaptic transmission. However, the role of glutamatergic neurotransmission modulating synaptic plasticity in mitragynine-induced synaptic changes is still unknown. Here, we determined the role of AMPA- and NMDA glutamate receptors in mitragynine-induced synaptic plasticity in the hippocampus. Male Sprague Dawley rats received either vehicle or mitragynine (10 mg/kg), with or without the AMPA receptor antagonist, NBQX (3 mg/kg), or the NMDA receptor antagonist, MK-801 (0.2 mg/kg). Field excitatory postsynaptic potentials (fEPSP) during baseline, paired-pulse facilitation (PPF) and long-term potentiation (LTP) were recorded in-vivo in the hippocampal CA1 area of anaesthetised rats. Basal synaptic transmission and LTP were significantly impaired after mitragynine, NBQX, and MK-801 alone, without an effect on PPF. Combined effects suggest a weak functional AMPA- as well as NMDA receptor antagonist action of mitragynine.
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| http://dx.doi.org/10.1016/j.bbr.2022.114169 | DOI Listing |
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