Background: 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. Aims: In the present study, we investigated the effects of mitragynine on spatial learning and synaptic transmission in the CA1 region of the hippocampus. Methods: 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 Ca 2+ influx was also examined in cultured primary neurons from E16-E18 rats. Results/outcomes: 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 Ca 2+ influx elicited by glutamate application was inhibited in neurons pre-treated with mitragynine. Conclusions/interpretation: These data suggest that high doses of mitragynine (5 and 10 mg/kg) cause memory deficits, possibly via inhibition of Ca 2+ influx and disruption of hippocampal synaptic transmission and long-term potentiation induction.
Cerebral ischemia is a result of insufficient blood flow to the brain. It leads to limited supply of oxygen and other nutrients to meet metabolic demands. These phenomena lead to brain damage. There are two types of cerebral ischemia: focal and global ischemia. This condition has significant impact on patient’s health and health care system requirements. Animal models such as transient occlusion of the middle cerebral artery and permanent occlusion of extracranial vessels have been established to mimic the conditions of the respective type of cerebral ischemia and to further understand pathophysiological mechanisms of these ischemic conditions. It is important to understand the pathophysiology of cerebral ischemia in order to identify therapeutic strategies for prevention and treatment. Here, we review the neuropathologies that are caused by cerebral ischemia and discuss the mechanisms that occur in cerebral ischemia such as reduction of cerebral blood flow, hippocampal damage, white matter lesions, neuronal cell death, cholinergic dysfunction, excitotoxicity, calcium overload, cytotoxic oedema, a decline in adenosine triphosphate (ATP), malfunctioning of Na+/K+-ATPase, and the blood-brain barrier breakdown. Altogether, the information provided can be used to guide therapeutic strategies for cerebral ischemia.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease that is currently affecting 40-50 million people worldwide. It is generally recognized from its main symptom dementia, in which the patient undergoes a progressive decline in their cognitive memory. Recent studies have shown that medicinal plants such as Clitoria ternatea equipped with antioxidant properties has high potential in treating AD. The study was conducted using zebrafish model of AD induced with aluminium chloride for 28 days. The treatment dose of C. ternatea extract (4.34 mg/L) was then given for 14 days. The behaviour of the zebrafish were evaluated through memory testing by using a T-maze test and novel tank diving test. Histological studies were also performed. 50% of the zebrafish tested showed improvement in memory through the T-maze test after treatment with C. ternatea extract. Zebrafish model of AD treated with C. ternatea extract also shows a decrease in anxiety in the novel tank diving test. A significant increase of purkinje cells were also observed from the histological study after treatment with C. ternatea extract. Nucleus elongation of oligodendrocytes from zebrafish model of AD induced with aluminium chloride were improved when treated with the C. ternatea extract. In conclusion, it was found that C. ternatea extract exhibits strong potential for treating zebrafish model of AD induced with aluminium chloride.
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