Brain-gut-microbiota axis: effect of basil oil on the gut microbiota and its contribution to the anticonvulsant properties

Abstract

Abstract Background Epilepsy is a chronic neurological condition that disrupts the normal functioning of the brain and it is characterized by seizures. Research suggests the involvement of the Brain-Gut-Microbiota axis in epilepsy. This study seeks to determine the role of the gut microbiota in the anticonvulsant effect of basil oil (BO) using antibiotic-depleted and altered mice against germ mice in PTZ induced seizure model. There has been ever growing interest to improve treatment outcome in epilepsy and also increase therapy options especially in the population of patients that do not attain seizure relief from available AEDs. According to research, gut microbiota can alter brain function and development and vice versa. This led to the study of the BGM axis and its involvement in neurological diseases such as epilepsy. Increasing evidence suggests that intestinal microbiota have effects on brain development and disrupting this delicate symbiotic balance existing between these two results in disease conditions. Also, the oil from Ocimum basilicum, BO has been proven scientifically to significantly block clonic seizures induced by PTZ and picrotoxin in seizure models. Methods The microbiota of mice were depleted or altered by administering cocktail antibiotics and individual antibiotics respectively. DNA was extracted from stool of mice and the 16S rRNA gene amplified in a quantitative RT-PCR. Amplicons were sequenced to determine the phylogenetic make-up of the bacteria involved. Metabolic profile of the serum and stool of mice were determined in a 1H NMR spectroscopy. Results Cocktail antibiotic pre-treatment significantly reversed the anticonvulsant effect of BO against frequency and duration of seizures but did not affect latency to seizure. The effect of BO in mice pre-treated with single antibiotics was lost against latency to seizures, frequency and duration compared to mice that received only BO. The phylogenetic make-up of antibiotic pre-treated groups showed distorted composition of the microbiota compared to the control group. Conclusion Depleted microbiota significantly reversed the anticonvulsant actions of BO. The concentrations of SCFAs in stool was higher than in serum. Administration of BO may not affect the distribution of microorganisms in the microbiota. The increased Firmicutes/Bacteroidetes ratio in groups with depleted microbiota may have enhanced the reversal of anticonvulsant actions of BO.