Abstract
Status epilepticus (SE) is one of the most significant complications in pediatric neurology. Clinical studies have shown positive effects of electroacupuncture (EA) as a therapeutic alternative in the control of partial seizures and secondary generalized clonic seizures. EA promotes the release of neurotransmitters such as GABA and some opioids. The present study aimed to evaluate the anticonvulsive and neuromodulatory effects of Shui Gou DM26 (SG_DM26) acupuncture point electrostimulation on the expression of the glutamate decarboxylase 67 (GAD67) enzyme and the glutamate transporter EAAC1 in an early SE model. At ten postnatal days (10-PD), male rats weighing 22–26 g were divided into 16 groups, including control and treatment groups: Simple stimulation, electrostimulation, anticonvulsant drug treatment, and combined treatment—electrostimulation and pentobarbital (PB). SE was induced with kainic acid (KA), and the following parameters were measured: Motor behavior, and expression of GAD67 and EAAC1. The results suggest an antiepileptic effect derived from SG DM26 point EA. The possible mechanism is most likely the increased production of the inhibitory neurotransmitter GABA, which is observed as an increase in the expression of both GAD67 and EAAC1, as well as the potential synergy between the neuromodulator effects of EA and PB.
Highlights
Status epilepticus (SE) is an acute epileptic condition characterized by repeated seizures
The results obtained in the present study show that the expression of the glutamate decarboxylase 67 (GAD67) enzyme and the glutamate transporter EAAC1 is not modified by simple stimulation, nor by the electro-stimulation of either the SG-DM26 point (KA-ACUP and kainic acid (KA)-EA) or the placebo points (KA-No-ACUP and KA-No-EA), in a model of SE induced by KA in immature rats
In the assessment of motor behavior, both the experimental and placebo groups maintained SE, demonstrating that the inhibitory effect of simple stimulation and electro-stimulation of the SG DM26 point does not act on GABA release during SE
Summary
Status epilepticus (SE) is an acute epileptic condition characterized by repeated seizures (partial or generalized, convulsive or non-convulsive). SE results from a failure of the mechanisms responsible for the termination of seizures, or from the initiation of mechanisms that lead to the development of seizures lasting more than 30 min [1]. The global incidence of seizures in neonates is estimated to be 50 to 100 cases per 100,000 births [2]. U.S and Mexico present with a first-time seizure disorder of different etiologies [3,4]. The immature nervous system is more likely to develop convulsive activity due to its structural and cellular liability.
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