Role of Intrahippocampal Sigma Receptor in Inhibiting Seizure by Electroacupuncture in Rats

Abstract

Abstract

Background:

The opioid receptors in the hippocampus are very important in regulating epilepsy. Previous studies showed that kappa, delta, and mu opioid receptors in the hippocampus play an important role in epilepsy and electroacupuncture (EA) anticonvulsion.

Objective:

To investigate the effects of intrahippocampal sigma receptor on EA anticonvulsant.

Design and Setting:

A randomized controlled animal experiment was conducted at the Department of Neurology, The Second Affiliated Hospital of Qingdao University Medical College in China. A total of 64 male Wistar rats, weighing 280–300 g, were randomized to 6 groups: DTG [1,3,di(2-tolyl)guanidine] (n = 10), dextrorphan (n = 10), artificial cerebrospinal fluid (n = 10), EA + DTG (n = 10), EA+ dextrorphan (n = 14), and EA+ artificial cerebrospinal fluid (n = 10).

Intervention:

The rat seizure model was achieved by repeated electroconvulsive shock (500 V, 60 mA, 50 Hz sine waves clipped on both ears 3 times with interval of 5 minutes), and the ictal behavioral and electroencephalographic (EEG) epileptiform were recorded with biosensor and EEG equipment respectively throughout whole experiments. EA was given between Fengfu Point (GV 16) and Jinshuo Point (GV 8) with continuous waveforms of 130 Hz and 1 mA.

Main Outcome Measure:

The ictal behavioral and EEG epileptiform were recorded. The histopathological study confirmed locations of intrahippocampal microinjection of DTG, 8.27 nmol, or dextrorphan, 1.5 nmol.

Results:

The ictal behavioral and EEG epileptiform was induced in all cases. EA extenuated the ictal behavioral and EEG epileptiform. Microinjection of DTG, an agonist of sigma receptor, into the hippocampus reduced the epileptiform activities and enhanced the EA anticonvulsion significantly (P < .01), whereas dextrorphan, antagonist of the sigma receptor, provoked epileptiform activities and resulted in disappearance of inhibitory effects of EA on seizure (P < .05).

Conclusions:

The results suggested that intrahippocampal sigma receptor was involved in seizure and EA anticonvulsion, and activation of sigma receptor might suppress seizure and facilitated effects of EA anticonvulsion.