Motor disturbances and thalamic electrical power of frequency bands' improve by grape seed extract in animal model of Parkinson's disease.

OBJECTIVE: Previous studies showed that grape seed extract (GSE) is an excellent natural substance with potent antioxidant effect and free radical scavenger. This study aimed to evaluate the effect of GSE on motor dysfunctions and thalamic local Electroencephalography (EEG) frequency bands' powers in rats with Parkinson's disease (PD). MATERIALS AND METHODS: In this study 8 µg 6-hydroxydopamine (6-OHDA) dissolved in 2 µl normal saline containing 0.01% ascorbic acid was infused into right medial forebrain bundle (MFB) to make an animal model of PD. Rats with PD received four weeks GSE (100 mg/kg, p.o.) after apomorphine-induced rotation test. Spontaneous motor tests and also thalamic ventroanterior nucleus (AV) local EEG recording were done in freely moving rats in all groups. RESULTS: Chronic treatment of PD rats with GSE could influence potentially frequency bands' powers of thalamic VA and improve post-lesion motor dysfunctions significantly (p<0.05 and p<0.01, respectively). CONCLUSION: Our findings suggest that GSE modulates the CNS function and has beneficial effects on the direct and indirect striato-thalamo-cortical pathways in PD. GSE acts as a new and potent natural free radical scavenger which removes oxidants produced by neurotoxin 6-OHDA in brain. Therefore, it reinforces electrical power of remained thalamic VA neurons and thereby improves post-lesion motor disorders.

Effect of the GABAergic system on memory formation and state-dependent learning induced by morphine in rats.

In the present study, the effects of intraperitoneal injections of GABA(A) receptor agonist and antagonist on memory formation and morphine state-dependent learning were investigated in rats. Pre-training administration of morphine (1-15 mg/kg) in a step-down passive avoidance task induced state-dependent learning with impaired memory retrieval on the test day. The impairment of memory was restored after the pre-test administration of the same dose of morphine. The pre-test administration of the GABA(A) receptor agonist, muscimol (0.01, 0.05 and 0.1 mg/kg), significantly decreased state-dependent retrieval induced by pre-test morphine (5 mg/kg). The state-dependency effect of morphine (1 mg/kg) was significantly potentiated by the pre-test administration of the GABA(A) receptor antagonist, bicuculline (0.125, 0.25 and 0.5 mg/kg). Furthermore, the pre-training injection of muscimol (0.01 mg/kg) impaired memory retrieval which was restored by pre-test morphine (1, 3 and 5 mg/kg) administration. However, the pre-training administration of bicuculline did not affect retention by itself. In addition, amnesia induced by pre-training morphine (5 mg/kg) was significantly reversed in rats which had received pre-test injections of muscimol (0.01, 0.05 and 0.1 mg/kg). Pre-test injections of bicuculline (0.125, 0.25 and 0.5 mg/kg) significantly decreased morphine-induced amnesia. It is concluded that the GABA(A) receptor mechanisms may be involved in the memory formation and it is postulated that these receptors may play an important role in morphine state-dependent learning.