کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3048012 | 1185070 | 2007 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Effects of GABAA and GABAB agonists on interhemispheric inhibition in man Effects of GABAA and GABAB agonists on interhemispheric inhibition in man](/preview/png/3048012.png)
ObjectiveAnimal studies on neurotransmitter systems that mediate interhemispheric inhibition (IHI) suggest that, (i) callosal transmission is regulated by presynaptic GABAB receptors, and (ii) GABAA-ergic neurones mediate early IHI, whereas GABAB-ergic neurones mediate later IHI. In humans the mechanism is unclear. Interactions between cortical inhibitory circuits suggest a postsynaptic GABAB-ergic mechanism. We will here test this hypothesis.MethodsShort-latency IHI (s-IHI) and long-latency IHI (l-IHI) were evaluated using the paired pulse paradigm before and under medication with (i) a GABAB-agonist (baclofen) in 17 subjects, and (ii) a GABAA-agonist (midazolam) in 10 subjects participating twice.ResultsBaclofen did not significantly enhance s-IHI. L-IHI between 20 and 50 ms was significantly strengthened, and obtained also at ISIs between 100 and 200 ms. Midazolam had no effect on s-IHI, whereas l-IHI was attenuated.ConclusionsOur results support the hypothesis, that l-IHI in humans is mediated by postsynaptic GABAB receptors. GABAA-ergic medication resulted in attenuation of l-IHI. Regarding s-IHI, our results are inconclusive and require further investigation.SignificanceThis is the first human study evaluating the effect of baclofen on IHI, indicating that l-IHI is mediated by GABAB-ergic neurones. Because interhemispheric interaction is now also been used as a therapeutic approach, understanding the underlying neurotransmitter systems will be increasingly relevant.
Journal: Clinical Neurophysiology - Volume 118, Issue 2, February 2007, Pages 308–316