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This Article Full Text Full Text (PDF) All Versions of this Article: 564/2/661    most recent jphysiol.2004.061747v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Di Lazzaro, V Articles by Tonali, P Search for Related Content PubMed PubMed Citation Articles by Di Lazzaro, V Articles by Tonali, P

¹ Istituto di Neurologia, Università Cattolica, L.go A. Gemelli 8, 00168 Rome, Italy
² Unidad de Neurologia Funcional, Hospital Nacional de Paraplejicos, Finca la Peraleda, 45071 Toledo, Spain
³ Department of Neurology, ‘F. Tappeiner’ Hospital, Via Rossini 5, 39012 (BZ), Merano, Italy

Experimental studies have demonstrated that the GABAergic system modulates acetylcholine release and, through GABA_A receptors, tonically inhibits cholinergic activity. Little is known about the effects of GABA on the cholinergic activity in the human central nervous system. In vivo evaluation of some cholinergic circuits of the human brain has recently been introduced using a transcranial magnetic stimulation (TMS) protocol based on coupling peripheral nerve stimulation with TMS of the motor cortex. Peripheral nerve inputs have an inhibitory effect on motor cortex excitability at short intervals (short latency afferent inhibition, SAI). We investigated whether GABA_A activity enhancement by lorazepam modifies SAI. We also evaluated the effects produced by lorazepam on a different TMS protocol of cortical inhibition, the short interval intracortical inhibition (SICI), which is believed to be directly related to GABA_A activity. In 10 healthy volunteers, the effects of lorazepam were compared with those produced by quetiapine, a psychotropic drug with sedative effects with no appreciable affinity at cholinergic muscarinic and benzodiazepine receptors, and with those of a placebo using a randomized double-blind study design. Administration of lorazepam produced a significant increase in SICI (F_3,9 = 3.19, P = 0.039). In contrast to SICI, SAI was significantly reduced by lorazepam (F_3,9 = 9.39, P = 0.0002). Our findings demonstrate that GABA_A activity enhancement determines a suppression of SAI and an increase of SICI.

(Received 23 December 2004; accepted after revision 16 February 2005; first published online 17 February 2005)
Corresponding author V. Di Lazzaro: Istituto di Neurologia, Università Cattolica, L.go A. Gemelli 8, 00168 Rome, Italy. Email: vdilazzaro{at}rm.unicatt.it

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