In neostriatal slices pretreated with sodium pentobarbital (100 microM) and 4-aminopyridine (50 microM), intrastriatal stimulation elicited EPSPs followed by a slowly decaying depolarization which lasted about 200 ms and was associated with a membrane conductance increase and a suppression of spike potentials. This depolarizing inhibitory synaptic action could be blocked by picrotoxin (50 microM) or bicuculline (50 microM). The reversal potential for the slowly decaying depolarization was -57 to -62 mV, i.e. it was positive with respect to the resting membrane potential (mean = -67 mV). GABA, injected into the tissue in the vicinity of the recording electrode by pressure application, or added to the perfusate (10 microM -1 mM), depolarized the cells and reduced both the membrane resistance and the amplitude of EPSPs. The reversal potential of GABA depolarization was found in a potential range approximating that of the slowing decaying depolarization. These results are compatible with the assumption that GABA is the transmitter of an intrinsic inhibition in rat neostriatum, but indicate that GABA-mediated IPSPs of neostriatal cells in vitro are depolarizing at the resting membrane potential. The possible reasons for this are discussed.

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In seven women and two men with Parkinson's disease, Hoehn and Yahr stage 1 or 2, the effect of repetitive transcranial magnetic stimulation (rTMS) was evaluated. Primary endpoint outcome measure was the changing of the motor items of the Unified Parkinson's Disease Rating Scale (subscale III of UP-DRS) 24 h after stimulation. Kinesiologic tests and writing samples were secondary outcome measures. After discontinuing all medication, stimulation was performed with 5 Hz at 90% of the motor threshold over the primary motor cortex of the more affected. There were 2250 stimuli applied, divided into 15 trains at intervals of 10 s. The identical treatment of the opposite side served as control treatment. Only treatment of the more affected side resulted in a significant improvement of the clinical symptoms of 46% as assessed by the UPDRS (p < 0.02). This effectiveness differed significantly from the control treatment (21%, p < 0.02). The kinesiological testing did not show any significant speeding of movements (p > 0.05). Some patients showed a normalisation of the previously disturbed handwriting specimen. These data confirm the previous observation that rTMS of primary motor regions leads to at least temporary clinical improvement of symptoms in patients with Parkinson's disease.

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