Publications by authors named "R Spehlmann"

The depressant effects of iontophoretically applied dopamine and noradrenaline on glutamate-induced neuronal firing in the amygdaloid complex of cats were significantly reduced 1 and 2 h after induction of a local epileptiform afterdischarge of the kind used in kindling. Neuronal excitation by glutamate and depression by GABA were not significantly changed. This suggests that kindling is associated with a reduction of the inhibitory effects of endogenous catecholamines.

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Microiontophoretic application of scopolamine and atropine usually induced or increased focal cortical slow waves of under 3 Hz and abolished or decreased focal fast waves of over 6 Hz whereas acetylcholine iontophoresis and electrical stimulation of the mesencephalic reticular formation had the opposite effect, suggesting that focal cortical slow waves may be due to the interruption of cholinergic input from the reticular formation.

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The effect of microiontophoretic application of GABA and its antagonist, picrotoxin, on the firing of neurons in the feline caudate nucleus (CN) was studied. Firing was elicited by stimulation of the CN a few millimeters from the recording site. Increasing ejection currents of GABA produced a dose-dependent decrease and eventual blockade of the firing of CN neurons.

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Because it is commonly believed that acetylcholine is a synaptic transmitter in the caudate nucleus and that the reduction of striatal biogenic amines in Parkinson's disease leads to acetylcholine supersensitivity in the caudate nucleus, we investigated the effects of the muscarinic blocking agent scopolamine on synaptic responses of neurons in the intact feline caudate nucleus and in the caudate nucleus depleted of dopamine by long-standing nigrostriatal lesions. In the intact caudate nucleus, micro-iontophoretic application of scopolamine selectively blocked the neuronal responses to stimulation of the caudate nucleus near the recording site without affecting the responses to stimulation of the sensorimotor cortex or the substantia nigra in the same fashion. This suggests that acetylcholine is a synaptic transmitter of caudate interneurons.

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