Convulsions or flaccid paralysis induced by ruthenium red depending on route of administration

Ruthenium red was administered to mice and cats intracranially or intraperitoneally. In mice, intracisternal administration produced status epilepticus and tonic convulsions. In contrast, intraperitoneal administration induced total flaccid paralysis lasting several hours. These effects of Ruthenium red were partially blocked by the simultaneous administration of CaCl2. EDTA, at doses much greater than those of Ruthenium red, produced effects similar to those of the dye, which were also blocked by CaCl2 administration. In cats, intraventricular or intrahippocampal administration of Ruthenium red through a permanently implanted cannula produced after a few minutes subclinical paroxysmal activity in all brain regions recorded. After several hours the animals developed typical grand mal seizures. Intraperitoneal injection of Ruthenium red to cats did not affect the EEG but markedly depressed muscular activity. Administration of carbachol to the latter animals produced myoclonic responses. These results are discussed in relation to the inhibitory effect of Ruthenium red on Ca2+ transport and binding to membranes, and to the role of this cation on neurotransmitter release.