nitroarginine and Paralysis

Iontophoretic application of L-arginine (L-Arg) resulted in a profound decrease in visually elicited and spontaneous activity in 22 of 77 (29%) cells in area 17 of the anaesthetized/paralysed cat. Duration was long, and cells did not recover pre-application activity levels, indicating permanent decline. This effect was obtained without change in the extracellularly recorded wave-form, demonstrating that this did not result from depolarization block. In the remaining 55 cells, application of L-Arg alone, at levels capable of eliciting inhibition as described above, was without effect. In 29 cells, L-Arg application was able to reverse the effect of inhibition of nitric oxide (NO) production. Populations of cells showing the depressive effect described above and those affected by NO modulation levels were mutually exclusive.

Topics: Action Potentials; Anesthesia, General; Animals; Arginine; Cats; Iontophoresis; Neurons; Nitric Oxide; Nitroarginine; Paralysis; Time Factors; Visual Cortex; Visual Perception

We have examined the responses of a population of 77 cells in the dorsal lateral geniculate nucleus (dLGN) of the anaesthetized, paralysed cat. Here the synthetic enzyme for the production of nitric oxide, nitric oxide synthase, is found only in the presynaptic terminals of the cholinergic input from the brainstem. In our hands, iontophoretic application of inhibitors of this enzyme resulted both in significant decreases in visual responses and decreased responses to exogenous application of NMDA, effects which were reversed by coapplication of the natural substrate for nitric oxide synthase, L-arginine, but not the biologically inactive isomer, D-arginine. Nitroprusside and S-nitroso-N-acetylpenicillamine (SNAP), nitric oxide donors, but not L-arginine, were able to increase markedly both spontaneous activity and the responsiveness to NMDA application. Furthermore, SNAP application facilitated visual responses. Responses of cells in animals without retinal, cortical and parabrachial input to the LGN suggest a postsynaptic site of action of nitric oxide. This modulation of the gain of visual signals transmitted to the cortex suggests a completely novel pathway for nitric oxide regulation of function, as yet described only in primary sensory thalamus of the mammalian central nervous system.

Topics: Afferent Pathways; Animals; Arginine; Cats; Electric Stimulation; Electroencephalography; Enzyme Inhibitors; gamma-Aminobutyric Acid; Geniculate Bodies; Iontophoresis; Models, Neurological; N-Methylaspartate; Nitric Oxide; Nitric Oxide Synthase; Nitroarginine; Nitroprusside; omega-N-Methylarginine; Paralysis; Penicillamine; Photic Stimulation; S-Nitroso-N-Acetylpenicillamine; Synapses; Time Factors; Visual Fields; Visual Perception