6533b7d9fe1ef96bd126c26f

RESEARCH PRODUCT

Nitric oxide-induced inhibition on striatal cells and excitation on globus pallidus neurons: a microiontophoretic study in the rat.

Giuseppe FerraroGiuseppe Di GiovanniVittorio La GruttaPierangelo Sardo

subject

MaleVasodilator AgentsAction PotentialsGlutamic AcidStriatumBiologyPharmacologyGlobus PallidusNitric OxideNitric oxidechemistry.chemical_compoundBasal gangliaPremovement neuronal activityAnimalsEnzyme InhibitorsRats WistarDose-Response Relationship DrugGeneral NeuroscienceGlutamate receptorIontophoresisCorpus StriatumRatsNitric oxide synthaseGlobus pallidusNG-Nitroarginine Methyl Esternervous systemchemistryMolsidomineExcitatory postsynaptic potentialbiology.proteinNeuroscience

description

Single units were recorded in the striatum and in the globus pallidus (GP) of urethane-anesthetized rats under microiontophoretic administration of either Nomega-nitro-L-arginine methyl ester (L-NAME, inhibitor of nitric oxide synthase), or 3-morpholino-sydnonimin-hydrocloride (SIN-1, nitric oxide, NO donor). A steady baseline firing of sporadically discharging striatal neurons (basal firing rate <0.1 spikes/s) was evoked by a pulsed microiontophoretic ejection of glutamate. On striatal neurons, microiontophoretic application of SIN-1 induced a current-dependent inhibition (11/13), whereas L-NAME administration produced a clear excitation (9/9). On GP cells, the administration of SIN-1 had excitatory effects (10/15), whereas the administration of L-NAME reduced the neuronal activity (6/6). We hypothesize that NO could exert an intrinsic regulatory action on the activity of both striatal and GP cells.

10.1016/s0304-3940(03)00350-1https://pubmed.ncbi.nlm.nih.gov/12759174