POSTNATAL NITRIC OXIDE INHIBITION MODIFIES NEUROTENSIN EFFECT ON ATPase ACTIVITY.

G. RODRÍGUEZ DE LORES ARNAIZ; A. ALVAREZ JULIÁ,; A. KEMLING; M. G. LÓPEZ ORDIERES

Charleston, Carolina sel Sur, EE.UU.

Congreso; XXXX Congreso de la Sociedad Americana de Neuroquímica (ASN); 2009

Sociedad Americana de Neuroquímica (ASN)

Postnatal nitric oxide inhibition modifies neurotensin effect onATPase activity. G. Rodríguez de Lores Arnaiz, A. Alvarez Juliá, A. Kemling, M. G. López Ordieres. Instituto de Biología Celular y Neurociencias "Prof. E. De Robertis”, Facultad de Medicina, Cátedra de Farmacología, Facultad de Farmacia y Bioquímica, UBA. Junín 956, 1113-Buenos Aires. glopez@ffyb.uba.ar In previous work the ability of peptide neurotensin to inhibit  neuronal Na⁺, K⁺-ATPase activity was described, an effect  involving high affinity neurotensin receptor (NTS1). Nitric oxide (NO) acts as a neurotransmitter or as a neuromodulator when it is synthesized by neuronal nitric oxide synthase (nNOS). Herein we evaluated neurotensin effect on cortical membranes isolated from Sprague-Dawley rats of either sex. Animals were injected at 3, 4 and 5 postnatal days with saline (control) or L-No-Arg, a nitric oxide synthase inhibitor (iNOS) and sacrificed 35 (juvenile) or 50 days (adult) later. The presence of neurotensin at 3.5 x 10^-8- 3.5 x 10^-6 M concentration decreased 6%-34% Na⁺, K⁺/-ATPase activity in synaptosomal membranes purified from control animals (female or male) whereas it failed to alter the enzyme in membranes obtained after iNOS treatment. Neurotensin at 1.0 x 10^-6 M concentration decreased only 12% [³H]-ouabain binding to membranes isolated from control animals whereas the effect was significantly higher in iNOS treated juvenile (- 37%) and adult (-53%) male rats. Results suggested that early postnatal NO dysfunction may exert a permanent change in neurotensin system that influence Na⁺, K⁺- ATPase activity.