Hippocampal participation in the neuropeptide W regulation of food intake

BIANCONI SANTIAGO; MEZA HERNAN; MARIA EMILIA SANTILLÁN; MARIA BELEN PORETTI; HELGI B. SCHIOTH; VALERIA PAOLA CARLINI

Mar del Plata

Congreso; Reunión Conjunta de la Sociedad Argentina de Investigación Clínica (SAIC), la Sociedad Argentina de Inmunología (SAI) y la Sociedad Argentina de Fisiología (SAFIS); 2018

SAIC, SAI, SAFIS

Hippocampal participation in the neuropeptide W regulation of food intakeBianconi S1,4, Meza H1, Santillán ME1, Poretti MB2,4, Schiöth HB4, and Carlini VP1,2,4.1: Instituto de Fisiología Humana, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina. 2: Instituto de Investigaciones en Ciencias de la Salud (INICSA), CONICET and Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina.3: IFEC-CONICET, Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba.4: Functional Pharmacology, Department of Neuroscience, Uppsala University, Uppsala, Sweden.The neuropeptide W (NPW) is involved in the regulation of feeding behavior and energy homeostasis. The peptide and its receptor NPBWR1 are expressed in several regions of the brain including the hypothalamus and hippocampus (Hi). Intracerebroventricular administration of NPW can produce anorectic/orexigenic effect when is administered in the dark/light phase respectively and the hypothalamic injection also stimulates food intake. The Hi is classically associated with learning and memory processes; however, recent studies implicate this structure in the control of food intake regulation. We have previously found that intrahippocampal infusion of NPW30 improved the hippocampal-dependent memory and reduced the threshold to generate long term potentiation. Objective: to investigate the hippocampal role of NPW30 on feeding. Male adult free-feeding rats were infused into the hippocampus (0.5 μl in each site) 1h after the onset of dark phase (feeding phase) with artificial cerebrospinal fluid (Control group) and 24h later, with a single dose of NPW30 (0.3 or 3 nmol/μl) (n≈13/group). Food intake was measured 1, 4, 12 and 24 h after the infusions. Only the highest dose of NPW30 increased cumulative food intake at the 12h (NPW30, 3 nmol/μl: 20.73±1.48g vs. Control: 16.74±1.38g; P<0.05) and the 24h time points (NPW30, 3 nmol/μl: 26.82±1.00g vs. Control: 23.61±0.68g; P<0.05). We have previously found that intrahippocampal infusion of NPW30 in the light phase is anorectic. Both results are in the opposite direction of those obtained from the ICV or hypothalamic administration. Both anorectic and orexigenic effects are possible after hippocampal infusion of NPW30 depending on which moment of the day the infusion is performed, suggesting that NPW30 influence on hippocampal feeding regulation could be modulated by diurnally variable factors. Further investigations on the biochemical and physiological functions of NPW will help us to better understand the hippocampal role on feeding and energy homeostasis.