GHERSI MARISA SOLEDAD
Congresos y reuniones científicas
Título:
NEURONOSTATIN ADMINISTRATION IMPAIRS MEMORY AND INDUCES ANXIOLYTIC EFFECTS IN RATS.
Autor/es:
CARLINI VP, ; GHERSI M, ; GABACH L, ; SCHIÖTH HB, ; PEREZ MF, ; RAMIREZ OA,; FIOL DE CUNEO M,; R DE BARIOGLIO S.
Lugar:
Huerta Grande, Córdoba
Reunión:
Congreso; Segunda Reunión Conjunta de Neurociencias. IIRCN: XXV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias (SAN); 2010
Institución organizadora:
Sociedad Argentina de Investigación en Neurociencias (SAN)
Resumen:
A 13-amino acid peptide named neuronostatin
(NST) encoded in the somatostatin pro-hormone has been
recently reported. It is produced throughout the body, particularly
in brain areas that have significant actions over the
metabolic and autonomic regulation. The present study was
performed in order to elucidate the functional role of NST on
memory, anxiety-like behavior and food intake and the hippocampal
participation in these effects. When the peptide
was intra-hippocampally administered at 3.0 nmol/ul, it impaired
memory retention in both, object recognition and stepdown
test. Also, this dose blocked the hippocampal longterm
potentiation (LTP) generation. When NST was intrahippocampally
administered at 0.3 nmol/ul and 3.0 nmol/ul,
anxiolytic effects were observed. Also, the administration in
the third ventricle at the higher dose (3.0 nmol/ul) induced
similar effects, and both doses reduced food intake. The main
result of the present study is the relevance of the hippocampal
formation in the behavioral effects induced by NST, and
these effects could be associated to a reduced hippocampal
synaptic plasticity.
(NST) encoded in the somatostatin pro-hormone has been
recently reported. It is produced throughout the body, particularly
in brain areas that have significant actions over the
metabolic and autonomic regulation. The present study was
performed in order to elucidate the functional role of NST on
memory, anxiety-like behavior and food intake and the hippocampal
participation in these effects. When the peptide
was intra-hippocampally administered at 3.0 nmol/ul, it impaired
memory retention in both, object recognition and stepdown
test. Also, this dose blocked the hippocampal longterm
potentiation (LTP) generation. When NST was intrahippocampally
administered at 0.3 nmol/ul and 3.0 nmol/ul,
anxiolytic effects were observed. Also, the administration in
the third ventricle at the higher dose (3.0 nmol/ul) induced
similar effects, and both doses reduced food intake. The main
result of the present study is the relevance of the hippocampal
formation in the behavioral effects induced by NST, and
these effects could be associated to a reduced hippocampal
synaptic plasticity.
