INVESTIGADORES
SOSA ESCUDERO Miguel Angel
congresos y reuniones científicas
Título:
Excitotoxic lesion by hypoxia-ischemia alters expression and distribution of AP-2 coat proteins and expression of NMDA-R in certain areas of rat brain.
Autor/es:
TRONCOSO M; FORMICA X; SOSA MA; SELTZER A
Lugar:
Huerta Grande (Córdoba)
Reunión:
Congreso; XXVIII Congreso Anual de la Sociedad Argentina de Investigacion en Neurociencias; 2013
Resumen:
Introduction: AP-2
is a protein adaptor complex involved in the clathrin-mediated endocytosis,that
interacts with motifs of the cytoplasmic domain of glutamate receptors, as a
step in formation of clathrin coated vesicles. These receptors are known to be
important players in the excitotoxic lesions and in neurodegenerative diseases.
Aims: As the NMDA
receptors (NMDA-R) are recognized by AP-2, and assuming
that membrane-bound AP-2 is an index of endocytic activity, we studied the
expression and distribution of AP-2 in areas of rat brain subjected to
excitotoxic lesion by hypoxia-ischemia, and attempted to
correlate with expression of NMDA-R. Methods:
AtPND8 7 days old rats received hypoxia-ischemia treatment by ligature of
the left carotid artery followed by short exposure to 100% N2..Brain tissues
were obtained 72 h after lesion, and..a-2 subunit of AP-2 was evaluated by WB in
membranes and cytosols from hippocampus (HIP), striatum (ST) and motor cortex
(MC). Expression of NMDA-R was also studied in the membranes of the areas under
study. Results: We observed that
AP-2 bound to membranes tends to increase in the MC and HIP but not in the ST. In
turn, expression of the NMDA-R was also increased in the injured tissues .Conclusions:These results indicate that
certain brain areas undergo modifications in the endocytic machinery due to
excitotoxic lesion, altering possibly the distribution of NMDA-R and,
consequently, the glutamatergic synapses.