Quinolinic acid induces changes in expresión of coat proteins in areas of rat brain.

BORGONOVO J; SOSA MA; SELTZER A

Pinamar

Congreso; XX Reunión Annual de la Sociedad Argentina de Neuroquimica.; 2005

Clathrin- mediated endocytosis (CME) is the best-understood mechanism of macromolecule internalization. In brain, CME is required for recycling of membrane proteins after the release of neurotransmitters in the synapse. Clathrin coated vesicle (CCV) formation is triggered by recruitment of assembly proteins as adaptors AP-2 or AP180 onto membrane domains where different receptors are concentrated. Association of GABA (A) receptors and AP2 represents an important mechanism in the postsynaptic modulation of inhibitory synaptic transmission. Striatal quinolinic acid (QA) injections induce loss of GABAergic medium spiny projection neurons, mimicking Huntington disease. We measured expression of coat proteins in areas of rat brain .AP-2 (alpha 1 and 2 subunits) and AP-180 expression were studied by WB analysis by using specific monoclonal antibodies. We observed that QA induce a decrease of both subunits of AP-2 in striatum at 48 hr, whereas the proteins significantly increase in the cerebellum. Alpha 1 subunit was increased in hippocampus and no changes were observed in cortex or brainstem . AP180 expression was not modified. We concluded that QA alters selectively the transport via CCV in striatum and cerebellum, two main areas involved in the control of movement.