Timed Changes of Synaptic Zinc in the Bed Nucleus of Medial Extended Amygdala in the Kainic Acid Model of Epilepsy are Suggestive of Reactive Neuroplasticity

PERENO, G; BALASZCZUK, V; BELTRAMINO, C

BIOCELL

Biocell

Lugar: Mendoza; Año: 2007 vol. 31 p. 97 - 97

0327-9545

Repeated seizures induce permanent alterations of the brain in experimental models and patients with intractable temporal lobe epilepsy (TLE). 15% of brain zinc is in presynaptic vesicles containing glutamate, and is co-released with it, increasing its effects on postsynaptic excitatory neuroreceptors. The changes in Zinc density in  the Bed Nucleus of Medial Extended Amygdala (BSTM), induced by  Kainic Acid as a model of TLE was studied. Adult male rats (n=4 per group) were perfused every 10 days after KA ip injection  up to 4 months. Controls were injected with saline. The brains were processed by the Timm's method to reveal synaptic Zinc, and analysed by densitometry. Images were captured  with a Zeiss microscope and a  Leica videocamera, using the  KS Lite v2.00 program to determine the grey value difference between control and experimental  animals. Student t test was used  for statistics, with a p < 0.05 as a significance limit. Results: normal dark  staining was seen in  BSTM sections of control animals. At 10 days post KA inj. a dramatic loss of staining was observed. A slow but steady recovery of Zinc density can be followed in the 4 months period studied.  We found significative loss of synaptic Zinc in from 10 days to 1 month exp animals, not observed in  the 2 to 4 months animals. This indicates an acute loss of synaptic Zinc in status epilepticus and a chronic neuroplasticity process of recovery through sprouting  in a 4 month period  post KA induced TLE.