Involvement of amygdalar extracellular zinc in rat behavior for passive avoidance.
On the basis of the evidence that zinc is released from glutamatergic neuron terminals in the amygdala, the effect of chelation of amygdalar extracellular zinc on glutamate release from the neuron terminals was studied by using in vivo microdialysis. When the amygdala was perfused with 100 microM CaEDTA to chelate extracellular zinc, glutamate concentration in the perfusate was decreased significantly, whereas that tended to be increased by perfusion with 100 microM ZnEDTA as a control. The effect of CaEDTA on extracellular glutamate levels was different between the amygdala and hippocampus, implying that modulation of glutamate signaling by zinc is different between them. To evaluate chelation of zinc in rat behavior, perfusion of the amygdala with CaEDTA was started 40 min before behavioral test for passive avoidance. The behavior for passive avoidance was impaired during perfusion with CaEDTA. On the other hand, the behavior during perfusion with ZnEDTA was more rapidly developed than that with vehicle only. These results suggest that amygdalar extracellular zinc is involved in the behavior for passive avoidance.
Takeda
Atsushi
A
Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Shizuoka 422-8526, Japan. takedaa@u-shizuoka-ken.ac.jp
Minami
Akira
A
Yamaide
Rie
R
Oku
Naoto
N
D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology*; D004492:Edetic Acid / Q000494:pharmacology; D045604:Extracellular Fluid / Q000187:drug effects / Q000502:physiology*; D017551:Microdialysis / Q000379:methods; D051381:Rats; D015032:Zinc / Q000037:antagonists & inhibitors / Q000502:physiology*
D004492:Edetic Acid; D015032:Zinc