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2005). The modulation of the nucleoside tranporter by CAMK II raises the intriguing question of what could be its function in the synaptic process. , 2002). , 2004), since it belongs to a category of enzymes that when activated can remain in the active state for a long period. , 2002). A model for the participation of adenosine transporters and CAMK II in a long-term synaptic modification is shown in figure XXX. Activation of NMDA receptors could promote calcium influx and formation of the calcium/calmodulin complex which could then activate CAMK II.
P. & Kelso, S. R. (1990). Apparent desensitization of NMDA responses in Xenopus oocytes involves calcium-dependent chloride current. , 4, 53-60. Ma, Z. , Wahle, P. & Hollmann, M. (2007). Quantitative analysis of cotransfection efficiencies in studies of ionotropic glutamate receptor complexes. , 85, 99-115. Marchetti, C. & Gavazzo, P. (2003). Subunit-dependent effects of nickel on NMDA receptor channels. Brain Res Mol Brain Res, 117, 139-44. Marchetti, C. & Gavazzo, P. (2005). NMDA receptors as targets of heavy metal interaction and toxicity.
This mechanism of neurotransmitter release was first suggested by Haycock and collaborators (1978). In cultures of chick retina cells, the neurochemical features of GABA transport were investigated by do Nascimento and collaborators (1998b). , 1998b). The results of several investigators using autoradiographic methods to analyze [3H]-GABA content of specific cell populations of fish and amphibian retinas reinforced the idea that most of the excitatory amino acids (EAAs)-evoked [3H]GABA release in retinas of different species occurs via a sodium-dependent, carrier-mediated process (Yazulla, 1983; Yazulla & Kleinschmidt, 1982; Schwartz, 1982; Tapias & Arias, 1982; Moran & Pasantes-Morales, 1983; Yazulla & Kleinschmidt, 1983; Ayoub & Lam, 1984).