Tong C K, Chesler M
Department of Physiology and Neuroscience, NYU Medical Center, 550 First Avenue, New York, NY 10016, USA.
Brain Res. 1999 Jan 9;815(2):373-81. doi: 10.1016/s0006-8993(98)01059-2.
Activity-dependent extracellular pH shifts were studied in slices of the rat dorsal lateral geniculate nucleus (dLGN) using double-barreled pH-sensitive microelectrodes. In 26 mM HCO3--buffered media, afferent activation (10 Hz, 5 s) elicited an early alkaline shift of 0.04+/-0.02 pH units associated with a later, slow acid shift of 0.05+/-0.03 pH units. Extracellular pH shifts in the ventral lateral geniculate nucleus were rare, and limited to acidifications of approximately 0.02 pH units. The alkaline shift in the dLGN increased in the presence of benzolamide (1-2 microM), an extracellular carbonic anhydrase inhibitor. The mean alkaline shift in benzolamide was 0.10+/-0.05 pH units. In 26 mM HEPES-buffered saline, the alkaline response averaged 0.09+/-0.03 pH units. The alkaline shifts persisted in 100 microM picrotoxin (PiTX) but were blocked by 25 microM CNQX/50 microM APV. If stimulation intensity was raised in the presence of CNQX/APV, a second alkalinization arose, presumably due to direct activation of dLGN neurons. The direct responses were amplified by benzolamide, and blocked by either 0 Ca2+/EGTA, Cd2+ or TTX. In 0 Ca2+, addition of 500 microM-5 mM Ba2+ restored the alkalosis. Alkaline shifts evoked with extracellular Ba2+ were larger and faster than those elicited by equimolar Ca2+. In summary, synchronous activation in the dLGN results in an extracellular H+ sink, via a Ca2+-dependent mechanism, similar to activity-dependent alkaline shifts in hippocampus.
使用双管pH敏感微电极，在大鼠背外侧膝状核（dLGN）切片中研究了活动依赖性细胞外pH变化。在26 mM HCO₃⁻缓冲介质中，传入激活（10 Hz，5 s）引发了0.04±0.02 pH单位的早期碱化变化，随后伴有0.05±0.03 pH单位的缓慢酸化变化。腹外侧膝状核中的细胞外pH变化很少见，且仅限于约0.02 pH单位的酸化。在细胞外碳酸酐酶抑制剂苯甲酰胺（1 - 2 μM）存在的情况下，dLGN中的碱化变化增加。苯甲酰胺中的平均碱化变化为0.10±0.05 pH单位。在26 mM HEPES缓冲盐溶液中，碱化反应平均为0.09±0.03 pH单位。碱化变化在100 μM苦味毒（PiTX）存在时持续存在，但被25 μM CNQX/50 μM APV阻断。如果在CNQX/APV存在的情况下提高刺激强度，会出现第二次碱化，可能是由于dLGN神经元的直接激活。直接反应被苯甲酰胺放大，并被0 Ca²⁺/EGTA、Cd²⁺或TTX阻断。在无Ca²⁺的情况下，加入500 μM - 5 mM Ba²⁺可恢复碱中毒。细胞外Ba²⁺引起的碱化变化比等摩尔Ca²⁺引起的更大、更快。总之，dLGN中的同步激活通过一种Ca²⁺依赖性机制导致细胞外H⁺汇，类似于海马体中的活动依赖性碱化变化。
