Glutamate activates a K+ conductance increase in Aplysia neurons that appears to be independent of G proteins.
A study was made of the role of G proteins in the K+ conductance increases elicited by cholinergic and glutamatergic agonists in identified Aplysia neurons. The cholinergic response, previously shown to be G protein mediated, was occluded by dialysis with either nonhydrolyzable GTP analogs (GTP gamma S or Gpp(NH)p) or beryllium fluoride and was blocked by pertussis toxin as well as by dialysis with a nonhydrolyzable GDP analog (GDP beta S). In contrast, the glutamatergic response, studied simultaneously in the same cell, persisted throughout all of the above manipulations and hence does not appear to depend upon G protein activation. This characteristic differentiates the glutamatergic response from most other transmitter- or hormone-induced increases in K+ conductance elicited in either neurons or other cell types, whether vertebrate or invertebrate.[1]References
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