A cGMP-dependent protein kinase, encoded by the gene, regulates neurotransmission through changes in synaptic structure and function.

A cGMP-dependent protein kinase (PKG) encoded by the () gene regulates both synaptic structure (nerve terminal growth) and function (neurotransmission) through independent mechanisms at the larval neuromuscular junction (nmj). Glial is known to restrict nerve terminal growth, whereas presynaptic inhibits synaptic vesicle (SV) exocytosis during low frequency stimulation. Presynaptic also facilitates SV endocytosis during high frequency stimulation. 's effects on neurotransmission can occur independent of any changes in nerve terminal growth. However, it remains unclear if 's effects on neurotransmission affect nerve terminal growth. Furthermore, it's possible that 's effects on synaptic structure contribute to changes in neurotransmission. In the present study, we examined these questions using RNA interference to selectively knockdown in presynaptic neurons or glia at the larval nmj. Consistent with our previous findings, presynaptic knockdown of impaired SV endocytosis, whereas knockdown of glial had no effect on SV endocytosis. Surprisingly, we found that knockdown of either presynaptic or glial increased neurotransmitter release in response to low frequency stimulation. Knockdown of presynaptic did not affect nerve terminal growth, demonstrating that 's effects on neurotransmission does not alter nerve terminal growth. In contrast, knockdown of glial enhanced nerve terminal growth. This enhanced nerve terminal growth was likely the cause of the enhanced neurotransmitter release seen following knockdown of glial . Overall, we show that can affect neurotransmitter release by regulating both synaptic structure and function.