Abstract
Synaptic transmission is highly plastic and subject to regulation by a wide variety of neuromodulators and neuropeptides. In the present study, we have examined the role of isoforms of the cytochrome b561 homologue called no extended memory (nemy) in regulation of synaptic strength and plasticity at the neuromuscular junction (NMJ) of third instar larvae in Drosophila. Specifically, we generated two independent excisions of nemy that differentially affect the expression of nemy isoforms. We show that the nemy 45 excision, which specifically reduces the expression of the longest splice form of nemy, leads to an increase in stimulus evoked transmitter release and altered synaptic plasticity at the NMJ. Conversely, the nemy 26.2 excision, which appears to reduce the expression of all splice forms except the longest splice isoform, shows a reduction in stimulus evoked transmitter release, and enhanced synaptic plasticity. We further show that nemy 45 mutants have reduced levels of amidated peptides similar to that observed in peptidyl-glycine hydryoxylating mono-oxygenase (PHM) mutants. In contrast, nemy 26.2 mutants show no defects in peptide amidation but rather display a decrease in Tyramine β hydroxylase activity (TβH). Taken together, these results show non-redundant roles for the different nemy isoforms and shed light on the complex regulation of neuromodulators.
Highlights
The strength of transmitter release is highly plastic and can be modulated both acutely and chronically
Since the effect of dietary octopamine was specific to nemy26.2 mutants, these results suggest that the rescue of synaptic function in octopamine fed nemy26.2 mutants must result from regulated release of octopamine from secretory vesicles
We found that nemy isoforms differentially affect peptidyl-glycine hydryoxylating mono-oxygenase (PHM) and Tyramine β hydroxylase activity (TβH) function and may indirectly influence some, or all, of the synapses that are modulated by amidated neuropeptides or octopamine
Summary
The strength of transmitter release is highly plastic and can be modulated both acutely and chronically. The modulation of synaptic strength in response to specific inputs facilitates learned behaviours and allows synapses to synchronize their outputs to specific environmental cues. Synaptic strength may be modulated by the action of various neuromodulators including neuropeptides and biogenic amines such as dopamine, octopamine and serotonin, which exert. The modulation of synaptic strength by such neuromodulators facilitates the integration and co-ordination of multiple inputs. In this manner, neuromodulators play an essential role in regulating synaptic plasticity, which is essential for the survival of an organism in an ever-changing environment. It is not surprising that there has been considerable interest in understanding the mechanisms by which neuromodulators regulate synaptic plasticity and behaviour
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