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• W2040252062 endingPage "182" @default.
• W2040252062 startingPage "170" @default.
• W2040252062 abstract "Development of neural circuitry relies on precise matching between correct synaptic partners and appropriate synaptic strength tuning. Adaptive developmental adjustments may emerge from activity and calcium-dependent mechanisms. Calcium/calmodulin-dependent protein kinase II (CaMKII) has been associated with developmental synaptic plasticity, but its varied roles in different synapses and developmental stages make mechanistic generalizations difficult. In contrast, we focused on synaptic development roles of CaMKII in a defined sensory-motor circuit. Thus, different forms of CaMKII were expressed with UAS-Gal4 in distinct components of the giant fiber system, the escape circuit of Drosophila , consisting of photoreceptors, interneurons, motoneurons, and muscles. The results demonstrate that the constitutively active CaMKII-T287D impairs development of cholinergic synapses in giant fiber dendrites and thoracic motoneurons, preventing light-induced escape behavior. The locus of the defects is postsynaptic as demonstrated by selective expression of transgenes in distinct components of the circuit. Furthermore, defects among these cholinergic synapses varied in severity, while the glutamatergic neuromuscular junctions appeared unaffected, demonstrating differential effects of CaMKII misregulation on distinct synapses of the same circuit. Limiting transgene expression to adult circuits had no effects, supporting the role of misregulated kinase activity in the development of the system rather than in acutely mediating escape responses. Overexpression of wild-type transgenes did not affect circuit development and function, suggesting but not proving that the CaMKII-T287D effects are not due to ectopic expression. Therefore, regulated CaMKII autophosphorylation appears essential in central synapse development, and particular cholinergic synapses are affected differentially, although they operate via the same nicotinic receptor." @default.
• W2040252062 created "2016-06-24" @default.
• W2040252062 creator A5021719922 @default.
• W2040252062 creator A5030891600 @default.
• W2040252062 creator A5037275128 @default.
• W2040252062 creator A5090286328 @default.
• W2040252062 date "2012-01-04" @default.
• W2040252062 modified "2023-10-15" @default.
• W2040252062 title "Constitutive Activation of Ca²⁺/Calmodulin-Dependent Protein Kinase II during Development Impairs Central Cholinergic Transmission in a Circuit Underlying Escape Behavior in<i>Drosophila</i>" @default.
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• W2040252062 doi "https://doi.org/10.1523/jneurosci.6583-10.2012" @default.
• W2040252062 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6621333" @default.
• W2040252062 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22219280" @default.
• W2040252062 hasPublicationYear "2012" @default.
• W2040252062 type Work @default.

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