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Concomitant alterations of physiological and developmental plasticity in Drosophila CaM kinase II-inhibited synapses
J Wang1, J J Renger, L C Griffith
1Department of Biological Sciences, University of Iowa, Iowa City 52242.
Abstract:
Ca2+/calmodulin-dependent protein kinase II (CaM kinase) has been implicated in neural plasticity that underlies learning and memory processes. Transformed strains of Drosophila, ala1 and ala2, expressing a specific inhibitor of CaM kinase are known to be impaired in an associative conditioning behavioral paradigm. We found that these transformants had altered short-term plasticity in synaptic transmission along with abnormal nerve terminal sprouting and directionality of outgrowth. These results represent an interesting parallel with the activity-dependent regulation of synaptic physiology and morphology by the cAMP cascade in Aplysia and Drosophila. In contrast to the learning mutants dunce and rutabaga, which are defective in the cAMP cascade, inhibition of CaM kinase in ala transformants caused increased sprouting at larval neuromuscular junctions near the nerve entry point, rather than altering the higher order branch segments. In addition, synaptic facilitation and potentiation were altered in a manner different from that observed in the cAMP mutants. Furthermore, synaptic currents in ala transformants were characterized by greater variability, suggesting an important role of CaM kinase in the stability of transmission.
Insights
Calcium/calmodulin-dependent protein kinase II (CaM kinase) inhibition in Drosophila alters synaptic plasticity and nerve terminal sprouting. This suggests CaM kinase is crucial for synaptic stability and learning.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Ca2+/calmodulin-dependent protein kinase II (CaM kinase) is involved in neural plasticity, learning, and memory.
- Drosophila strains ala1 and ala2, which inhibit CaM kinase, show impaired associative conditioning.
- Previous studies linked cAMP cascade to synaptic plasticity and morphology in Aplysia and Drosophila.
Purpose of the Study:
- To investigate the role of CaM kinase in synaptic transmission, plasticity, and nerve terminal morphology in Drosophila.
- To compare the effects of CaM kinase inhibition with known cAMP cascade mutants (dunce, rutabaga).
Main Methods:
- Utilized transformed Drosophila strains (ala1, ala2) with specific CaM kinase inhibitors.
- Analyzed short-term plasticity in synaptic transmission.
- Examined nerve terminal sprouting and outgrowth directionality at larval neuromuscular junctions.
- Assessed synaptic facilitation, potentiation, and synaptic currents.
Main Results:
- CaM kinase inhibition led to altered short-term synaptic plasticity and abnormal nerve terminal sprouting near the nerve entry point.
- Sprouting patterns differed from cAMP mutants, which affected higher-order branches.
- Synaptic facilitation and potentiation were altered differently compared to cAMP mutants.
- Synaptic currents in ala transformants exhibited increased variability, indicating a role in transmission stability.
Conclusions:
- CaM kinase plays a significant role in regulating synaptic physiology and morphology, distinct from the cAMP cascade.
- CaM kinase is important for the stability of synaptic transmission.
- These findings highlight CaM kinase's contribution to neural plasticity underlying learning and memory.