Fruit fly study points way to prevention of neurodegeneration
A collaborative study by an international team of researchers at German Center for Neurodegenerative Diseases (DZNE) and Tokyo Institute of Technology (Tokyo Tech) revealed that neurons in the eye change on the molecular level when they are exposed to prolonged light. The innate neuronal property might be utilized to protect neurons from degeneration or cell death in the future.
Our ability to adapt to environmental changes has enabled our ‘synapses’, functional connections between neurons, to change. However, little was known about the signaling underlying such ‘synaptic plasticity’. Investigations of fruit flies now reveal details of the mechanisms behind synaptic plasticity.
As suggested by recent studies, changes in a region at the presynaptic membrane, described as the active zone, control synapse function. The research teams exposed living fruit flies, Drosophila, to different light regimes and then compared the active zones in the photoreceptors. The release of neurotransmitters to the postsynaptic neuron is controlled by T-shaped structures at the presynaptic membrane that tether synaptic vesicles. The teams tagged proteins that are crucial to these T-shaped structures to reveal drop in a subset of active zone proteins, while others remained unchanged. Further, they found that corresponding to the loss of structural proteins, the number of T-shaped structures was also reduced.
The synaptic changes that have been identified might reflect an innate neuronal property that leads to protection from excessive stimuli. By enhancing this property, it might be possible to protect neurons from degeneration. Further, the researchers were also able to identify that a feedback mechanism was responsible for these changes and that it relied on the signaling protein Wnt.
The results contribute to a better understanding of the molecular mechanisms underlying brain functions such as learning and memory. Future investigation may reveal how modifying the Wnt signal can be used to manipulate synaptic plasticity, with possible therapeutic applications for neurodegenerative or mental diseases.