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Synapses between neurons are critical sites of modulation and plasticity, both in health and in disease. Therefore a detailed knowledge of the cellular mechanisms that regulate synaptic transmission at the level of individual synapses is prerequisite for understanding the operation of complex neuronal circuits. Recently we have devised a new way of investigating the events leading up to the release of chemical neurotransmitters at individual synapses. This is based on measuring, with fluorescence microscopy, rapid changes in the concentration of calcium ions, as well as the rate at which small vesicles containing chemical neurotransmitters are discharged. Using this approach we aim to investigate how different channels that transmit calcium ions into the terminal control the release of vesicles, how they influence synaptic plasticity, and how synapses are influenced by other modulatory neurotransmitters acting upon presynaptic terminals. Interestingly, some inherited cases of migraine, ataxia (incoordination caused by abnormal cerebellar function) and epilepsy are due to mutations of P/Q type of calcium channels. We investigate how these mutations affect calcium signals in nerve terminals, and how they affect neurotransmitter release. We hope that our results will allow us not only to establish how the desiase-linked mutations destabilise neurotransmission at the level of individual synapses, but also to understand how changes in basic synaptic parameters affect the function of neuronal circuits and behaviour.
Synapses between neurons are critical sites of modulation and plasticity, both in health and in disease. Therefore a detailed knowledge of the cellular mechanisms that regulate synaptic transmission at the level of individual synapses is prerequisite for understanding the operation of complex neuronal circuits. Recently we have devised a new way of investigating the events leading up to the release of chemical neurotransmitters at individual synapses. This is based on measuring, with fluorescence microscopy, rapid changes in the concentration of calcium ions, as well as the rate at which small vesicles containing chemical neurotransmitters are discharged. Using this approach we aim to investigate how different channels that transmit calcium ions into the terminal control the release of vesicles, how they influence synaptic plasticity, and how synapses are influenced by other modulatory neurotransmitters acting upon presynaptic terminals. Interestingly, some inherited cases of migraine, ataxia (incoordination caused by abnormal cerebellar function) and epilepsy are due to mutations of P/Q type of calcium channels. We investigate how these mutations affect calcium signals in nerve terminals, and how they affect neurotransmitter release. We hope that our results will allow us not only to establish how the desiase-linked mutations destabilise neurotransmission at the level of individual synapses, but also to understand how changes in basic synaptic parameters affect the function of neuronal circuits and behaviour.
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bioRxiv : the preprint server for biology (2024)
Research squareno. 1 (2023): 1091-13
semanticscholar(2021)
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