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Topic: presynaptic terminals

Seminar
2 seminars
ePoster
1 ePoster

In Neuroscience and Cell Biology

Seminar · Optogenetics

Optogenetic silencing of synaptic transmission with a mosquito rhodopsin

Ofer Yizhar · Weizmann Institute

Thu, May 27, 2021 · 15:00 UTC

Long-range projections link distant circuits in the brain, allowing efficient transfer of information between regions and synchronization of distributed patterns of neural activity. Understanding the functional roles of defined neuronal projection pathways requires temporally precise manipulation of their activity, and optogenetic tools appear to be an obvious choice for such experiments. However, we and others have previously shown that commonly-used inhibitory optogenetic tools have low efficacy and off-target effects when applied to presynaptic terminals. In my talk, I will present a new so

Seminar · Cell Biology

Protein Synthesis at Neuronal Synapses

Erin Schuman · Max Planck Institute for Brain Research

Tue, Oct 27, 2020 · 15:00 UTC

The complex morphology of neurons, with synapses located 100’s of microns from the cell body, necessitates the localization of important cell biological machines and processes within dendrites and axons. Using expansion microscopy together with metabolic labeling we have discovered that both postsynaptic spines and presynaptic terminals exhibit rapid translation, which exhibits differential sensitivity to different neurotransmitters and neuromodulators. In addition, we have explored the unique mechanisms neurons use to meet protein demands at synapses, identifying the transcriptome and transla

ePoster · Neuroscience

Dopamine dysregulation in Parkinson's Disease

Chaitanya Chintaluri, Tim Vogels · Bernstein Conference 2024

Parkinson's disease (PD), characterized by the absence of dopamine in the striatum[1], is caused by the death of the substantia nigra pars compacta dopamine (SNcDA) neurons in the midbrain. The loss of these autonomously pacemaking[2] neurons is attributed to irreparable damage due to a dysregulation cascade starting from excess cytosolic dopamine and its decomposition into its aldehyde[3]. However, it is unresolved if dopamine dysregulation in SNcDA neurons themselves is the cause of PD or if it is a mere symptom. Here, we applied a recent theory of metabolic spikes[4] to SNcDA neurons, to