The Role of Calcium in Vesicle Priming and Exocytosis During Neurotransmitter Release |
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| Air date: | Wednesday, October 31, 2007, 3:00:00 PM |
| Category: | Wednesday Afternoon Lectures |
| Runtime: | 75 minutes |
| NLM Title: | The role of calcium in vesicle priming and exocytosis during neurotransmitter release [electronic resource] / Erwin Neher. |
| Series: | NIH director's Wednesday afternoon lecture series |
| Author: | Neher, Erwin. National Institutes of Health (U.S.) |
| Publisher: | [Bethesda, Md. : National Institutes of Health, 2007] |
| Other Title(s): | NIH director's Wednesday afternoon lecture series |
| Abstract: | (CIT): Synaptic transmission is a multi-step process, which involves Ca++ influx into the nerve terminal, Ca-dependent exocytosis, and postsynaptic transmitter action. When synaptic strength changes during 'plasticity' this can be a consequence of changes in any of these steps. Unfortunately, most nerve terminals are very small and not readily accessible to detailed investigation, such that it is usually very difficult to assign a given change to one of the molecular steps involved. More recently, however, it was discovered that a specialized synapse in the auditory pathway, the 'Calyx of Held', has presynaptic terminals, which are large enough that quantitative biophysical techniques can be applied. Particularly, the postsynaptic current can be measured precisely, while the presynaptic calcium concentration ([Ca++]) can be manipulated in a controlled fashion either by opening and closing of Ca++ channels or by photoreleasing Ca++ from a chemically caged form. Furthermore, [Ca++] can be measured by introducing fluorescent Ca++ indicators into the terminal. Using these experimental possibilities, we have studied the role of Ca++ and other second messengers in short-term changes of synaptic strength. We found that the concentration of free calcium ([Ca++]i) has at least three roles in neurotransmitter release and its modulation: i it triggers release within microdomains of highly elevated [Ca++]i around open channels ii it enhances the supply of new vesicles during ongoing activity and after short-term depression iii during high-frequency stimulation action potentials become more efficient in eliciting exocytosis due to the buildup of 'residual Calcium', and to facilitation of Ca-current. |
| Subjects: | Calcium Signaling--physiology Exocytosis--physiology Neurotransmitter Agents--secretion Synaptic Vesicles--physiology |
| Publication Types: | Government Publications Lectures |
| Download: | Download
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| NLM Classification: | QV 126 |
| NLM ID: | 101322980 |
| CIT File ID: | 14115 |
| CIT Live ID: | 6198 |
| Permanent link: | http://videocast.nih.gov/launch.asp?14115 |
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Enhanced Audio Podcast | 1:08:24 |
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Enhanced Video Podcast | 1:08:24 | |