Amplification of calcium signals at dendritic spines provides a method for CNS quantal analysis

• Published in: Canadian journal of physiology and pharmacology Vol. 77; no. 9; pp. 651 - 659
• Main Authors: Wang, Sabrina, Prange, Oliver, Murphy, Timothy H
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Ottawa, Canada NRC Research Press 10.10.1999; National Research Council of Canada; Canadian Science Publishing NRC Research Press
• Subjects: Animals; Biochemistry and metabolism; Biological and medical sciences; Brain - physiology; Calcium; Calcium - metabolism; Calcium Signaling; Central nervous system; Dendrites - metabolism; Female; Fundamental and applied biological sciences. Psychology; Magnesium - physiology; Nervous system; Pregnancy; Rats; Receptors, N-Methyl-D-Aspartate - physiology; Synapses; Synaptic Transmission; Vertebrates: nervous system and sense organs; Cerebral cortex; Calcium; Rat; Rodentia; Glutamate receptor; Ionic current; Vertebrata; Mammalia; Synaptic transmission; Dendritic spine; NMDA receptor; Neurotransmission; Release; Brain (vertebrata)
• ISSN: 0008-4212; 1205-7541
• DOI: 10.1139/y99-073

It has been proposed that the small volume of a dendritic spine can amplify Ca 2+ signals during synaptic transmission. Accordingly, we have performed calculations to determine whether the activation of N-methyl- D -aspartate (NMDA) type glutamate receptors during synaptic transmission results in significant elevation in intracellular Ca 2+ levels, permitting optical detection of synaptic signals within a single spine. Simple calculations suggest that the opening of even a single NMDA receptor would result in the influx of ~ 310 000 Ca 2+ ions into the small volume of a spine, producing changes in Ca 2+ levels that are readily detectable using high affinity Ca 2+ indicators such as fura-2 or fluo-3. Using fluorescent Ca 2+ indicators, we have imaged local Ca 2+ transients mediated by NMDA receptors in spines and dendritic shafts attributed to spontaneous miniature synaptic activity. Detailed analysis of these quantal events suggests that the current triggering these transients is attributed to the activation of <10 NMDA receptors. The frequency of these miniature synaptic Ca 2+ transients is not randomly distributed across synapses, as some synapses can display a >10-fold higher frequency of transients than others. As expected for events mediated by NMDA receptors, miniature synaptic Ca 2+ transients were suppressed by extracellular Mg 2+ at negative membrane potentials; however, the Mg 2+ block could be removed by depolarization.Key words: miniature release, N-methyl- D -aspartate (NMDA), calcium, glutamate, spine.