A memory for extracellular Ca2+ by speeding recovery of P2X receptors from desensitization
| Autor: | S. P. Cook, K. D. Rodland, Edwin W. McCleskey |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Nervous system
Patch-Clamp Techniques Sensory system Stimulus (physiology) Kidney Article Adenosine Triphosphate Memory Ganglia Spinal medicine Extracellular Animals Humans Learning Neurons Afferent Receptor Ion channel Cells Cultured Nerve Endings Chemistry Receptors Purinergic P2 General Neuroscience Neuropeptides Nociceptors Rats Calcium Channel Agonists medicine.anatomical_structure Hyperalgesia Biophysics Nociceptor Calcium Neuroscience Free nerve ending Ion Channel Gating Mechanoreceptors Receptors Purinergic P2X3 |
| Zdroj: | The Journal of neuroscience : the official journal of the Society for Neuroscience. 18(22) |
| ISSN: | 0270-6474 |
| Popis: | Nerve endings of nociceptors (pain-sensing neurons) express an unusual subtype of ATP-gated ion channel, the P2X3 receptor, that rapidly desensitizes (20 min). Here we show that Ca2+, or certain other polyvalent cations, binds to an extracellular site on rat sensory neurons and can increase current through P2X3 channels more than 10-fold. Importantly, Ca2+facilitates P2X3 current to precisely the same level whether a transient Ca2+change occurred just before or several minutes before activating the channels with ATP. This memory for past changes in Ca2+is integrative in that a 90 sec Ca2+stimulus delivered just before an ATP application has the same effect as an earlier series of three, separated 30 sec Ca2+stimuli. These diverse phenomena are explained by a single mechanism: Ca2+speeds recovery of P2X channels from desensitization. Recovery follows an exponential growth curve that depends on the duration, but not the timing, of changes in recovery rate. Modulation of desensitization underlies a well described short-term memory in bacteria, and it might be similarly used in the nervous system. |
| Databáze: | OpenAIRE |
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