Neuroscience 2004 Abstract
| Presentation Number: | 656.12 |
|---|---|
| Abstract Title: | Dependence on metabotropic glutamate receptor activation but not Ca<sup>2+</sup> entry in the genesis of novel convulsant-induced bursting in rat spinal cord. |
| Authors: |
Hochman, S.*1
; Wilhelm, J. L.1
; Dougherty, K. J.1
; Machacek, D.1
; Aduonum, A.1,2
1Dept Physiol, Emory Univ Sch Med, Atlanta, GA 2GA, 615 Michaesl St, 30322, |
| Primary Theme and Topics |
Motor Systems - Spinal Cord -- Physiology |
| Secondary Theme and Topics | Motor Systems<br />- Spinal Cord<br />-- Damage and recovery |
| Session: |
656. Spinal Cord: Physiology and Anatomy Poster |
| Presentation Time: | Tuesday, October 26, 2004 11:00 AM-12:00 PM |
| Location: | San Diego Convention Center - Hall A-H, Board # FF16 |
| Keywords: | RHYTHM, SYNCHRONY, MGLUR, CALCIUM CHANNEL |
Using the isolated in vitro rat spinal cord, Dougherty et al (2001; SFN Abst) showed that spike broadening following application of the convulsants TEA & 4AP resulted in the emergence of novel forms of synchronous bursting throughout the spinal neuraxis: (1) bursting mediated via electrical transmission, independent of ionotropic receptors, and (2) bursting mediated chemically in the absence of external Ca2+ but requiring release from internal Ca2+ stores. The present study further characterized these bursting patterns. Motor activity was recorded from various ventral roots in the isolated neonatal rat spinal cord.
(1) Synchronous activity induced by bicuculline/strychnine/5-HT but blocked by the glutamate receptor blockers CNQX/APV re-emerged after applying TEA/4AP. Activity block by carbenoxolone implicated electrical coupling. Here, we support this conclusion by showing that blockade of all known voltage-gated Ca2+ channels does not block the TEA/4AP evoked synchronous activity. This bursting was blocked with the broad-spectrum mGluR antagonist MCPG (n=3/3) & the group I mGluR subtype 1 antagonist AIDA (n=3/4).
(2) Synchronous activity induced following application of TEA/4AP in nominally Ca2+-free saline initiates an intracellular Ca2+ store and CNQX/APV-sensitive bursting. Here we show that extracellular Ca2+ is not required since block of cell surface Ca2+ receptors does not alter bursting. Thus, epileptiform activity via chemical synaptic transmission occurs in the absence of external Ca2+ entry. Interestingly this bursting was blocked with the metabotropic glutamate antagonist MCPG implicating mGluRs in the Ca2+ release from internal stores.
Thus, 2 novel forms of spinal epileptiform activity are expressed independent of extracellular Ca2+ but require activation of metabotropic glutamate receptors.
(1) Synchronous activity induced by bicuculline/strychnine/5-HT but blocked by the glutamate receptor blockers CNQX/APV re-emerged after applying TEA/4AP. Activity block by carbenoxolone implicated electrical coupling. Here, we support this conclusion by showing that blockade of all known voltage-gated Ca2+ channels does not block the TEA/4AP evoked synchronous activity. This bursting was blocked with the broad-spectrum mGluR antagonist MCPG (n=3/3) & the group I mGluR subtype 1 antagonist AIDA (n=3/4).
(2) Synchronous activity induced following application of TEA/4AP in nominally Ca2+-free saline initiates an intracellular Ca2+ store and CNQX/APV-sensitive bursting. Here we show that extracellular Ca2+ is not required since block of cell surface Ca2+ receptors does not alter bursting. Thus, epileptiform activity via chemical synaptic transmission occurs in the absence of external Ca2+ entry. Interestingly this bursting was blocked with the metabotropic glutamate antagonist MCPG implicating mGluRs in the Ca2+ release from internal stores.
Thus, 2 novel forms of spinal epileptiform activity are expressed independent of extracellular Ca2+ but require activation of metabotropic glutamate receptors.
Supported by NINDS NS40440
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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