Neuroscience 2001 Abstract
| Presentation Number: | 918.13 |
|---|---|
| Abstract Title: | NON-α-NON-β-ADRENERGIC DEPOLARIZATION IN GUINEA PIG COCHLEAR SPIRAL MODIOLAR ARTERY INVOLVES CHLORIDE CHANNEL ACTIVATION. |
| Authors: |
Si, J. Q.*1,2
; Jiang, Z. G.1
; Nuttall, A. L.1
1OHRC, Oregon Health Sciences University, Portland, OR, OR 2Physiology, Shihezi University Medical College, Xinjiang, China |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Synaptic Transmission -- Postsynaptic mechanisms: Excitatory |
| Secondary Theme and Topics | Autonomic, Limbic and Other Systems<br />- Autonomic<br />-- Cardiovascular regulation |
| Session: |
918. Synaptic transmission: postsynaptic mechanisms--excitatory VIII Poster |
| Presentation Time: | Thursday, November 15, 2001 8:00 AM-9:00 AM |
| Location: | Exhibit Hall F-37 |
| Keywords: | adrenoceptors, electrophysiology, neuromuscular junction, neurotransmission |
We previously reported that both nerve-released and exogenously applied norepinephrine (NE) elicits a depolarization in cochlear vascular muscle cells that is perhaps mediated partially by a novel but poorly defined γ-adrenoceptor, in addition to the partial mediation by α-adrenoceptors [Jiang,SFN Abstr. 2000]. It is known that chloride currents contribute to NE-induced vasocontraction. Our further intracellular recording study found that: 1) in the presence of α1 & α2 adrenergic antagonists (1 μM prazosin & idazoxan), the residual NE-depolarization was not affected by diphenhydramine, ritanserin or haloperidol (antagonists for H1, 5-HT2 and D2,3,4 receptors, respectively); 2) the depolarization was significantly inhibited by the chloride channel blocker niflumic acid (NFA,0.01-1 mM), IAA-94 (10 μM) or DIDS (0.1-1 mM); 3) the depolarization was enhanced by low extracellular Cl- (60 mM, which shifted ECl from ~-25 to ~0 mV); 4) in the presence of α1 & α2 antagonists plus a P2X antagonist (PPADS,10 μM), the residual component of evoked excitatory junction potential (EJP) was also suppressed by NFA, IAA-94 or DIDS and enhanced by low Cl- (60 mM). Finally, 5) the residual EJP in the presence of α- & P2X antagonists was significantly suppressed by a persistent application of NE (50-100 μM). It is concluded that the intrinsic and extrinsic NE-induced non-α-non-β-excitation does not result from a cross activation of other known amine receptors, rather, it is likely mediated by a novel adrenoceptor that is positively coupled to a chloride conductance.
Supported by grants of DRF, Oregon MRF & NIH NIDCD DC00105
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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