![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
|
|
|
|
|
||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Received for publication December 24, 2003.
Revised December 22, 2003.
Accepted for publication December 31, 2003.
The rostral ventromedial medulla (RVM) is a major locus for the descending control of nociception and opioid analgesia. However, it is not clear how opioids affect synaptic inputs to RVM neurons. In this study, we determined the effect of µ opioid receptor activation on excitatory and inhibitory synaptic transmission in spi nally projecting RVM neurons. RVM neurons were retrogradely labeled with a fluorescent tracer injected into the dorsal horn of the spinal cord in rats. Whole-cell voltage-clamp recordings were performed on labeled RVM neurons in brain slices in vitro. The µ receptor agonist, (D-Ala2, N-Me-Phe4, Gly-ol5)-enkephalin (DAMGO, 1 µM), significantly decreased the amplitude of evoked excitatory postsynaptic currents (EPSCs) in 52% (9 of 17) of labeled cells. DAMGO also significantly reduced the amplitude of evoked inhibitory postsynaptic currents (IPSCs) in 69% (11/16) of cells examined. Furthermore, DAMGO significantly decreased the frequency of miniature EPSCs in 55% (15 of 27) of cells and significantly decreased the frequency of miniature IPSCs in all 12 cells studied. Although most EPSCs and IPSCs were mediated by glutamate and GABA, the nicotinic and glycine receptor antagonists attenuated EPSCs and IPSCs, respectively, in some labeled RVM neurons. Immunocytochemical labeling revealed that only 35% recorded RVM neurons were tryptophan hydroxylase-positive, and 15% cells had GABA immunoreactivity. Thus, this study provides important functional evidence that activation of m opioid receptors decreases the release of both excitatory and inhibitory neurotransmitters onto most spinally projecting RVM neurons.
Key words:
GABA, Synapse, brainstem, opioids, presynaptic, spinal cord
This article has been cited by other articles:
|
|
 |
|
  K. T. Sykes, S. R. White, R. W. Hurley, H. Mizoguchi, L. F. Tseng, and D. L. Hammond Mechanisms Responsible for the Enhanced Antinociceptive Effects of {micro}-Opioid Receptor Agonists in the Rostral Ventromedial Medulla of Male Rats with Persistent Inflammatory Pain J. Pharmacol. Exp. Ther., August 1, 2007; 322(2): 813 - 821. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Sah Canonical Organization of Opioid Modulation of Nociceptive Circuits. Focus on "{micro} Opioid Receptor Activation Inhibits GABAergic Inputs to Basolateral Amygdala Neurons Through Kv1.1/Kv1.2 Channels" J Neurophysiol, April 1, 2006; 95(4): 2029 - 2030. [Full Text] [PDF]
|
|
|
|
|
|
T. F. Finnegan, S.-R. Chen, and H.-L. Pan {micro} Opioid Receptor Activation Inhibits GABAergic Inputs to Basolateral Amygdala Neurons Through Kv1.1/1.2 Channels J Neurophysiol, April 1, 2006; 95(4): 2032 - 2041. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Zhang, K. T. Sykes, A. V. Buhler, and D. L. Hammond Electrophysiological Heterogeneity of Spinally Projecting Serotonergic and Nonserotonergic Neurons in the Rostral Ventromedial Medulla J Neurophysiol, March 1, 2006; 95(3): 1853 - 1863. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. F. Finnegan, S.-R. Chen, and H.-L. Pan Effect of the {micro} Opioid on Excitatory and Inhibitory Synaptic Inputs to Periaqueductal Gray-Projecting Neurons in the Amygdala J. Pharmacol. Exp. Ther., February 1, 2005; 312(2): 441 - 448. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D.-P. Li, L. M. Atnip, S.-R. Chen, and H.-L. Pan Regulation of Synaptic Inputs to Paraventricular-Spinal Output Neurons by {alpha}2 Adrenergic Receptors J Neurophysiol, January 1, 2005; 93(1): 393 - 402. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
