Canonical Organization of Opioid Modulation of Nociceptive Circuits. Focus on “μ Opioid Receptor Activation Inhibits GABAergic Inputs to Basolateral Amygdala Neurons Through Kv1.1/Kv1.2 Channels”

2006 ◽  
Vol 95 (4) ◽  
pp. 2029-2030 ◽  
Author(s):  
Pankaj Sah
Keyword(s):  
Opioid Receptor ◽  
Basolateral Amygdala ◽  
Receptor Activation ◽  
Μ Opioid Receptor

μ Opioid Receptor Activation Inhibits GABAergic Inputs to Basolateral Amygdala Neurons Through Kv1.1/1.2 Channels

2006 ◽  
Vol 95 (4) ◽  
pp. 2032-2041 ◽  
Author(s):  
Thomas F. Finnegan ◽  
Shao-Rui Chen ◽  
Hui-Lin Pan
Keyword(s):  
Opioid Receptor ◽  
Opioid Receptors ◽  
Basolateral Amygdala ◽  
Receptor Activation ◽  
Peak Amplitude ◽  
Amygdaloid Nucleus ◽  
Synaptic Inputs ◽  
Μ Opioid Receptor ◽  
Immunofluorescence Labeling ◽  
Μ Opioid Receptors

The basolateral amygdala (BLA) is the major amygdaloid nucleus distributed with μ opioid receptors. The afferent input from the BLA to the central nucleus of the amygdala (CeA) is considered important for opioid analgesia. However, little is known about the effect of μ opioids on synaptic transmission in the BLA. In this study, we examined the effect of μ opioid receptor stimulation on the inhibitory and excitatory synaptic inputs to CeA-projecting BLA neurons. BLA neurons were retrogradely labeled with a fluorescent tracer injected into the CeA of rats. Whole cell voltage-clamp recordings were performed on labeled BLA neurons in brain slices. The specific μ opioid receptor agonist, (d-Ala2, N-Me-Phe4,Gly5-ol)-enkephalin (DAMGO, 1 μM), significantly reduced the frequency of miniature inhibitory postsynaptic currents (mIPSCs) in 77% of cells tested. DAMGO also significantly decreased the peak amplitude of evoked IPSCs in 75% of cells examined. However, DAMGO did not significantly alter the frequency of mEPSCs or the peak amplitude of evoked EPSCs in 90% and 75% of labeled cells, respectively. Bath application of the Kv channel blockers, 4-AP (Kv1.1, 1.2, 1.3, 1.5, 1.6, 3.1, 3.2), α-dendrotoxin (Kv1.1, 1.2, 1.6), dendrotoxin-K (Kv1.1), or tityustoxin-Kα (Kv1.2) each blocked the inhibitory effect of DAMGO on mIPSCs. Double immunofluorescence labeling showed that some of the immunoreactivities of Kv1.1 and Kv1.2 were colocalized with synaptophysin in the BLA. This study provides new information that activation of presynaptic μ opioid receptors primarily attenuates GABAergic synaptic inputs to CeA-projecting neurons in the BLA through a signaling mechanism involving Kv1.1 and Kv1.2 channels.

scholarly journals Author Correction: Structural insights into μ-opioid receptor activation

Nature ◽  
2020 ◽  
Vol 584 (7820) ◽  
pp. E16-E16
Author(s):  
Weijiao Huang ◽  
Aashish Manglik ◽  
A. J. Venkatakrishnan ◽  
Toon Laeremans ◽  
Evan N. Feinberg ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Receptor Activation ◽  
Μ Opioid Receptor ◽  
Structural Insights

scholarly journals μ-Opioid Receptor Activation Directly Modulates Intrinsically Photosensitive Retinal Ganglion Cells

Neuroscience ◽  
2019 ◽  
Vol 408 ◽  
pp. 400-417 ◽  
Author(s):  
Allison M. Cleymaet ◽  
Shannon K. Gallagher ◽  
Ryan E. Tooker ◽  
Mikhail Y. Lipin ◽  
Jordan M. Renna ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Opioid Receptor ◽  
Ganglion Cells ◽  
Receptor Activation ◽  
Retinal Ganglion ◽  
Μ Opioid Receptor

scholarly journals Tonic GABAA receptor conductance in medial subnucleus of the tractus solitarius neurons is inhibited by activation of μ-opioid receptors

2012 ◽  
Vol 107 (3) ◽  
pp. 1022-1031 ◽  
Author(s):  
Melissa A. Herman ◽  
Richard A. Gillis ◽  
Stefano Vicini ◽  
Kenneth L. Dretchen ◽  
Niaz Sahibzada
Keyword(s):  
Opioid Receptor ◽  
Opioid Receptors ◽  
Receptor Activation ◽  
Membrane Excitability ◽  
Selective Blockade ◽  
Medial Nucleus ◽  
Opioid Receptor Agonist ◽  
Gaba Signaling ◽  
Μ Opioid Receptor ◽  
Μ Opioid Receptors

Our laboratory previously reported that gastric activity is controlled by a robust GABAA receptor-mediated inhibition in the medial nucleus of the tractus solitarius (mNTS) ( Herman et al. 2009 ), and that μ-opioid receptor activation inhibits gastric tone by suppression of this GABA signaling ( Herman et al. 2010 ). These data raised two questions: 1) whether any of this inhibition was due to tonic GABAA receptor-mediated conductance in the mNTS; and 2) whether μ-opioid receptor activation suppressed both tonic and phasic GABA signaling. In whole cell recordings from rat mNTS neurons, application of three GABAA receptor antagonists (gabazine, bicuculline, and picrotoxin) produced a persistent reduction in holding current and decrease in population variance or root mean square (RMS) noise, suggesting a blockade of tonic GABA signaling. Application of gabazine at a lower concentration abolished phasic currents, but had no effect on tonic currents or RMS noise. Application of the δ-subunit preferring agonist gaboxadol (THIP) produced a dose-dependent persistent increase in holding current and RMS noise. Pretreatment with tetrodotoxin prevented the action of gabazine, but had no effect on the THIP-induced current. Membrane excitability was unaffected by the selective blockade of phasic inhibition, but was increased by blockade of both phasic and tonic currents. In contrast, activation of tonic currents decreased membrane excitability. Application of the μ-opioid receptor agonist DAMGO produced a persistent reduction in holding current that was not observed following pretreatment with a GABAA receptor antagonist and was not evident in mice lacking the δ-subunit. These data suggest that mNTS neurons possess a robust tonic inhibition that is mediated by GABAA receptors containing the δ-subunit, that determines membrane excitability, and that is partially regulated by μ-opioid receptors.

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