Effects of [mu]-opioids on neurons of the medical geniculate nucleus
Immunohistochemical and hybridization studies have revealed the presence of μ-, but not k- and δ-opioid receptors in the medial geniculate body. Using whole-cell patch clamp techniques, I examined the effects of opioid agonists on gerbil MGB neurons (P9-P16) in vitro. The opioid effects were conc...
Main Author: | |
---|---|
Format: | Others |
Language: | English |
Published: |
2009
|
Online Access: | http://hdl.handle.net/2429/10738 |
id |
ndltd-UBC-oai-circle.library.ubc.ca-2429-10738 |
---|---|
record_format |
oai_dc |
spelling |
ndltd-UBC-oai-circle.library.ubc.ca-2429-107382018-01-05T17:35:28Z Effects of [mu]-opioids on neurons of the medical geniculate nucleus Ota, Takayo Immunohistochemical and hybridization studies have revealed the presence of μ-, but not k- and δ-opioid receptors in the medial geniculate body. Using whole-cell patch clamp techniques, I examined the effects of opioid agonists on gerbil MGB neurons (P9-P16) in vitro. The opioid effects were concentration-dependent. Opioids produced different actions on the input conductance (G[sub i]) when applied in low, compared with high concentrations. The increase in G[sub i] might be due to increase in K⁺ conductance whereas the decrease in G[sub i] might be due to l[sub H] inactivation. When Gi was increased, the reversal potential was —65 mV; this implicates opioid actions on K+ , among other ion channels. In the case of decreased G[sub i], the opioid currents did not reverse from -100 mV to -50 mV, implying the involvement of cationic channels, other than K⁺ . DAMGO, a μ-selective opioid agonist, had a reversal potential that was similar to that observed when morphine increased G[sub i], implying that opioids activate u-opioid receptors in MGB neurons. Tetrodotoxin altered the concentration-dependent action of morphine. Here, the suggestion is morphine's actions involve neurons that presynaptic to the patch clamped neuron. Morphine application blocked spike-frequency adaptation and reduced firing rates in response to depolarizing current pulse injection. Morphine application may block Ca²⁺-mediated K⁺ channels that inhibited spike-frequency adaptation. Such blockade may be expected to increase the spike frequency. However, the increased conductance due to morphine would shunt the Na⁺ current, resulting in a lower spike frequency. The results of this study have revealed that opioids have both excitatory and inhibitory effects on MGB neurons. Medicine, Faculty of Anesthesiology, Pharmacology and Therapeutics, Department of Graduate 2009-07-13T20:18:18Z 2009-07-13T20:18:18Z 2000 2000-11 Text Thesis/Dissertation http://hdl.handle.net/2429/10738 eng For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use. 3387871 bytes application/pdf |
collection |
NDLTD |
language |
English |
format |
Others
|
sources |
NDLTD |
description |
Immunohistochemical and hybridization studies have revealed the presence of μ-,
but not k- and δ-opioid receptors in the medial geniculate body. Using whole-cell
patch clamp techniques, I examined the effects of opioid agonists on gerbil MGB
neurons (P9-P16) in vitro. The opioid effects were concentration-dependent.
Opioids produced different actions on the input conductance (G[sub i]) when applied in
low, compared with high concentrations. The increase in G[sub i] might be due to
increase in K⁺ conductance whereas the decrease in G[sub i] might be due to l[sub H]
inactivation. When Gi was increased, the reversal potential was —65 mV; this
implicates opioid actions on K+ , among other ion channels. In the case of decreased
G[sub i], the opioid currents did not reverse from -100 mV to -50 mV, implying the
involvement of cationic channels, other than K⁺ . DAMGO, a μ-selective opioid
agonist, had a reversal potential that was similar to that observed when morphine
increased G[sub i], implying that opioids activate u-opioid receptors in MGB neurons.
Tetrodotoxin altered the concentration-dependent action of morphine. Here, the
suggestion is morphine's actions involve neurons that presynaptic to the patch
clamped neuron. Morphine application blocked spike-frequency adaptation and
reduced firing rates in response to depolarizing current pulse injection. Morphine
application may block Ca²⁺-mediated K⁺ channels that inhibited spike-frequency
adaptation. Such blockade may be expected to increase the spike frequency.
However, the increased conductance due to morphine would shunt the Na⁺ current,
resulting in a lower spike frequency. The results of this study have revealed that
opioids have both excitatory and inhibitory effects on MGB neurons. === Medicine, Faculty of === Anesthesiology, Pharmacology and Therapeutics, Department of === Graduate |
author |
Ota, Takayo |
spellingShingle |
Ota, Takayo Effects of [mu]-opioids on neurons of the medical geniculate nucleus |
author_facet |
Ota, Takayo |
author_sort |
Ota, Takayo |
title |
Effects of [mu]-opioids on neurons of the medical geniculate nucleus |
title_short |
Effects of [mu]-opioids on neurons of the medical geniculate nucleus |
title_full |
Effects of [mu]-opioids on neurons of the medical geniculate nucleus |
title_fullStr |
Effects of [mu]-opioids on neurons of the medical geniculate nucleus |
title_full_unstemmed |
Effects of [mu]-opioids on neurons of the medical geniculate nucleus |
title_sort |
effects of [mu]-opioids on neurons of the medical geniculate nucleus |
publishDate |
2009 |
url |
http://hdl.handle.net/2429/10738 |
work_keys_str_mv |
AT otatakayo effectsofmuopioidsonneuronsofthemedicalgeniculatenucleus |
_version_ |
1718588646860259328 |