Kappa Opioid Receptor Agonist Administration in Olfactory Bulbectomized Mice Restores Cognitive Impairment through Cholinergic Neuron Activation
Olfactory bulbectomized (OBX) mice are characterized by impaired performance in the passive avoidance test and decreased number of cholinergic neurons in the hippocampus. Several studies have reported that κ-opioid receptor agonists improve cognitive function in mice. However, their influence on OBX...
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| Published in | Biological & pharmaceutical bulletin Vol. 41; no. 6; pp. 957 - 960 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
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Japan
The Pharmaceutical Society of Japan
01.06.2018
Pharmaceutical Society of Japan Japan Science and Technology Agency |
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| Abstract | Olfactory bulbectomized (OBX) mice are characterized by impaired performance in the passive avoidance test and decreased number of cholinergic neurons in the hippocampus. Several studies have reported that κ-opioid receptor agonists improve cognitive function in mice. However, their influence on OBX-induced cognitive dysfunction remains unclear. To address this question, we evaluated the effects of the endogenous κ-opioid receptor agonist dynorphin A (Dyn A) and the selective agonist trans-(−)-U-50488 on the behavior of OBX mice in the passive avoidance test. The cognitive dysfunction of OBX mice was significantly recovered by the intracerebroventricular administration of Dyn A or trans-(−)-U-50488. The effects of these two agonists were counteracted by the selective κ-opioid receptor antagonist nor-binaltorphimine or the inhibitor of acetylcholine release β-bungarotoxin. These findings suggest that κ-opioid receptor agonists produce anti-dementia effects through activation of cholinergic neurons in OBX mice. |
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| AbstractList | Olfactory bulbectomized (OBX) mice are characterized by impaired performance in the passive avoidance test and decreased number of cholinergic neurons in the hippocampus. Several studies have reported that κ-opioid receptor agonists improve cognitive function in mice. However, their influence on OBX-induced cognitive dysfunction remains unclear. To address this question, we evaluated the effects of the endogenous κ-opioid receptor agonist dynorphin A (Dyn A) and the selective agonist trans-(−)-U-50488 on the behavior of OBX mice in the passive avoidance test. The cognitive dysfunction of OBX mice was significantly recovered by the intracerebroventricular administration of Dyn A or trans-(−)-U-50488. The effects of these two agonists were counteracted by the selective κ-opioid receptor antagonist nor-binaltorphimine or the inhibitor of acetylcholine release β-bungarotoxin. These findings suggest that κ-opioid receptor agonists produce anti-dementia effects through activation of cholinergic neurons in OBX mice. Graphical Abstract Olfactory bulbectomized (OBX) mice are characterized by impaired performance in the passive avoidance test and decreased number of cholinergic neurons in the hippocampus. Several studies have reported that κ-opioid receptor agonists improve cognitive function in mice. However, their influence on OBX-induced cognitive dysfunction remains unclear. To address this question, we evaluated the effects of the endogenous κ-opioid receptor agonist dynorphin A (Dyn A) and the selective agonist trans-(-)-U-50488 on the behavior of OBX mice in the passive avoidance test. The cognitive dysfunction of OBX mice was significantly recovered by the intracerebroventricular administration of Dyn A or trans-(-)-U-50488. The effects of these two agonists were counteracted by the selective κ-opioid receptor antagonist nor-binaltorphimine or the inhibitor of acetylcholine release β-bungarotoxin. These findings suggest that κ-opioid receptor agonists produce anti-dementia effects through activation of cholinergic neurons in OBX mice. Olfactory bulbectomized (OBX) mice are characterized by impaired performance in the passive avoidance test and decreased number of cholinergic neurons in the hippocampus. Several studies have reported that κ-opioid receptor agonists improve cognitive function in mice. However, their influence on OBX-induced cognitive dysfunction remains unclear. To address this question, we evaluated the effects of the endogenous κ-opioid receptor agonist dynorphin A (Dyn A) and the selective agonist trans-(−)-U-50488 on the behavior of OBX mice in the passive avoidance test. The cognitive dysfunction of OBX mice was significantly recovered by the intracerebroventricular administration of Dyn A or trans-(−)-U-50488. The effects of these two agonists were counteracted by the selective κ-opioid receptor antagonist nor-binaltorphimine or the inhibitor of acetylcholine release β-bungarotoxin. These findings suggest that κ-opioid receptor agonists produce anti-dementia effects through activation of cholinergic neurons in OBX mice. |
| Author | Nemoto, Wataru Sugawara, Masae Tan-No, Koichi Takahashi, Kohei Nakagawasai, Osamu Sato, Atsushi Tadano, Takeshi |
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| Cites_doi | 10.1016/j.bbr.2016.11.008 10.1016/j.biopsych.2006.08.032 10.1016/j.brainres.2007.07.095 10.1016/j.bbr.2015.10.033 10.1016/S0166-4328(02)00383-2 10.1046/j.1471-4159.1997.68010313.x 10.2174/1570159X13666150727220944 10.1016/0006-8993(93)91615-Y 10.1016/S0163-7258(97)00004-1 10.1523/JNEUROSCI.3769-07.2007 10.1254/jphs.SC0070155 10.1038/sj.bjp.0701671 10.1016/j.bbr.2016.09.029 10.1016/0041-0101(83)90274-X 10.1016/S0166-4328(02)00183-3 10.1016/j.bbr.2010.02.042 10.1016/j.bbr.2010.07.002 10.1159/000353848 10.1016/j.euroneuro.2017.08.071 10.1016/j.npep.2005.10.003 10.1113/jphysiol.1967.sp008332 10.1016/j.bbr.2010.07.012 10.1159/000381525 10.1016/S0304-3940(97)00757-X 10.1248/bpb.b14-00006 10.1523/JNEUROSCI.2980-11.2012 |
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| SubjectTerms | Acetylcholine Activation Avoidance Bungarotoxin Cholinergic nerves cholinergic neuron Cognitive ability Dementia disorders Dynorphin Dynorphin A Intracerebroventricular administration memory Mice Narcotics Neurons olfactory bulbectomy Opioid receptors (type kappa) κ-opioid |
| Title | Kappa Opioid Receptor Agonist Administration in Olfactory Bulbectomized Mice Restores Cognitive Impairment through Cholinergic Neuron Activation |
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