title: Activation of kappa opioid receptors decreases synaptic transmission and inhibits long-term potentiation in the basolateral amygdala of the mouse.
abstract: BACKGROUND
  The amygdala plays an important role in the processing of chronic pain and pain memory formation. Particularly, it is involved in the emotional and affective components of the pain circuitry. The role of kappa opioid receptors in these pain conditions is only partly known. The present study investigates the effect of kappa receptor activation on synaptic transmission and synaptic plasticity in the amygdala.
  
  
  METHODS
  Electrophysiological in vitro experiments were carried out in brain slices of male C57BL/6JOlaHsd mice. The effect of the kappa opioid receptor agonist U50,488H (5 microM) and the selective kappa opioid receptor antagonist nor-BNI (3 microM) on field potential (FP) amplitude and the induction of long-term potentiation (LTP) in the basolateral amygdala (BLA) was examined.
  
  
  RESULTS
  High frequency stimulation (HFS) of afferents in the lateral amygdala with two trains of 100 pulses at 50 Hz increased the FP amplitudes to 119+/-2% (mean+/-SEM; n=6) in the BLA. U50,488H decreased synaptic transmission (baseline: 100+/-0.5%; U50,488H: 86.3+/-2.4%; n=6) and blocked the induction of LTP (U50,488H: 100+/-4.1%; HFS: 102.6+/-7%; n=6). The effect on synaptic transmission and on LTP was completely reversed or prevented by application of nor-BNI, which itself had no effect on synaptic transmission or the induction of LTP.
  
  
  CONCLUSIONS
  Kappa opioid receptor activation decreases synaptic transmission and inhibits the induction of LTP in the BLA of the mouse. These findings may be associated with the effects of kappa opioid agonists in chronic pain and pain memory formation.
authors.affiliation: Clinical Neuropharmacology Group, Max-Planck-Institut für Psychiatrie, Kraepelinstrasse 2-10, 80804 Munich, Germany. vhuge@med.uni-muenchen.de
authors.forename: Volker
authors.initials: V
authors.lastname: Huge
authors.forename: Gerhard
authors.initials: G
authors.lastname: Rammes
authors.forename: Antje
authors.initials: A
authors.lastname: Beyer
authors.forename: Walter
authors.initials: W
authors.lastname: Zieglgänsberger
authors.forename: Shahnaz C
authors.initials: SC
authors.lastname: Azad
mesh_terms: D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer / Q000494:pharmacology; D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D018712:Analgesics, Non-Narcotic / Q000494:pharmacology; D000818:Animals; D002908:Chronic Disease; D004558:Electric Stimulation; D004594:Electrophysiology; D004644:Emotions / Q000502:physiology; D005108:Extinction, Psychological / Q000187:drug effects; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009271:Naltrexone / Q000031:analogs & derivatives / Q000494:pharmacology; D010146:Pain / Q000503:physiopathology / Q000523:psychology*; D017473:Receptors, Opioid, kappa / Q000819:agonists*; D009435:Synaptic Transmission / Q000187:drug effects*
chemical_list: D018712:Analgesics, Non-Narcotic; D017473:Receptors, Opioid, kappa; C051844:norbinaltorphimine; D009271:Naltrexone; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer