PMID- 9394782
OWN - NLM
STAT- MEDLINE
DCOM- 19971223
LR  - 20190826
IS  - 0165-5728 (Print)
IS  - 0165-5728 (Linking)
VI  - 79
IP  - 2
DP  - 1997 Nov
TI  - Conditioned immunomodulation: investigations of the role of endogenous activity 
      at mu, kappa, and delta opioid receptor subtypes.
PG  - 101-12
AB  - The present investigations were designed to determine the role of activity at mu, 
      kappa, and delta opioid receptor subtypes in conditioned immunomodulation by 
      evaluating the effects of selective opioid receptor antagonists on conditioned 
      stimulus-induced alterations in immune status. Lewis rats were exposed to an 
      aversive conditioned stimulus that was developed through pairings with electric 
      footshock. This aversive conditioned stimulus induces a reduction in splenic 
      natural killer cell activity, splenocyte proliferation in response to mitogens, 
      and diminished levels of interferon-gamma (IFN-gamma) production by splenocytes. 
      Intracerebroventricular (i.c.v.) administration of the opioid antagonist 
      naltrexone or the mu 1-selective antagonist naloxonazine blocked conditioned 
      alterations of immune status, indicating that activity at mu-opioid receptors is 
      involved in conditioned immunomodulation. Further support for the involvement of 
      mu-opioid receptors within the central nervous system is provided by data showing 
      that peripheral administration of naloxonazine, at doses shown to be effective 
      when administered i.c.v., had no effect on conditioned alterations of immune 
      status. Ventricular administration of the kappa receptor antagonist 
      nor-binaltorphimine (nor-BNI) did not antagonize the immunomodulatory effects of 
      the conditioned stimulus. Administration of the delta receptor antagonist 
      naltrindole also did not antagonize the conditioned alterations of immune status. 
      Collectively, the results of this study indicate that the alterations of immune 
      status produced by an aversive conditioned stimulus require activity at mu-opioid 
      receptors, possibly mu 1, within the central nervous system.
FAU - Perez, L
AU  - Perez L
AD  - University of North Carolina at Chapel Hill 27599-3270, USA.
FAU - Lysle, D T
AU  - Lysle DT
LA  - eng
GR  - DA00334/DA/NIDA NIH HHS/United States
GR  - DA10167/DA/NIDA NIH HHS/United States
GR  - MH46284/MH/NIMH NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Narcotic Antagonists)
RN  - 0 (Receptors, Opioid, delta)
RN  - 0 (Receptors, Opioid, kappa)
RN  - 0 (Receptors, Opioid, mu)
RN  - 36B82AMQ7N (Naloxone)
RN  - 36OOQ86QM1 (norbinaltorphimine)
RN  - 5S6W795CQM (Naltrexone)
RN  - 82824-01-9 (naloxonazine)
RN  - G167Z38QA4 (naltrindole)
SB  - IM
MH  - Animals
MH  - Avoidance Learning/physiology
MH  - Cell Division/drug effects
MH  - Conditioning, Classical/*physiology
MH  - Electroshock
MH  - Immune System/drug effects/*physiology
MH  - Killer Cells, Natural/drug effects
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - Naloxone/analogs & derivatives/pharmacology
MH  - Naltrexone/analogs & derivatives/pharmacology
MH  - Narcotic Antagonists/pharmacology
MH  - Rats
MH  - Rats, Inbred Lew
MH  - Receptors, Opioid, delta/*physiology
MH  - Receptors, Opioid, kappa/*physiology
MH  - Receptors, Opioid, mu/*physiology
MH  - Spleen/cytology/drug effects
EDAT- 1997/12/12 02:44
MHDA- 2000/06/01 09:00
CRDT- 1997/12/12 02:44
PHST- 1997/12/12 02:44 [pubmed]
PHST- 2000/06/01 09:00 [medline]
PHST- 1997/12/12 02:44 [entrez]
AID - S0165-5728(97)00106-9 [pii]
AID - 10.1016/s0165-5728(97)00106-9 [doi]
PST - ppublish
SO  - J Neuroimmunol. 1997 Nov;79(2):101-12. doi: 10.1016/s0165-5728(97)00106-9.