PMID- 8930844
OWN - NLM
STAT- MEDLINE
DCOM- 19970310
LR  - 20190512
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 496 ( Pt 3)
IP  - Pt 3
DP  - 1996 Nov 1
TI  - Activation of oxytocin neurones by systemic cholecystokinin is unchanged by 
      morphine dependence or withdrawal excitation in the rat.
PG  - 787-94
AB  - 1. Morphine inhibits supraoptic nucleus oxytocin neurones directly and 
      presynaptically via inhibition of afferent noradrenergic endings. 2. We studied 
      whether morphine tolerance/dependence (induced by intracerebroventricular 
      (I.C.V.) morphine infusion) alters the responsiveness of oxytocin neurones to 
      systemic cholecystokinin (CCK), a stimulus which activates oxytocin neurones via 
      the release of noradrenaline. 3. CCK (20 micrograms kg-1, i.v.) increased plasma 
      oxytocin concentrations similarly in urethane-anaesthetized morphine-naive and 
      -dependent rats. In naive rats, I.C.V. (10 micrograms) and i.v. morphine (0.5 mg 
      kg-1) reduced CCK-induced oxytocin secretion by 95 +/- 4 and 49 +/- 10%, 
      respectively. In dependent rats, i.v. morphine reduced CCK-induced release by 
      only 8 +/- 9%, indicating tolerance. 4. In urethane-anaesthetized rats, i.v. CCK 
      increased the firing rates of oxytocin neurones similarly in morphine-naive and 
      -dependent rats (by 1.2 +/- 0.2 and 1.4 +/- 0.3 spikes s-1 maximum, respectively, 
      over 5 min). Naloxone did not alter spontaneous or CCK-induced activity in naive 
      rats but increased activity in dependent rats (by 3.4 +/- 0.5 spikes s-1), 
      indicative of withdrawal excitation; however, the response to CCK remained 
      unchanged after naloxone. 5. Systemic CCK did not trigger withdrawal, nor did it 
      have a greater excitatory effect in dependent rats. Thus, morphine withdrawal 
      excitation of oxytocin neurones does not involve supersensitivity to the 
      noradrenergic input, or hypersensitivity of this input to i.v. CCK. Tolerance 
      apparently occurs both at the cell bodies of oxytocin neurones in the supraoptic 
      nucleus and in their noradrenergic input. However, dependence is apparent only at 
      the cell bodies.
FAU - Brown, C H
AU  - Brown CH
AD  - Department of Physiology, University Medical School, Edinburgh, UK.
FAU - Munro, G
AU  - Munro G
FAU - Murphy, N P
AU  - Murphy NP
FAU - Leng, G
AU  - Leng G
FAU - Russell, J A
AU  - Russell JA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 50-56-6 (Oxytocin)
RN  - 76I7G6D29C (Morphine)
RN  - 9011-97-6 (Cholecystokinin)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Afferent Pathways/physiology/physiopathology
MH  - Animals
MH  - Cerebral Ventricles/drug effects/*physiology/physiopathology
MH  - Cholecystokinin/*pharmacology
MH  - Drug Tolerance
MH  - Electric Stimulation
MH  - Female
MH  - Infusions, Parenteral
MH  - Injections, Intravenous
MH  - Morphine/administration & dosage/*pharmacology
MH  - Morphine Dependence/*physiopathology
MH  - Neurons/drug effects/*physiology
MH  - Norepinephrine/metabolism
MH  - Oxytocin/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - *Substance Withdrawal Syndrome
MH  - Supraoptic Nucleus/drug effects/*physiology/physiopathology
PMC - PMC1160864
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
PMCR- 1996/11/01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
PHST- 1996/11/01 00:00 [pmc-release]
AID - 10.1113/jphysiol.1996.sp021727 [doi]
PST - ppublish
SO  - J Physiol. 1996 Nov 1;496 ( Pt 3)(Pt 3):787-94. doi: 
      10.1113/jphysiol.1996.sp021727.