PMID- 21554582
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20110510
IS  - 0953-8194 (Print)
IS  - 0953-8194 (Linking)
VI  - 4
IP  - 1
DP  - 1992 Feb
TI  - Morphine but not Naloxone Enhances Luteinizing Hormone-Releasing Hormone Neuronal 
      Responsiveness to Norepinephrine.
PG  - 91-9
LID - 10.1111/j.1365-2826.1992.tb00350.x [doi]
AB  - Some axon terminals of hypothalamic opiate neurons directly synapse on 
      luteinizing hormone-releasing hormone (LHRH) neurons. To determine whether such 
      synaptic connections affect LHRH neuronal activity, we have examined the profiles 
      and concentrations of LH released in response to intracerebroventricular (icv) 
      norepinephrine (NE, 45 mug) infusions alone or following medial preoptic area 
      (MPOA) electrochemical stimulation (ECS) in estrogen-treated ovariectomized rats. 
      Similar studies were performed in rats treated with naloxone (5 mg/kg ip) or 
      morphine (20 mg/kg sc) given 15 min prior to MPOA-ECS or 30 min prior to icv NE. 
      Naloxone neither augmented nor suppressed the LH response obtained with NE alone. 
      MPOA-ECS evoked a significant increase in plasma LH. When the preoptic area was 
      stimulated (0 min) and NE was infused at 30 min, a significant amplification of 
      LH release occurred. Prior treatment of rats (-15 min) with naloxone had no 
      effect on LH responses elicited by either preoptic stimulation alone or combined 
      with icv NE. In the second study, morphine was given sc and had no effect on 
      basal plasma LH levels. However, when morphine was given (-15 min) and icv NE 
      infusions were made (30 min), the rise in plasma LH induced by NE was 
      significantly enhanced. Preoptic ECS (0 min) evoked a rise in plasma LH and this 
      response was also enhanced by morphine pretreatment. The major effect on LH 
      release occurred when sc morphine injections (-15 min) were combined with 
      MPOA-ECS (0 min) followed by icv NE (30 min). In these rats, a remarkable and 
      highly significant release of LH occurred which reached peak levels even greater 
      than those observed during spontaneous LH surges (2,392 versus 16 to 1,800 
      ng/ml). Since morphine has profound effects on the serotonergic system, in the 
      third series of studies, morphine was infused into the dorsal raphe nucleus (DRN) 
      and LH responses to MPOA-ECS or icv NE alone or following combined ECS + NE were 
      examined. DRN morphine did not affect basal LH release but it produced a rapid 
      and highly significant rise in plasma prolactin. When DRN morphine was given (-15 
      min) and NE was infused icv (30 min), there was marked amplification in LH 
      release compared to those values observed after only NE. However, there were no 
      appreciable differences in LH values obtained after sc versus DRN morphine 
      injections in response to NE. Similarly, the amplification of LH release which 
      occurred following DRN morphine (-15 min) + MPOA-ECS (0 min) was not different 
      from that obtained after sc morphine. In the final group of rats, DRN morphine 
      was given (-15 min), the preoptic area was stimulated (0 min) and NE was infused 
      (30 min). Following this treatment, plasma LH release was also markedly enhanced 
      and did not differ appreciably (except at 60 and 120 min) from the levels of LH 
      released after sc morphine. Prolactin concentrations rose slowly after icv NE to 
      reach peak levels 75 min after treatment. Combinations of morphine + MPOA-ECS 
      without or with NE neither augmented nor suppressed the high prolactin 
      concentrations achieved after only DRN morphine infusions. We conclude from these 
      data that: 1) those opiate neuronal terminals which synapse directly on LHRH 
      neurons do not affect LHRH neuronal responsiveness to either NE, to MPOA-ECS or 
      to combined preoptic stimulation+ NE, and 2) morphine has profound effects on 
      LHRH neuronal responsiveness to both NE, to MPOA-ECS and, in particular, to 
      combined ECS + NE. Since amplification of LH release occurs after treatment of 
      rats with morphine either by sc injections or DRN infusions, the augmented LH and 
      prolactin responses observed are most likely due to the morphine-induced release 
      of serotonin and not to direct morphine effects on LHRH neurons.
FAU - He, J R
AU  - He JR
AD  - Center for Studies in Reproduction and Department of Physiology, School of 
      Medicine, University of Maryland, Baltimore, Maryland 21201, USA.
FAU - Barraclough, C A
AU  - Barraclough CA
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Neuroendocrinol
JT  - Journal of neuroendocrinology
JID - 8913461
EDAT- 1992/02/01 00:00
MHDA- 1992/02/01 00:01
CRDT- 2011/05/11 06:00
PHST- 2011/05/11 06:00 [entrez]
PHST- 1992/02/01 00:00 [pubmed]
PHST- 1992/02/01 00:01 [medline]
AID - 10.1111/j.1365-2826.1992.tb00350.x [doi]
PST - ppublish
SO  - J Neuroendocrinol. 1992 Feb;4(1):91-9. doi: 10.1111/j.1365-2826.1992.tb00350.x.