PMID- 8391665
OWN - NLM
STAT- MEDLINE
DCOM- 19930730
LR  - 20181130
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 57
IP  - 3
DP  - 1993 Mar
TI  - Responses of anterior pituitary hormones and hypothalamic histamine to blockade 
      of histamine synthesis and to selective activation or inactivation of presynaptic 
      histamine H3 receptors in stressed rats.
PG  - 532-40
AB  - The stress-induced release of anterior pituitary hormones and changes in 
      hypothalamic content of histamine (HA) and its metabolite tele-methylHA (t-meHA) 
      were studied in male rats during inhibition of HA synthesis or activation or 
      blockade of HA H3 receptors. Pretreatment with the HA synthesis inhibitor 
      alpha-fluoromethylhistidine (alpha-FMH; 200 micrograms intracerebroventricularly 
      (icv) at -120 min) or the specific H3 receptor agonist R(alpha)methylhistamine 
      (RmHA; 10 mg/kg intraperitoneally (ip) at -180 and -60 min) inhibited by 30-80% 
      the responses of prolactin (PRL), corticotropin (ACTH) and beta-endorphin 
      (beta-END) immunoreactivity to 1, 2.5 or 5 min of restraint stress (p < 
      0.05-0.01), but had no effect on basal secretion of the hormones. The inhibitory 
      effect of the H3 receptor agonist RmHA (10 mg/kg x 2) on the hormone response to 
      5 min of restraint stress was prevented by simultaneous ip administration of the 
      H3 receptor antagonist thioperamide. alpha-FMH reduced the hypothalamic content 
      of HA 60% and that of t-meHA 30%, while RmHA had no effect on the HA content. 
      Restraint stress for 5 min did not affect the HA and t-meHA contents, which may 
      be due to the short duration of stress exposure. Pretreatment with the H3 
      receptor antagonist thioperamide (5 or 10 mg/kg ip at -120 min) had no effect on 
      basal or restraint stress-induced release of PRL, ACTH or beta-END, although the 
      compound increased the hypothalamic content of t-meHA 2-fold.(ABSTRACT TRUNCATED 
      AT 250 WORDS)
FAU - Soe-Jensen, P
AU  - Soe-Jensen P
AD  - Department of Medical Physiology, Panum Institute, University of Copenhagen, 
      Denmark.
FAU - Knigge, U
AU  - Knigge U
FAU - Garbarg, M
AU  - Garbarg M
FAU - Kjaer, A
AU  - Kjaer A
FAU - Rouleau, A
AU  - Rouleau A
FAU - Bach, F W
AU  - Bach FW
FAU - Schwartz, J C
AU  - Schwartz JC
FAU - Warberg, J
AU  - Warberg J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Histamine Antagonists)
RN  - 0 (Insulin)
RN  - 0 (Methylhistamines)
RN  - 0 (Methylhistidines)
RN  - 0 (Piperidines)
RN  - 0 (Pituitary Hormones, Anterior)
RN  - 0 (Receptors, Histamine)
RN  - 0 (Receptors, Histamine H3)
RN  - 60617-12-1 (beta-Endorphin)
RN  - 6986-90-9 (alpha-methylhistamine)
RN  - 70050-43-0 (alpha-fluoromethylhistidine)
RN  - 820484N8I3 (Histamine)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - 9002-62-4 (Prolactin)
RN  - II4319BWUI (thioperamide)
SB  - IM
MH  - Adrenocorticotropic Hormone/metabolism
MH  - Animals
MH  - Histamine/biosynthesis/*metabolism
MH  - Histamine Antagonists
MH  - Hypoglycemia/metabolism
MH  - Hypothalamus/*metabolism
MH  - Insulin/pharmacology
MH  - Kinetics
MH  - Male
MH  - Methylhistamines/pharmacology
MH  - Methylhistidines/pharmacology
MH  - Piperidines/pharmacology
MH  - Pituitary Hormones, Anterior/*metabolism
MH  - Prolactin/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Histamine/*physiology
MH  - Receptors, Histamine H3
MH  - Restraint, Physical
MH  - Stress, Physiological/*physiopathology
MH  - beta-Endorphin/metabolism
EDAT- 1993/03/01 00:00
MHDA- 1993/03/01 00:01
CRDT- 1993/03/01 00:00
PHST- 1993/03/01 00:00 [pubmed]
PHST- 1993/03/01 00:01 [medline]
PHST- 1993/03/01 00:00 [entrez]
AID - 10.1159/000126402 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1993 Mar;57(3):532-40. doi: 10.1159/000126402.