PMID- 11640977
OWN - NLM
STAT- MEDLINE
DCOM- 20020102
LR  - 20190826
IS  - 0166-4328 (Print)
IS  - 0166-4328 (Linking)
VI  - 124
IP  - 2
DP  - 2001 Oct 15
TI  - Involvement of central histamine in amygdaloid kindled seizures in rats.
PG  - 243-50
AB  - The involvement of central histamine in amygdaloid kindled seizures in rats was 
      investigated using histamine-related compounds. Histamine contents in the 
      amygdala of electrical stimulation site was significantly decreased after 
      development of amygdaloid kindling. Intracerebroventricular (i.c.v.) injection of 
      histamine resulted in inhibition of amygdaloid kindled seizures. The 
      H(1)-agonists 2-methylhistamine and 2-thiazolylethylamine also inhibited 
      amygdaloid kindled seizures. In addition, intraperitoneal (i.p.) injection of 
      histidine and metoprine inhibited amygdaloid kindled seizures at doses that 
      caused increases in histamine contents of the brain. H(1)-antagonists 
      (diphenhydramine and chlorpheniramine) attenuated histamine (i.c.v.)-induced 
      inhibition of amygdaloid kindled seizures, however, no significant antagonism was 
      observed with H(2)-antagonists (cimetidine, ranitidine or zolantidine). 
      Intracerebroventricular injection of H(3)-antagonists (thioperamide and AQ 0145) 
      resulted in a dose-related inhibition of amygdaloid kindled seizures. The same 
      findings were observed when thioperamide and clobenpropit were injected i.p. The 
      effects of thioperamide (i.p.) and AQ 0145 (i.p.) were inhibited by an 
      H(3)-agonist [(R)-alpha-methylhistamine] and H(1)-antagonists (diphenhydramine 
      and chlorpheniramine). On the other hand, H(2)-antagonists (cimetidine and 
      ranitidine) showed no antagonistic effects. These findings suggested that a 
      histaminergic mechanism plays an important role in suppressing amygdaloid kindled 
      seizures through histamine H(1)-receptors.
FAU - Kamei, C
AU  - Kamei C
AD  - Department of Pharmacology, Faculty of Pharmaceutical Sciences, Okayama 
      University, Okayama 700-8530, Japan. kamei@pheasant.okayama-u.ac.jp
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Behav Brain Res
JT  - Behavioural brain research
JID - 8004872
RN  - 0 (Receptors, Histamine H1)
RN  - 820484N8I3 (Histamine)
SB  - IM
MH  - Amygdala/*physiopathology
MH  - Animals
MH  - Brain Mapping
MH  - Cerebral Cortex/physiopathology
MH  - Dominance, Cerebral/physiology
MH  - Hippocampus/physiopathology
MH  - Histamine/*physiology
MH  - Hypothalamus/physiopathology
MH  - Kindling, Neurologic/*physiology
MH  - Rats
MH  - Receptors, Histamine H1/physiology
MH  - Seizures/*physiopathology
EDAT- 2001/10/20 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/10/20 10:00
PHST- 2001/10/20 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/10/20 10:00 [entrez]
AID - S0166432801002182 [pii]
AID - 10.1016/s0166-4328(01)00218-2 [doi]
PST - ppublish
SO  - Behav Brain Res. 2001 Oct 15;124(2):243-50. doi: 10.1016/s0166-4328(01)00218-2.