PMID- 11879358
OWN - NLM
STAT- MEDLINE
DCOM- 20020318
LR  - 20190813
IS  - 0013-9580 (Print)
IS  - 0013-9580 (Linking)
VI  - 42
IP  - 12
DP  - 2001 Dec
TI  - Mechanism of the inhibitory effect of histamine on amygdaloid-kindled seizures in 
      rats.
PG  - 1494-500
AB  - PURPOSE: The mechanism of the inhibitory effect of histamine on 
      amygdaloid-kindled seizures was investigated in rats. METHODS: Under 
      pentobarbital anesthesia, rats were fixed to a stereotaxic apparatus, and bipolar 
      electrodes were implanted into the right amygdala. A guide cannula made of 
      stainless steel tubing was implanted into the right lateral ventricle. Electrodes 
      were connected to a miniature receptacle, which was embedded in the skull with 
      dental cement. EEG was recorded with an electroencephalograph; stimulation of the 
      amygdala was applied bipolarly every day by a constant-current stimulator and 
      continued until a generalized convulsion was obtained. RESULTS: 
      Intracerebroventricular (i.c.v.) injection of histamine at doses of 2-10 microg 
      resulted in a dose-related inhibition of amygdaloid-kindled seizures. I.c.v. 
      injection of calcium chloride at doses of 10-50 microg and A23187 at doses of 
      2-10 microg also caused dose-dependent inhibition of amygdaloid-kindled seizures. 
      Calcium chloride at a dose of 10 microg, which showed no significant effect on 
      amygdaloid-kindled seizures when used alone, significantly potentiated the effect 
      of histamine. Similar findings were observed with A23187 at a dose of 2 microg. 
      In addition, EGTA and EGTA/AM antagonized the inhibition of kindled seizures 
      induced by histamine. Moreover, the inhibition of kindled seizures induced by 
      histamine was antagonized by KN62. However, calphostin C did not antagonize the 
      inhibitory effect of histamine. CONCLUSIONS: These results indicated that 
      histamine-induced inhibition of amygdaloid-kindled seizures may be closely 
      associated with a calcium calmodulin-dependent protein kinase II activation 
      pathway.
FAU - Okuma, C
AU  - Okuma C
AD  - Department of Pharmacology, Faculty of Pharmaceutical Sciences, Okayama 
      University, Okayama, Japan.
FAU - Hirai, T
AU  - Hirai T
FAU - Kamei, C
AU  - Kamei C
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Epilepsia
JT  - Epilepsia
JID - 2983306R
RN  - 0 (Naphthalenes)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 37H9VM9WZL (Calcimycin)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 820484N8I3 (Histamine)
RN  - 99590-86-0 (EGTA acetoxymethyl ester)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.1.- (calcium-dependent protein kinase)
RN  - I271P23G24 (calphostin C)
RN  - M4I0D6VV5M (Calcium Chloride)
SB  - IM
MH  - Amygdala/drug effects/enzymology/*physiology
MH  - Animals
MH  - Calcimycin/pharmacology
MH  - Calcium Chloride/pharmacology
MH  - Egtazic Acid/*analogs & derivatives/pharmacology
MH  - Electric Stimulation
MH  - Electroencephalography/drug effects
MH  - Histamine/*pharmacology
MH  - Kindling, Neurologic/*drug effects/physiology
MH  - Male
MH  - Naphthalenes/pharmacology
MH  - Protein Kinase Inhibitors
MH  - Protein Kinases/physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Seizures/enzymology/physiopathology/*prevention & control
EDAT- 2002/03/07 10:00
MHDA- 2002/03/19 10:01
CRDT- 2002/03/07 10:00
PHST- 2002/03/07 10:00 [pubmed]
PHST- 2002/03/19 10:01 [medline]
PHST- 2002/03/07 10:00 [entrez]
AID - 05601 [pii]
AID - 10.1046/j.1528-1157.2001.05601.x [doi]
PST - ppublish
SO  - Epilepsia. 2001 Dec;42(12):1494-500. doi: 10.1046/j.1528-1157.2001.05601.x.