Abstract— The intraperitoneal administration of L‐histidine in a dose of 1000 mg/kg increased threefold the whole brain levels of histamine in the mouse. This increase was evident in all brain regions except the medulla oblongata‐pons. The subcellular localization of histamine and histidine was the same in mice administered bhistidine as in salinetreated animals. Cold exposure and restraint further augmented the elevation of histamine elicited by histidine treatment. a‐Hydrazino‐histidine and 4‐bromo‐3‐hydroxybenzyloxyamine (NSD‐1055) but not a‐methyl‐DOPA inhibited histidine decarboxylase [EC 188.8.131.52 activity in mouse brain homogenates and prevented the increase in brain histamine after histidine administration. NSD‐1055 and a‐hydrazino‐histidine also lowered brain levels of histamine by 50 per cent. NSD‐1055 lowered whole brain levels of histamine rapidly, with a half‐life for the depletable histamine pool of about 5 min. Assuming that inhibition of histidine decarboxylase accounted for the reduction in histamine, then the rate of histamine decline reflects the rate of histamine turnover, and our results suggest that a portion of mouse brain histamine turns over quite rapidly. Reserpine lowered brain levels of histamine by about 50 per cent, whereas the antihistaminic agent, dexbrompheniramine, and sodium pentobarbital elevated histamine levels.
|Original language||English (US)|
|Number of pages||14|
|Journal||Journal of Neurochemistry|
|State||Published - Feb 1972|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience