Concentration of histamine in different parts of the brain and hypophysis of rabbit: effect of treatment with histidine, certain other amino acids and histamine

Abstract

4. In conscious rabbits, intravenous infusion of histidine in the dose range 62 to 1,500 mg/kg, raised significantly (P<0-01) the concentration of histamine in all regions of the brain examined, the pattern of distribution remaining unchanged. The largest increases occurred in the mid brain (90 to 320%) and in the hypothalamus (50 to 250%); in these areas the higher doses produced higher concentrations. Elsewhere in the brain the concentration rose in response to the lowest dose of histidine, but was not increased when higher doses were given. Concentrations in the anterior lobe of the hypophysis were unaltered. 5. The infusion of histidine, unlike that of amino acid precursors, of the monoamines, produced no obvious disturbance in the animals. 6. The rise in brain histamine after dosage with histidine persisted for several hours, depending on the dose; with 500 mg/kg, the rise was virtually unchanged after 16 hours. 7. Histamine (5 mg/kg by intravenous infusion) raised the concentration of histamine in the hypophysis but not in the brain.8. After the infusion of DOPA, a-methyldopa or 5-hydroxytryptophan, the histamine concentration rose in the mid-brain but not in other parts of the brain.9. These amino acids, when infused singly with histidine, did not interfere with the histidine-induced rise of brain histamine.

Role of histamine in rodent antinociception

“…The latter dose might seem to be high, but it should be considered that another amino acid, L-DOPA, also needs to be administered at a dose of 1000 mg kg-' in order to show any effect (Blaschko & Chrusciel, 1960). Nevertheless, even at the highest dose of L-histidine, the gross behaviour of animals was not modified during our experiments, as formerly reported by Schwartz et al (1972) for rats and by Abou et al (1973) for rabbits.…”

“…The choice of histidine as a tool for studying the role of endogenous histamine in antinociception was made on the basis that, as Schwartz et al (1972) and Abou et al (1973) demonstrated, its decarboxylating enzyme is not saturated in normal conditions. Systemic administrations of L-histidine are therefore able to enhance brain histamine levels.…”

Measurement of tele-methylhistamine and histamine in human cerebrospinal fluid, urine, and plasma

“…Analogously, in spinal cord the HA concentration does not exceed that in brain [50,56]; the cord contains HMT [55]. It is also unlikely that the HA in CSF derives from plasma, for, among other reasons, the plasma level is about one-twentieth that of CSF Sources of CSF HA could be the leptomeninges, including the choroid plexus, which has HA-containing mast cells [50,52,[57][58][59][60][61]; the circumventricular organs, which contain mast cells [62] and a high concentration of HA [63]; and mast cells associated with blood vessels [59,64]. Peritoneal mast cells of the rat [65] and neoplastic cells of the mouse do not metabolize histamine, but rather release it [65,66].…”

Antidepressant‐like effects of endogenous histamine and of two histamine H1 receptor agonists in the mouse forced swim test

“…Histamine synthesis can be enhanced by systemic administration of the precursor, L‐histidine, since the enzyme HDC is not saturated in physiological conditions (Schwartz et al , 1972; Abou et al , 1973). Furthermore, histidine loads (1000 mg kg ‐1 ) in mice produce a rise in histamine whole brain levels with a maximum occurring 1 h after treatment, and a slowly decreasing plateau thereafter (Taylor & Snyder, 1972).…”