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

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Abstract
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 α-fluoromethylhistidine (α-FMH; 200 µg intracerebroventricularly (icv) at –120 min) or the specific H3 receptor agonist R(α)methylhistamine (RmHA; 10 mg/kg intraperitoneally (ip) at –180 and –60 min) inhibited by 30–80% the responses of prolactin (PRL), corticotropin (ACTH) and β-endorphin (β-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 × 2) on the hormone response to 5 min of restraint stress was prevented by simultaneous ip administration of the H3 receptor antagonist thioperamide. α-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 β-END, although the compound increased the hypothalamic content of t-meHA 2-fold. Insulin-induced (1 IU/kg ip) hypoglycemia increased the plasma concentration of ACTH and β-END 2- and 1.5-fold, respectively, and increased the hypothalamic content of t-meHA almost 2-fold, which indicates an increased turnover of neuronal HA. α-FMH or RmHA prevented the insulin-induced release of ACTH and β-END. Insulin had no significant effect on PRL secretion. In conclusion, the findings that the response of PRL, ACTH and α-END to stress or insulin-induced hypoglycemia was inhibited by blockade of HA synthesis or activation of H3 receptors and that hypothalamic HA turnover increased in response to hypoglycemia further implicate a role of hypothalamic histaminergic neurons in the neuroendocrine regulation of pituitary hormone secretion.

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