In vivo release by histamine agonists and antagonists of endogenous catecholamines in the cat hypothalamus

Philippu, A.; Bald, Martin; Kraus, Anja; Dietl, H.

doi:10.1007/bf00517307

Cited by 46 publications

(14 citation statements)

References 24 publications

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“…Levels rose early in the light phase and were highest during illumination for levels of norepinephrine [55,56], gammaaminobutyric acid [57], cortisol [58,59], vasopressin [60] and oxytocin [60][61][62]. Although no causal relationship has been demonstrated to link these rhythmic changes in monkey CSF, it is interesting to note that histamine and histamine agonists were shown to stimulate in vivo release of catecholamines in the hypothalamus of the cat [63] and peptide hormones in rodents and man [see 8].…”

Section: Discussionmentioning

confidence: 97%

Diurnal fluctuation in levels of histamine metabolites in cerebrospinal fluid of rhesus monkey

Prell

Khandelwal²,

Burns³

et al. 1989

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In samples of ventricular cerebrospinal fluid (CSF) that were collected from a conscious, restrained rhesus monkey at intervals of 30 90 min, levels of the histamine metabolites, tele-methylhistamine (t-MH) and tele-methylimidazoleacetic acid (t-MIAA), were determined by gas chromatography-mass spectrometry. Levels of t-MH and t-MIAA each showed time-related fluctuations. Peak and trough concentrations of t-MIAA, the product of t-MH, paralleled, but lagged about 2 h behind, the levels of t-MH. Within the first 3 h of illumination, metabolite levels increased more than 3-fold; they fell sharply within the first 3 h of darkness. Mean levels of t-MH and t-MIAA were significantly higher during periods of illumination than of darkness. Fluctuations in the levels of pros-methylimidazoleacetic acid (p-MIAA), an endogenous isomer of t-MIAA that is not a histamine metabolite, were markedly different from those of t-MH or t-MIAA; p-MIAA levels peaked only at the middle of the dark period. The time-related fluctuations in levels of t-MH and t-MIAA, but not p-MIAA, are similar to the daily rhythmic changes observed in monkey CSF for the levels of other central neurotransmitters and peptide neurohormones.

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Section: Discussionmentioning

confidence: 97%

Diurnal fluctuation in levels of histamine metabolites in cerebrospinal fluid of rhesus monkey

Prell

Khandelwal²,

Burns³

et al. 1989

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“…These data implied a possibility that a putative histamine transporter would have a similar structure to other monoamine transporters. Accordingly, we investigated the effects of monoamine uptake inhibitors on [ [1,6,25,41,46] , and also has many interactions with other neurotransmitters [22] . Histamine agonists and antagonists modulate dopamine release and dopamine turnover via histamine H 3 receptors and dopamine agonists, and antagonists modulate histamine release via dopamine receptors in the hypothalamus [3,4,22,24,27,37,38] .…”

Section: Discussionmentioning

confidence: 99%

Evidence for the Presence of Histamine Uptake into the Synaptosomes of Rat Brain

Sakurai

Oreland

et al. 2006

Pharmacology

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Histamine has many physiological roles in the brain and periphery. Neuronal histamine is metabolized almost exclusively by histamine N-methyltransferase. Although several neurotransmitter systems such as dopamine and 5-hydroxytryptamine have their specific reuptake system in their neurons and glial cells, a specific histamine reuptake system into the corresponding nerve terminals or glial cells has not yet been clearly elucidated. We characterized the uptake of histamine into the P2 fractions of rat brain homogenized in 0.32 mol/l sucrose using in vitro uptake techniques. [³H]histamine uptake increased with the increment of added protein amount and elapsed time. [³H]histamine uptake was also temperature-dependent. The uptake of [³H]histamine into the P2 fractions occurs by two saturable processes, a high-affinity and a low-affinity, characterized by K_m values of 0.16 and 1.2 µmol/l, respectively. Na⁺, Cl^– and HCO₃^– ions were essential for the uptake of histamine in P2 fractions. [³H]histamine uptake was inhibited in the presence of several tricyclic antidepressants. In accordance with this, the endogenous release of histamine from brain slices evoked by 100 mmol/l K⁺ was augmented in the presence of 20 µmol/l imipramine. These results further support the existence of a specific histamine uptake system in the brain, although the precise molecular entities have not been identified until now.

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“…The possibility that the inhibitory effect of RmHA is mediated via H3 heteroreceptors located on serotonergic or adren ergic neurons would seem to be in accordance with the fact that serotonin exerts stimulatory and norepinephrine exerts both inhibitory and stimulatory actions on the re lease of PRL, ACTH and (TEND [29][30][31], Inhibition of serotonin and norepinephrine release by RmHA-or HAinduced activation of Hi heteroreceptors might therefore lead to a decreased hormone response to stress. However, interpretation of the data is intricate, since it has also been found that HA stimulates hypothalamic norepi nephrine release by activation of Hi or Hj receptors [32,33] and that HA increases synaptosomal release of sero tonin [34] and its turnover in the hypothalamus probably by activation of H: receptors [35]. Furthermore, hista minergic stimulation of PRL secretion seems to involve serotonergic neurons [36], Blockade of Hi receptors by the antagonist thiopera mide prevented the inhibitory effect of the H?…”

Section: Discussionmentioning

confidence: 99%

Responses of Anterior Pituitary Hormones and Hypothalamic Histamine to Blockade of Histamine Synthesis and to Selective Activation or Inactivation of Presynaptic Histamine H<sub>3</sub> Receptors in Stressed Rats

et al. 1993

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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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In vivo release by histamine agonists and antagonists of endogenous catecholamines in the cat hypothalamus

Cited by 46 publications

References 24 publications

Diurnal fluctuation in levels of histamine metabolites in cerebrospinal fluid of rhesus monkey

Diurnal fluctuation in levels of histamine metabolites in cerebrospinal fluid of rhesus monkey

Evidence for the Presence of Histamine Uptake into the Synaptosomes of Rat Brain

Responses of Anterior Pituitary Hormones and Hypothalamic Histamine to Blockade of Histamine Synthesis and to Selective Activation or Inactivation of Presynaptic Histamine H<sub>3</sub> Receptors in Stressed Rats

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