Autoregulation of histamine release in medulla oblongata via H3-receptors in rabbits

Kanamaru, Mitsuko; Iwase, Michiko; Homma, Ikuo

doi:10.1016/s0168-0102(98)00023-6

Cited by 17 publications

(12 citation statements)

References 28 publications

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“…These results are consistent with previous studies (Jansen et al. , 1998; Kanamaru et al. , 1998; Westerink et al.…”

Section: Discussionsupporting

confidence: 94%

“…It was found that intra-TMN administration of immepip decreases, and of thioperamide increases, local histamine levels. These results are consistent with previous studies (Jansen et al, 1998;Kanamaru et al, 1998;Westerink et al, 2002;Giannoni et al, 2009Giannoni et al, , 2010. However, intra-TMN administration of immepip or thioperamide had no effect on the cortical histamine levels.…”

Section: Discussionsupporting

confidence: 93%

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The role of cortical and hypothalamic histamine‐3 receptors in the modulation of central histamine neurotransmission: an in vivo electrophysiology and microdialysis study

Flik

Dremencov

Cremers

et al. 2011

Eur J of Neuroscience

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The current study aimed to investigate the effect of histamine-3 (H(3)) receptors, expressed in the tuberomammillary nucleus (TMN) of the hypothalamus and in the prefrontal cortex (PFC), on histamine neurotransmission in the rat brain. The firing activity of histamine neurons in the TMN was measured using in vivo extracellular single-unit electrophysiology, under propofol anesthesia. Extracellular histamine levels were determined using the dual (PFC and TMN) probe microdialysis, in freely-moving animals. Histamine levels in dialysates were determined using high-performance liquid chromatography (HPLC) and fluorescence detection. It was found that systemic administration of the selective H(3)-agonist, immepip, decreases, and the reverse H(3) /H(4)-agonist, thioperamide, increases the firing activity of histamine neurons in the TMN and the release of histamine in TMN and PFC. Local perfusion of immepip into the TMN increased, and thioperamide decreased, histamine levels in the TMN but not in the PFC. Local perfusion of immepip into the PFC, however, decreased extracellular histamine levels in both TMN and PFC. It can be concluded that brain H(3) receptors, and especially those expressed in the PFC, play an important role in the autoregulation of histamine neurotransmission. It is possible that H(3) receptors in the PFC are expressed on pyramidal neurons projecting to the TMN, and activation of these receptors diminishes glutamate excitatory input from PFC to the TMN. As the brain histamine system has a role in pathophysiology of psychotic, affective, cognitive, sleep and eating disorders, H(3) receptors are potential targets for future CNS medications.

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“…These results are consistent with previous studies (Jansen et al. , 1998; Kanamaru et al. , 1998; Westerink et al.…”

Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 93%

The role of cortical and hypothalamic histamine‐3 receptors in the modulation of central histamine neurotransmission: an in vivo electrophysiology and microdialysis study

Flik

Dremencov

Cremers

et al. 2011

Eur J of Neuroscience

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“…H-3 receptors reportedly decrease histamine release presynaptically also in the brainstem [14], and consequently H-3 receptor activation should evoke respiratory suppression by down-regulation of the tonically active histaminergic transmitter system. In the present study, however, the opposite was the case.…”

Section: Histaminergic Neuromodulation Under Normoxiamentioning

confidence: 99%

Histaminergic modulation of the intact respiratory network of adult mice

Dutschmann

Büsselberg

et al. 2003

Pflugers Arch - Eur J Physiol

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Histaminergic modulation of neuronal activity in the respiratory network was investigated under normoxic and hypoxic conditions in the working heart-brainstem preparation of adult mice. Systemic application of histamine, as well as the H-1 and H-3 receptor agonists 6-[2-(4-imidazolyl)ethylamino]- N-(4-trifluoromethylphenyl) heptanecarboxamide (HTMT) and imetit, 0.5-10 micro M, significantly increased the frequency of respiratory burst discharges. Dimaprit, an H-2 receptor agonist, had no effect on respiratory activity. To test for ongoing histaminergic modulation we applied the histamine receptor antagonists pyrilamine (H-1); cimetidine (H-2) and thioperamide (H-3), each 0.5-10 micro M. Only the H-1 receptor antagonist had significant effects, viz. reduction of respiratory frequency and depression of burst amplitude. Underlying effects of histamine receptor activation were identified at the cellular level. Intracellular recordings showed that histamine mediated an increase in synaptic drive potentials in inspiratory neurones while augmentation of inhibitory and excitatory synaptic activity was observed in expiratory neurones. The augmented synaptic depolarisation of inspiratory neurones was blocked by the H-1 receptor antagonist. Histaminergic modulation is also involved in the hypoxic response of the respiratory network. Blockade of H-1 receptors significantly attenuated secondary depression of the biphasic hypoxic responses, while hypoxic augmentation was not affected. We conclude that histamine is a functional neuromodulator, which is tonically active in the respiratory network and is activated further during hypoxia. The data indicate that histaminergic neuromodulation acts predominantly via H-1 receptors.

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“…There are at least three possible ways of the effect -the blockage of brain stem H 2 histamine receptors which mediate the hypotensive action [18], the agonistic properties of H 2 antagonists or the affinity of H 2 antagonists to H 3 receptors controlling histamine biosynthesis and release [19]. Furthermore, blockage of pre-synaptic central histamine H 3 receptors with thioperamide also leads to the pressor reaction which may result from the increase in endogenous histamine release [19,20]. In addition, the regulatory role of H 3 histamine receptors in the secretion of other central neurotransmitters may take place, since there are interactions between central histaminergic and other neuronal systems, including noradrenergic [21], muscarinic cholinergic [22] and opioidergic [23] systems, in cardiovascular regulation.…”

Section: Fig 1 Skf 91488-induced Maximal Increases In Map (A) and Hmentioning

confidence: 99%

Endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats – studies with histamine N-methyltransferase inhibitor SKF 91488

Jochem¹

2002

Inflamm. res.

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Autoregulation of histamine release in medulla oblongata via H3-receptors in rabbits

Cited by 17 publications

References 28 publications

The role of cortical and hypothalamic histamine‐3 receptors in the modulation of central histamine neurotransmission: an in vivo electrophysiology and microdialysis study

The role of cortical and hypothalamic histamine‐3 receptors in the modulation of central histamine neurotransmission: an in vivo electrophysiology and microdialysis study

Histaminergic modulation of the intact respiratory network of adult mice

Endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats – studies with histamine N-methyltransferase inhibitor SKF 91488

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