Endogenous serotonin modulates histamine release in the rat hypothalamus as measured by in vivo microdialysis

Laitinen, Kirsti; Tuomisto, Leena; Laitinen, Jarmo T.

doi:10.1016/0014-2999(95)00397-4

Cited by 26 publications

(10 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although it cannot be entirely ruled out, some involvement of endogenous serotonin in the enhancing effect of methamphetamine on t-MeHA levels seems unlikely. Serotonin was reported to induce histamine release after local perfusion in the rat hypothalamus (Laitinen et al, 1995) and to increase the firing rate of tuberomammillary neurons in vitro (Eriksson et al, 2001). However, these local stimulations may play a minor part in the overall in vivo regulation of histamine neurons by endogenous serotonin because we recently showed that histamine neuron activity is under tonic inhibition by endogenous serotonin via 5-HT 2 receptors (Morisset et al, 1999).…”

Section: Discussionmentioning

confidence: 98%

Acute and Chronic Effects of Methamphetamine on Tele-Methylhistamine Levels in Mouse Brain: Selective Involvement of the D₂ and not D₃Receptor

Morisset-Lopez¹,

Pilon²,

Tardivel-Lacombe³

et al. 2002

J Pharmacol Exp Ther

View full text Add to dashboard Cite

We have explored the role of endogenous dopamine in the control of histaminergic neuron activity in mouse brain regions evaluated by changes in tele-methylhistamine (t-MeHA) levels. In vitro, methamphetamine released [ 3 H]noradrenaline but failed to release [ 3 H]histamine from synaptosomes. In vivo, methamphetamine enhanced t-MeHA levels by about 2-fold with ED 50 values of ϳ1 mg/kg in caudate putamen, nucleus accumbens, cerebral cortex, and hypothalamus. This response selectively involved the D 2 and not the D 3 receptor as indicated by its blockade by haloperidol and by its persistence after administration of nafadotride, a D 3 receptor preferential ligand, or in (Ϫ/Ϫ) D 3 receptor-deficient mice. The t-MeHA response to methamphetamine was delayed compared with the locomotoractivating effect of this drug, suggesting that it is of compensatory nature. In agreement, ciproxifan, an inverse agonist known to enhance histamine neuron activity, decreased the hyperlocomotion induced by methamphetamine. Repeated methamphetamine administration resulted in the expected sensitization to the hyperlocomotor effect of the drug but did not modify either the ED 50 or the E max regarding t-MeHA levels. However, it resulted in an enhanced basal t-MeHA level (ϩ30 -40%), which was sustained for at least 11 days after withdrawal in hypothalamus, striatum, and cerebral cortex and suppressed by haloperidol. Hence, both the acute and chronic administration of methamphetamine enhance histamine neuron activity, presumably in a compensatory manner. Repeated methamphetamine administration also resulted in a modified balance in the opposite influences of dopamine and serotonin on histaminergic neurons as revealed by the enhanced response to haloperidol and abolished response to ketanserin, respectively.Histamine neurons originate from the tuberomammillary nucleus in the hypothalamus and project in a highly divergent manner to many brain regions, namely, in the limbic system where the highest density of terminals is encountered Onodera et al., 1994). Whereas the function of these neurons in physiological processes such as arousal, attention, or hormonal controls is well documented, very little was known about their possible involvement in brain disorders.Recently, however, several pieces of evidence have started to suggest a possible involvement of brain histaminergic neurons in the pathophysiology of schizophrenia and/or the action of typical and atypical antipsychotic agents. Overdose of various H 1 receptor antagonists of the first generation was repeatedly reported to result in toxic psychoses with hallucinations resembling schizophrenia and the hallucinogenic potential of these drugs has even led to abuse (Sangalli, 1997). In several open studies famotidine, an H 2 receptor antagonist, was found to improve schizophrenic patients, a finding that remains to be confirmed in control studies.Methamphetamine, a psychotogenic drug that induces an enhanced dopamine release in schizophrenic patients (Laruelle et al., 1996), was shown ...

show abstract

Section: Discussionmentioning

confidence: 98%

Acute and Chronic Effects of Methamphetamine on Tele-Methylhistamine Levels in Mouse Brain: Selective Involvement of the D₂ and not D₃Receptor

Morisset-Lopez¹,

Pilon²,

Tardivel-Lacombe³

et al. 2002

J Pharmacol Exp Ther

View full text Add to dashboard Cite

show abstract

“…In vivo microdialysis studies were performed 3 months after the operation, as previously described (Laitinen et al 1995). The rats were anesthetized with chloral hydrate (400 mg/kg, i.p.)…”

Section: Methodsmentioning

confidence: 99%

Brain histamine H3 receptors in rats with portacaval anastomosis: in vitro and in vivo studies

Lozeva

Attila

Anttila

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

The long-term effects of portacaval anastomosis (PCA) on histamine H3 receptors in rat brain were studied by in vitro and in vivo methods. The overflow of histamine from the anterior hypothalamus and from cortex after long-term PCA was determined by in vivo microdialysis. The binding properties of [3H]-R-alpha-methylhistamine in membranes from cortex, cerebellum, and rest of brain (ROB) were examined with saturation binding experiments. The regional distribution of [3H]-R-alpha-methylhistamine binding sites in the brain of sham- and PCA-operated rats was assessed also with autoradiography. The tissue levels of histamine were significantly elevated in cortex and ROB of PCA-operated rats. In addition, the spontaneous and K+-evoked overflow of histamine from anterior hypothalamus, and the thioperamide-induced overflow from both anterior hypothalamus and cortex were increased after chronic PCA. In spite of the significantly elevated tissue concentrations and the moderate increase in histamine release, the binding properties of [3HI-R-alpha-methylhistamine to cortical membranes were not significantly changed. However, the autoradiography study did reveal a decrease in [3H]-R-alpha-methylhistamine binding density, particularly in striatum and cortex, where H3 receptors are located mainly at non-histaminergic neurons. In conclusion, we suggest that there is a region-selective increase in the histaminergic activity in chronic PCA, which leads to the down-regulation of somadendritic and pre-synaptic H3 receptors located at non-histaminergic neurons. At the same time, the autoreceptor mediated control of histamine neuronal activity via pre-synaptic H3 receptors located at histaminergic neurons is preserved after long-term PCA.

show abstract

“…Histamine is synthesized from histidine by histidine-decarboxylase (HDC) ( Haas et al, 2008 ) in neurons restricted to the hypothalamic tuberomamillary nucleus (TMN) and innervating most of the brain, including the raphe nuclei ( Watanabe et al, 1983 ). Experimental studies demonstrated functional interactions between histaminergic and serotonergic systems ( Airaksinen et al, 1989 ; Laitinen et al, 1995 ; Brown et al, 2002 ) that share control of functions impaired in depression, such as appetite, cognition, emotion, and sleep ( Passani et al, 2004 ; Haas et al, 2008 ). Histamine H 1 -receptor activation increased the firing rate of serotonergic neurons ( Eriksson et al, 2001 ).…”

Section: Introductionmentioning

confidence: 99%

Brain Histamine Is Crucial for Selective Serotonin Reuptake Inhibitors‘ Behavioral and Neurochemical Effects

Munari¹,

Provensi²,

Passani³

et al. 2015

IJNPPY

View full text Add to dashboard Cite

Backgound:The neurobiological changes underlying depression resistant to treatments remain poorly understood, and failure to respond to selective serotonin reuptake inhibitors may result from abnormalities of neurotransmitter systems that excite serotonergic neurons, such as histamine.Methods:Using behavioral (tail suspension test) and neurochemical (in vivo microdialysis, Western-blot analysis) approaches, here we report that antidepressant responses to selective serotonin reuptake inhibitors (citalopram or paroxetine) are abolished in mice unable to synthesize histamine due to either targeted disruption of histidine decarboxylase gene (HDC-/-) or injection of alpha-fluoromethylhistidine, a suicide inhibitor of this enzyme.Results:In the tail suspension test, all classes of antidepressants tested reduced the immobility time of controls. Systemic reboxetine or imipramine reduced the immobility time of histamine-deprived mice as well, whereas selective serotonin reuptake inhibitors did not even though their serotonergic system is functional. In in vivo microdialysis experiments, citalopram significantly increased histamine extraneuronal levels in the cortex of freely moving mice, and methysergide, a serotonin 5-HT1/5-HT2 receptor antagonist, abolished this effect, thus suggesting the involvement of endogenous serotonin. CREB phosphorylation, which is implicated in the molecular mechanisms of antidepressant treatment, was abolished in histamine-deficient mice treated with citalopram. The CREB pathway is not impaired in HDC-/- mice, as administration of 8-bromoadenosine 3’, 5’-cyclic monophosphate increased CREB phosphorylation, and in the tail suspension test it significantly reduced the time spent immobile by mice of both genotypes.Conclusions:Our results demonstrate that selective serotonin reuptake inhibitors selectively require the integrity of the brain histamine system to exert their preclinical responses.

show abstract

Endogenous serotonin modulates histamine release in the rat hypothalamus as measured by in vivo microdialysis

Cited by 26 publications

References 36 publications

Acute and Chronic Effects of Methamphetamine on Tele-Methylhistamine Levels in Mouse Brain: Selective Involvement of the D₂ and not D₃Receptor

Acute and Chronic Effects of Methamphetamine on Tele-Methylhistamine Levels in Mouse Brain: Selective Involvement of the D₂ and not D₃Receptor

Brain histamine H3 receptors in rats with portacaval anastomosis: in vitro and in vivo studies

Brain Histamine Is Crucial for Selective Serotonin Reuptake Inhibitors‘ Behavioral and Neurochemical Effects

Contact Info

Product

Resources

About

Endogenous serotonin modulates histamine release in the rat hypothalamus as measured by in vivo microdialysis

Cited by 26 publications

References 36 publications

Acute and Chronic Effects of Methamphetamine on Tele-Methylhistamine Levels in Mouse Brain: Selective Involvement of the D2 and not D3Receptor

Acute and Chronic Effects of Methamphetamine on Tele-Methylhistamine Levels in Mouse Brain: Selective Involvement of the D2 and not D3Receptor

Brain histamine H3 receptors in rats with portacaval anastomosis: in vitro and in vivo studies

Brain Histamine Is Crucial for Selective Serotonin Reuptake Inhibitors‘ Behavioral and Neurochemical Effects

Contact Info

Product

Resources

About

Acute and Chronic Effects of Methamphetamine on Tele-Methylhistamine Levels in Mouse Brain: Selective Involvement of the D₂ and not D₃Receptor

Acute and Chronic Effects of Methamphetamine on Tele-Methylhistamine Levels in Mouse Brain: Selective Involvement of the D₂ and not D₃Receptor