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[PMID]:28274820
[Au] Autor:Andersson R; Galter D; Papadia D; Fisahn A
[Ad] Endereço:Neuronal Oscillations Laboratory, Neurogeriatrics Division, Center for Alzheimer Research, Dept. of Neurobiology, Care Sciences and Society, Karolinska Institutet, 14186 Stockholm, Sweden.
[Ti] Título:Histamine induces KCNQ channel-dependent gamma oscillations in rat hippocampus via activation of the H1 receptor.
[So] Source:Neuropharmacology;118:13-25, 2017 May 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Histamine is an aminergic neurotransmitter, which regulates wakefulness, arousal and attention in the central nervous system. Histamine receptors have been the target of efforts to develop pro-cognitive drugs to treat disorders such as Alzheimer's disease and schizophrenia. Cognitive functions including attention are closely associated with gamma oscillations, a rhythmical electrical activity pattern in the 30-80 Hz range, which depends on the synchronized activity of excitatory pyramidal cells and inhibitory fast-spiking interneurons. We set out to explore whether histamine has a role in promoting gamma oscillations in the hippocampus. Using in-situ hybridization we demonstrate that histamine receptor subtypes 1, 2 and 3 are expressed in stratum pyramidale of area CA3 in rats. We show that both pyramidal cells and fast-spiking interneurons depolarize and increase action potential firing in response to histamine in vitro. The activation of histamine receptors generates dose-dependent, transient gamma oscillations in area CA3 of the hippocampus - the locus of the gamma rhythm generator. We also demonstrate that this histamine effect is independent of muscarinic receptors. Using specific antagonists we provide evidence that histamine gamma rhythmogenesis specifically depends on the H1 receptor. Histamine also depolarized both pyramidal cells and fast-spiking interneurons and increased membrane resistance in pyramidal cells. The increased membrane resistance is potentially mediated by the inhibition of potassium channels because application of the KCNQ channel opener ICA110381 abolished the oscillations. Taken together our data demonstrate a novel and physiological mechanism for generating gamma oscillations in hippocampus and suggest a role for KCNQ channels in this cognition-relevant brain activity.
[Mh] Termos MeSH primário: Ritmo Gama/efeitos dos fármacos
Hipocampo
Histamínicos/farmacologia
Histamina/farmacologia
Canais de Potássio KCNQ/metabolismo
Receptores Histamínicos/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Animais Recém-Nascidos
Benzamidas/farmacologia
Glutamato Descarboxilase/metabolismo
Hipocampo/citologia
Hipocampo/efeitos dos fármacos
Hipocampo/fisiologia
Técnicas In Vitro
Masculino
Moduladores de Transporte de Membrana/farmacologia
Rede Nervosa/efeitos dos fármacos
Rede Nervosa/fisiologia
Neurônios/efeitos dos fármacos
Neurotransmissores/farmacologia
Piridinas/farmacologia
Ratos
Ratos Sprague-Dawley
Ubiquitina Tiolesterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-chloro-N-(6-chloropyridin-3-yl)benzamide); 0 (Benzamides); 0 (Histamine Agents); 0 (KCNQ Potassium Channels); 0 (Membrane Transport Modulators); 0 (Neurotransmitter Agents); 0 (Pyridines); 0 (Receptors, Histamine); 820484N8I3 (Histamine); EC 3.4.19.12 (Ubiquitin Thiolesterase); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE


  2 / 98 MEDLINE  
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[PMID]:27807161
[Au] Autor:Uygun DS; Ye Z; Zecharia AY; Harding EC; Yu X; Yustos R; Vyssotski AL; Brickley SG; Franks NP; Wisden W
[Ad] Endereço:Department of Life Sciences and.
[Ti] Título:Bottom-Up versus Top-Down Induction of Sleep by Zolpidem Acting on Histaminergic and Neocortex Neurons.
[So] Source:J Neurosci;36(44):11171-11184, 2016 Nov 02.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Zolpidem, a GABA receptor-positive modulator, is the gold-standard drug for treating insomnia. Zolpidem prolongs IPSCs to decrease sleep latency and increase sleep time, effects that depend on α2 and/or α3 subunit-containing receptors. Compared with natural NREM sleep, zolpidem also decreases the EEG power, an effect that depends on α1 subunit-containing receptors, and which may make zolpidem-induced sleep less optimal. In this paper, we investigate whether zolpidem needs to potentiate only particular GABAergic pathways to induce sleep without reducing EEG power. Mice with a knock-in F77I mutation in the GABA receptor γ2 subunit gene are zolpidem-insensitive. Using these mice, GABA receptors in the frontal motor neocortex and hypothalamic (tuberomammillary nucleus) histaminergic-neurons of γ2I77 mice were made selectively sensitive to zolpidem by genetically swapping the γ2I77 subunits with γ2F77 subunits. When histamine neurons were made selectively zolpidem-sensitive, systemic administration of zolpidem shortened sleep latency and increased sleep time. But in contrast to the effect of zolpidem on wild-type mice, the power in the EEG spectra of NREM sleep was not decreased, suggesting that these EEG power-reducing effects of zolpidem do not depend on reduced histamine release. Selective potentiation of GABA receptors in the frontal cortex by systemic zolpidem administration also reduced sleep latency, but less so than for histamine neurons. These results could help with the design of new sedatives that induce a more natural sleep. SIGNIFICANCE STATEMENT: Many people who find it hard to get to sleep take sedatives. Zolpidem (Ambien) is the most widely prescribed "sleeping pill." It makes the inhibitory neurotransmitter GABA work better at its receptors throughout the brain. The sleep induced by zolpidem does not resemble natural sleep because it produces a lower power in the brain waves that occur while we are sleeping. We show using mouse genetics that zolpidem only needs to work on specific parts and cell types of the brain, including histamine neurons in the hypothalamus, to induce sleep but without reducing the power of the sleep. This knowledge could help in the design of sleeping pills that induce a more natural sleep.
[Mh] Termos MeSH primário: Neocórtex/fisiologia
Neurônios/fisiologia
Piridinas/administração & dosagem
Receptores de GABA-A/metabolismo
Sono/efeitos dos fármacos
Sono/fisiologia
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Feminino
Histamínicos/administração & dosagem
Hipnóticos e Sedativos/administração & dosagem
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neocórtex/citologia
Neocórtex/efeitos dos fármacos
Neurônios/citologia
Neurônios/efeitos dos fármacos
Medicamentos Indutores do Sono/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine Agents); 0 (Hypnotics and Sedatives); 0 (Pyridines); 0 (Receptors, GABA-A); 0 (Sleep Aids, Pharmaceutical); 7K383OQI23 (zolpidem)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161104
[St] Status:MEDLINE


  3 / 98 MEDLINE  
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[PMID]:27260166
[Au] Autor:Rocha SM; Saraiva T; Cristóvão AC; Ferreira R; Santos T; Esteves M; Saraiva C; Je G; Cortes L; Valero J; Alves G; Klibanov A; Kim YS; Bernardino L
[Ad] Endereço:Health Sciences Research Centre, Faculty of Health Sciences, University of Beira Interior, Covilhã, Portugal.
[Ti] Título:Histamine induces microglia activation and dopaminergic neuronal toxicity via H1 receptor activation.
[So] Source:J Neuroinflammation;13(1):137, 2016 Jun 04.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Histamine is an amine widely known as a peripheral inflammatory mediator and as a neurotransmitter in the central nervous system. Recently, it has been suggested that histamine acts as an innate modulator of microglial activity. Herein, we aimed to disclose the role of histamine in microglial phagocytic activity and reactive oxygen species (ROS) production and to explore the consequences of histamine-induced neuroinflammation in dopaminergic (DA) neuronal survival. METHODS: The effect of histamine on phagocytosis was assessed both in vitro by using a murine N9 microglial cell line and primary microglial cell cultures and in vivo. Cells were exposed to IgG-opsonized latex beads or phosphatidylserine (PS) liposomes to evaluate Fcγ or PS receptor-mediated microglial phagocytosis, respectively. ROS production and protein levels of NADPH oxidases and Rac1 were assessed as a measure of oxidative stress. DA neuronal survival was evaluated in vivo by counting the number of tyrosine hydroxylase-positive neurons in the substantia nigra (SN) of mice. RESULTS: We found that histamine triggers microglial phagocytosis via histamine receptor 1 (H1R) activation and ROS production via H1R and H4R activation. By using apocynin, a broad NADPH oxidase (Nox) inhibitor, and Nox1 knockout mice, we found that the Nox1 signaling pathway is involved in both phagocytosis and ROS production induced by histamine in vitro. Interestingly, both apocynin and annexin V (used as inhibitor of PS-induced phagocytosis) fully abolished the DA neurotoxicity induced by the injection of histamine in the SN of adult mice in vivo. Blockade of H1R protected against histamine-induced Nox1 expression and death of DA neurons in vivo. CONCLUSIONS: Overall, our results highlight the relevance of histamine in the modulation of microglial activity that ultimately may interfere with neuronal survival in the context of Parkinson's disease (PD) and, eventually, other neurodegenerative diseases which are accompanied by microglia-induced neuroinflammation. Importantly, our results also open promising new perspectives for the therapeutic use of H1R antagonists to treat or ameliorate neurodegenerative processes.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/efeitos dos fármacos
Agonistas dos Receptores Histamínicos/toxicidade
Histamina/toxicidade
Microglia/efeitos dos fármacos
Receptores Histamínicos H1/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Anexina A5/metabolismo
Encéfalo/citologia
Antígeno CD11b/genética
Antígeno CD11b/metabolismo
Células Cultivadas
Citoesqueleto/efeitos dos fármacos
Citoesqueleto/patologia
Histamínicos/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
NADH NADPH Oxirredutases/genética
NADH NADPH Oxirredutases/metabolismo
NADPH Oxidase 1
Fagocitose/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (CD11b Antigen); 0 (Histamine Agents); 0 (Histamine Agonists); 0 (Reactive Oxygen Species); 0 (Receptors, Histamine H1); 820484N8I3 (Histamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 1.6.- (NADH, NADPH Oxidoreductases); EC 1.6.3.- (NADPH Oxidase 1); EC 1.6.3.- (NOX1 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160605
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-016-0600-0


  4 / 98 MEDLINE  
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[PMID]:27010896
[Au] Autor:Jochem J; Altinbas B; Yalcin M; Ottani A; Giuliani D; Savci V; Kasperska-Zajac A; Guarini S
[Ad] Endereço:Department of Basic Medical Sciences, School of Public Health in Bytom, Medical University of Silesia, Katowice, Poland. jjochem@poczta.onet.pl.
[Ti] Título:Involvement of the histaminergic system in the resuscitating effect of centrally acting leptin in haemorrhagic shock in rats.
[So] Source:J Physiol Pharmacol;67(1):67-74, 2016 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Leptin, acting centrally as a neuromodulator, induces the activation of the sympathetic nervous system, which may lead to a pressor action in normotensive animals. In haemorrhagic shock, leptin administered intracerebroventricularly (icv.) evokes the resuscitating effect, with long-lasting rises in mean arterial pressure (MAP) and heart rate (HR), subsequent increase in peripheral blood flows, and a 100% survival at 2 h. Since leptin is able to activate histaminergic neurons, and centrally acting histamine also induces the resuscitating effect with the activation of the sympathetic nervous system, in the present study, we investigated an involvement of the histaminergic system in leptin-evoked cardiovascular effects in haemorrhagic shock. The model of irreversible haemorrhagic shock, with MAP decreased to and stabilised at 20 - 25 mmHg, has been used. Leptin (20 µg) given icv. at 5 min of critical hypotension evoked 181.5% increase in extracellular hypothalamic histamine concentration during the first 10 min after injection. Rises in MAP, HR and renal, mesenteric and hindquarters blood flows induced by leptin were inhibited by icv. pre-treatment with histamine H1 receptor antagonist chlorpheniramine (50 nmol). In contrast, there was no effect of H2, H3 and H4 receptor antagonists ranitidine (25 nmol), VUF 5681 (25 nmol) and JNJ 10191584 (25 nmol), respectively. In conclusion, the histaminergic system is involved in centrally-acting leptin-induced resuscitating effect in haemorrhagic shock in rats.
[Mh] Termos MeSH primário: Histamínicos/farmacologia
Leptina/farmacologia
Choque Hemorrágico/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Benzimidazóis/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Sistema Cardiovascular/efeitos dos fármacos
Clorfeniramina/farmacologia
Frequência Cardíaca/efeitos dos fármacos
Histamina/farmacologia
Injeções Intraventriculares/métodos
Masculino
Neurônios/efeitos dos fármacos
Ranitidina/farmacologia
Ratos
Ratos Wistar
Fluxo Sanguíneo Regional/efeitos dos fármacos
Choque Hemorrágico/fisiopatologia
Sistema Nervoso Simpático/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzimidazoles); 0 (Histamine Agents); 0 (JNJ 10191584); 0 (Leptin); 3U6IO1965U (Chlorpheniramine); 820484N8I3 (Histamine); 884KT10YB7 (Ranitidine)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160325
[St] Status:MEDLINE


  5 / 98 MEDLINE  
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[PMID]:26811198
[Au] Autor:Liu ZL; Wu X; Luo YJ; Wang L; Qu WM; Li SQ; Huang ZL
[Ad] Endereço:Department of Pulmonary Medicine, Center of Snoring and Sleep Apnea Medicine, Zhongshan Hospital of Fudan University, Shanghai, China.
[Ti] Título:Signaling mechanism underlying the histamine-modulated action of hypoglossal motoneurons.
[So] Source:J Neurochem;137(2):277-86, 2016 Apr.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Histamine, an important modulator of the arousal states of the central nervous system, has been reported to contribute an excitatory drive at the hypoglossal motor nucleus to the genioglossus (GG) muscle, which is involved in the pathogenesis of obstructive sleep apnea. However, the effect of histamine on hypoglossal motoneurons (HMNs) and the underlying signaling mechanisms have remained elusive. Here, whole-cell patch-clamp recordings were conducted using neonatal rat brain sections, which showed that histamine excited HMNs with an inward current under voltage-clamp and a depolarization membrane potential under current-clamp via histamine H1 receptors (H1Rs). The phospholipase C inhibitor U-73122 blocked H1Rs-mediated excitatory effects, but protein kinase A inhibitor and protein kinase C inhibitor did not, indicating that the signal transduction cascades underlying the excitatory action of histamine on HMNs were H1R/Gq/11 /phospholipase C/inositol-1,4,5-trisphosphate (IP3). The effects of histamine were also dependent on extracellular Na(+) and intracellular Ca(2+), which took place via activation of Na(+)-Ca(2+) exchangers. These results identify the signaling molecules associated with the regulatory effect of histamine on HMNs. The findings of this study may provide new insights into therapeutic approaches in obstructive sleep apnea. We proposed the post-synaptic mechanisms underlying the modulation effect of histamine on hypoglossal motoneuron. Histamine activates the H1Rs via PLC and IP3, increases Ca(2+) releases from intracellular stores, promotes Na(+) influx and Ca(2+) efflux via the NCXs, and then produces an inward current and depolarizes the neurons. Histamine modulates the excitability of HMNs with other neuromodulators, such as noradrenaline, serotonin and orexin. We think that these findings should provide an important new direction for drug development for the treatment of obstructive sleep apnea.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Histamínicos/farmacologia
Histamina/farmacologia
Neurônios Motores/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/farmacologia
Estrenos/farmacologia
Líquido Extracelular/efeitos dos fármacos
Líquido Extracelular/metabolismo
Técnicas In Vitro
Bulbo/citologia
Técnicas de Patch-Clamp
Pirrolidinonas/farmacologia
Ratos
Ratos Sprague-Dawley
Sódio/metabolismo
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Estrenes); 0 (Histamine Agents); 0 (Pyrrolidinones); 0 (Sodium Channel Blockers); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 4368-28-9 (Tetrodotoxin); 820484N8I3 (Histamine); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160411
[Lr] Data última revisão:
160411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160127
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.13548


  6 / 98 MEDLINE  
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[PMID]:26781158
[Au] Autor:Lladó-Pelfort L; Troyano-Rodriguez E; van den Munkhof HE; Cervera-Ferri A; Jurado N; Núñez-Calvet M; Artigas F; Celada P
[Ad] Endereço:Department of Neurochemistry and Neuropharmacology, Institut d'Investigacions Biomèdiques de Barcelona (IIBB-CSIC) (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Madrid, Spain; Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barc
[Ti] Título:Phencyclidine-induced disruption of oscillatory activity in prefrontal cortex: Effects of antipsychotic drugs and receptor ligands.
[So] Source:Eur Neuropsychopharmacol;26(3):614-25, 2016 Mar.
[Is] ISSN:1873-7862
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The non-competitive NMDA receptor (NMDA-R) antagonist phencyclidine (PCP) markedly disrupts thalamocortical activity, increasing excitatory neuron discharge and reducing low frequency oscillations (LFO, <4Hz) that temporarily group neuronal discharge. These actions are mainly driven by PCP interaction with NMDA-R in GABAergic neurons of the thalamic reticular nucleus and likely underlie PCP psychotomimetic activity. Here we report that classical (haloperidol, chlorpromazine, perphenazine) and atypical (clozapine, olanzapine, quetiapine, risperidone, ziprasidone, aripripazole) antipsychotic drugs--but not the antidepressant citalopram--countered PCP-evoked fall of LFO in the medial prefrontal cortex (mPFC) of anesthetized rats. PCP reduces LFO by breaking the physiological balance between excitatory and inhibitory transmission. Next, we examined the role of different neurotransmitter receptors to reverse PCP actions. D2-R and D1-R blockade may account for classical antipsychotic action since raclopride and SCH-23390 partially reversed PCP effects. Atypical antipsychotic reversal may additionally involve 5-HT1A-R activation (but not 5-HT2A-R blockade) since 8-OH-DPAT and BAYx3702 (but not M100907) fully countered PCP effects. Blockade of histamine H1-R (pyrilamine) and α1-adrenoceptors (prazosin) was without effect. However, the enhancement of GABAA-R-mediated neurotransmission (using muscimol, diazepam or valproate) and the reduction of excitatory neurotransmission (using the mGluR2/3 agonist LY379268 and the preferential kainite/AMPA antagonist CNQX--but not the preferential AMPA/kainate antagonist NBQX) partially or totally countered PCP effects. Overall, these results shed new light on the neurobiological mechanisms used by antipsychotic drugs to reverse NMDA-R antagonist actions and suggest that agents restoring the physiological excitatory/inhibitory balance altered by PCP may be new targets in antipsychotic drug development.
[Mh] Termos MeSH primário: Potenciais Evocados/efeitos dos fármacos
Antagonistas de Aminoácidos Excitatórios/toxicidade
Fenciclidina/toxicidade
Córtex Pré-Frontal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Antipsicóticos/farmacologia
Dopaminérgicos/farmacologia
Relação Dose-Resposta a Droga
Eletroencefalografia
Análise de Fourier
Histamínicos/farmacologia
Masculino
Ratos
Ratos Wistar
Serotoninérgicos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Dopamine Agents); 0 (Excitatory Amino Acid Antagonists); 0 (Histamine Agents); 0 (Serotonin Agents); J1DOI7UV76 (Phencyclidine)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160120
[St] Status:MEDLINE


  7 / 98 MEDLINE  
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[PMID]:26693882
[Au] Autor:Buoli M; Serati M; Cahn W
[Ad] Endereço:a Department of Psychiatry, Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico , University of Milan , Milan , Italy.
[Ti] Título:Alternative pharmacological strategies for adult ADHD treatment: a systematic review.
[So] Source:Expert Rev Neurother;16(2):131-44, 2016.
[Is] ISSN:1744-8360
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adult Attention Deficit Hyperactivity Disorder (ADHD) is a prevalent psychiatric condition associated with high disability and frequent comorbidity. Current standard pharmacotherapy (methylphenidate and atomoxetine) improves ADHD symptoms in the short-term, but poor data were published about long-term treatment. In addition a number of patients present partial or no response to methylphenidate and atomoxetine. Research into the main database sources has been conducted to obtain an overview of alternative pharmacological approaches in adult ADHD patients. Among alternative compounds, amphetamines (mixed amphetamine salts and lisdexamfetamine) have the most robust evidence of efficacy, but they may be associated with serious side effects (e.g. psychotic symptoms or hypertension). Antidepressants, particularly those acting as noradrenaline or dopamine enhancers, have evidence of efficacy, but they should be avoided in patients with comorbid bipolar disorder. Finally metadoxine and lithium may be particularly suitable in case of comorbid alcohol misuse or bipolar disorder.
[Mh] Termos MeSH primário: Antidepressivos/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico
Estimulantes do Sistema Nervoso Central/uso terapêutico
Dopaminérgicos/uso terapêutico
Agonistas Nicotínicos/uso terapêutico
[Mh] Termos MeSH secundário: Agonistas alfa-Adrenérgicos/uso terapêutico
Adulto
Anfetaminas/uso terapêutico
Compostos Benzidrílicos/uso terapêutico
Compostos Bicíclicos Heterocíclicos com Pontes/uso terapêutico
Bupropiona/uso terapêutico
Desipramina/uso terapêutico
Droxidopa/uso terapêutico
Combinação de Medicamentos
Cloridrato de Duloxetina/uso terapêutico
Guanfacina/uso terapêutico
Histamínicos/uso terapêutico
Seres Humanos
Dimesilato de Lisdexanfetamina/uso terapêutico
Compostos de Lítio/uso terapêutico
Lobelina/uso terapêutico
Mecamilamina/uso terapêutico
Memantina/uso terapêutico
Morfolinas/uso terapêutico
Antagonistas Nicotínicos/uso terapêutico
Nomifensina/uso terapêutico
Paroxetina/uso terapêutico
Piridinas/uso terapêutico
Piridoxina/uso terapêutico
Ácido Pirrolidonocarboxílico/uso terapêutico
Quinazolinonas/uso terapêutico
Cloridrato de Venlafaxina/uso terapêutico
Promotores da Vigília/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (3-(5-chloro-2-furoyl)-3,7-diazabicyclo(3.3.0)octane); 0 (Adderall); 0 (Adrenergic alpha-Agonists); 0 (Amphetamines); 0 (Antidepressive Agents); 0 (Benzhydryl Compounds); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Central Nervous System Stimulants); 0 (Dopamine Agents); 0 (Drug Combinations); 0 (Histamine Agents); 0 (Lithium Compounds); 0 (MK-0249); 0 (Morpholines); 0 (Nicotinic Agonists); 0 (Nicotinic Antagonists); 0 (Pyridines); 0 (Quinazolinones); 0 (Wakefulness-Promoting Agents); 01ZG3TPX31 (Bupropion); 1LGS5JRP31 (Nomifensine); 30OMY4G3MK (Guanfacine); 3E05NBH9V5 (ispronicline); 41VRH5220H (Paroxetine); 6EE945D3OK (Mecamylamine); 7D7RX5A8MO (Venlafaxine Hydrochloride); 9044SC542W (Duloxetine Hydrochloride); 947S0YZ36I (reboxetine); D0P25S3P81 (Lobeline); EJQ7M98H5J (metadoxine); J7A92W69L7 (Droxidopa); KV2JZ1BI6Z (Pyridoxine); R3UK8X3U3D (modafinil); SJT761GEGS (Lisdexamfetamine Dimesylate); SZB83O1W42 (Pyrrolidonecarboxylic Acid); TG537D343B (Desipramine); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:170103
[Lr] Data última revisão:
170103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151224
[St] Status:MEDLINE
[do] DOI:10.1586/14737175.2016.1135735


  8 / 98 MEDLINE  
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[PMID]:26581501
[Au] Autor:Sadek B; Stark H
[Ad] Endereço:Department of Pharmacology and Therapeutics, College of Medicine & Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates. Electronic address: bassem.sadek@uaeu.ac.ae.
[Ti] Título:Cherry-picked ligands at histamine receptor subtypes.
[So] Source:Neuropharmacology;106:56-73, 2016 Jul.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Histamine, a biogenic amine, is considered as a principle mediator of multiple physiological effects through binding to its H1, H2, H3, and H4 receptors (H1-H4Rs). Currently, the HRs have gained attention as important targets for the treatment of several diseases and disorders ranging from allergy to Alzheimer's disease and immune deficiency. Accordingly, medicinal chemistry studies exploring histamine-like molecules and their physicochemical properties by binding and interacting with the four HRs has led to the development of a diversity of agonists and antagonists that display selectivity for each HR subtype. An overview on H1-R4Rs and developed ligands representing some key steps in development is provided here combined with a short description of structure-activity relationships for each class. Main chemical diversities, pharmacophores, and pharmacological profiles of most innovative H1-H4R agonists and antagonists are highlighted. Therefore, this overview should support the rational choice for the optimal ligand selection based on affinity, selectivity and efficacy data in biochemical and pharmacological studies. This article is part of the Special Issue entitled 'Histamine Receptors'.
[Mh] Termos MeSH primário: Histamínicos/farmacologia
Receptores Histamínicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Histamínicos/química
Histamínicos/farmacocinética
Seres Humanos
Receptores Histamínicos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Histamine Agents); 0 (Receptors, Histamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151120
[St] Status:MEDLINE


  9 / 98 MEDLINE  
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[PMID]:26529287
[Au] Autor:Schou M; Varnäs K; Jureus A; Ahlgren C; Malmquist J; Häggkvist J; Tari L; Wesolowski SS; Throner SR; Brown DG; Nilsson M; Johnström P; Finnema SJ; Nakao R; Amini N; Takano A; Farde L
[Ad] Endereço:AstraZeneca Translational Science Centre at Karolinska Institutet, PET Centre of Excellence, Department of Clinical Neuroscience, S-17176 Stockholm, Sweden.
[Ti] Título:Discovery and Preclinical Validation of [(11)C]AZ13153556, a Novel Probe for the Histamine Type 3 Receptor.
[So] Source:ACS Chem Neurosci;7(2):177-84, 2016 Feb 17.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: The histamine type 3 receptor (H3) is a G protein-coupled receptor implicated in several disorders of the central nervous system. Herein, we describe the radiolabeling and preclinical evaluation of a candidate radioligand for the H3 receptor, 4-(1S,2S)-2-(4-cyclobutylpiperazine-1-carbonyl)cyclopropyl]-N-methyl-benzamide (5), and its comparison with one of the frontrunner radioligands for H3 imaging, namely, GSK189254 (1). Compounds 1 and 5 were radiolabeled with tritium and carbon-11 for in vitro and in vivo imaging experiments. The in vitro binding of [(3)H]1 and [(3)H]5 was examined by (i) saturation binding to rat and nonhuman primate brain tissue homogenate and (ii) in vitro autoradiography on tissue sections from rat, guinea pig, and human brain. The in vivo binding of [(11)C]1 and [(11)C]5 was examined by PET imaging in mice and nonhuman primates. Bmax values obtained from Scatchard analysis of [(3)H]1 and [(3)H]5 binding were in good agreement. Autoradiography with [(3)H]5 on rat, guinea pig, and human brain slices showed specific binding in regions known to be enhanced in H3 receptors, a high degree of colocalization with [(3)H]1, and virtually negligible nonspecific binding in tissue. PET measurements in mice and nonhuman primates demonstrated that [(11)C]5 binds specifically and reversibly to H3 receptors in vivo with low nonspecific binding in brain tissue. Whereas [(11)C]1 showed similar binding characteristics in vivo, the binding kinetics appeared faster for [(11)C]5 than for [(11)C]1. CONCLUSIONS: [(11)C]5 has suitable properties for quantification of H3 receptors in nonhuman primate brain and has the potential to offer improved binding kinetics in man compared to [(11)C]1.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Encéfalo/diagnóstico por imagem
Radioisótopos de Carbono/farmacocinética
Histamínicos/farmacologia
Receptores Histamínicos H3/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/patologia
Animais
Autorradiografia
Benzamidas/química
Benzamidas/farmacologia
Benzazepinas/farmacologia
Relação Dose-Resposta a Droga
Feminino
Cobaias
Haplorrinos
Histamínicos/química
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Niacinamida/análogos & derivados
Niacinamida/farmacologia
Piperazinas/química
Piperazinas/farmacologia
Ligação Proteica/efeitos dos fármacos
Ratos
Reprodutibilidade dos Testes
Fatores de Tempo
Distribuição Tecidual/efeitos dos fármacos
Distribuição Tecidual/fisiologia
Trítio/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(1S,2S)-2-(4-cyclobutylpiperazine-1-carbonyl)cyclopropyl)-N-methyl-benzamide); 0 (6-((3-cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy)-N-methyl-3-pyridinecarboxamide); 0 (Benzamides); 0 (Benzazepines); 0 (Carbon Radioisotopes); 0 (Histamine Agents); 0 (Piperazines); 0 (Receptors, Histamine H3); 10028-17-8 (Tritium); 25X51I8RD4 (Niacinamide)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151104
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.5b00268


  10 / 98 MEDLINE  
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[PMID]:26387685
[Au] Autor:Yu L; Zhang XY; Cao SL; Peng SY; Ji DY; Zhu JN; Wang JJ
[Ad] Endereço:State Key Laboratory of Pharmaceutical Biotechnology, Department of Biological Science and Technology, School of Life Sciences, Nanjing University, Nanjing, China.
[Ti] Título:Na(+) -Ca(2+) Exchanger, Leak K(+) Channel and Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel Comediate the Histamine-Induced Excitation on Rat Inferior Vestibular Nucleus Neurons.
[So] Source:CNS Neurosci Ther;22(3):184-93, 2016 Mar.
[Is] ISSN:1755-5949
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: Antihistaminergic drugs have traditionally been used to treat vestibular disorders in the clinic. As a potential central target for antihistaminergic drugs, the inferior vestibular nucleus (IVN) is the largest subnucleus of the central vestibular nuclear complex and is considered responsible for vestibular-autonomic responses and integration of vestibular, cerebellar, and multisensory signals. However, the role of histamine on the IVN, particularly the underlying mechanisms, is still not clear. METHODS: Using whole-cell patch-clamp recordings on rat brain slices, histamine-induced effect on IVN neurons and the underlying receptor and ionic mechanisms were investigated. RESULTS: We found that histamine remarkably depolarized both spontaneous firing neurons and silent neurons in IVN via both histamine H1 and histamine H2 receptors. Furthermore, Na(+) -Ca(2+) exchangers (NCXs) and background leak K(+) channels linked to H1 receptors and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels coupled to H2 receptors comediate the histamine-induced depolarization on IVN neurons. CONCLUSION: These results demonstrate the multiple ionic mechanisms underlying the excitatory modulation of histamine/central histaminergic system on IVN neurons and the related vestibular reflexes and functions. The findings also suggest potential targets for the treatment of vestibular disorders in the clinic, at the level of ionic channels in central vestibular nuclei.
[Mh] Termos MeSH primário: Canais de Cátion Regulados por Nucleotídeos Cíclicos/metabolismo
Histamina/farmacologia
Neurônios/efeitos dos fármacos
Canais de Potássio/metabolismo
Trocador de Sódio e Cálcio/metabolismo
Núcleos Vestibulares/citologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Compostos de Benzil/farmacologia
Césio/farmacologia
Cloretos/farmacologia
Canais de Cátion Regulados por Nucleotídeos Cíclicos/antagonistas & inibidores
Relação Dose-Resposta a Droga
Histamínicos/farmacologia
Técnicas In Vitro
Potenciais da Membrana/efeitos dos fármacos
Técnicas de Patch-Clamp
Bloqueadores dos Canais de Potássio/farmacologia
Pirimidinas/farmacologia
Ratos
Bloqueadores dos Canais de Sódio/farmacologia
Trocador de Sódio e Cálcio/antagonistas & inibidores
Tetrodotoxina/farmacologia
Tiazolidinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2-(4-(4-nitrobenzyloxy)benzyl)thiazolidine-4-carboxylic acid ethyl ester); 0 (Benzyl Compounds); 0 (Chlorides); 0 (Cncg protein, rat); 0 (Cyclic Nucleotide-Gated Cation Channels); 0 (Histamine Agents); 0 (Potassium Channel Blockers); 0 (Potassium Channels); 0 (Pyrimidines); 0 (Sodium Channel Blockers); 0 (Sodium-Calcium Exchanger); 0 (Thiazolidines); 133059-99-1 (ICI D2788); 1KSV9V4Y4I (Cesium); 4368-28-9 (Tetrodotoxin); 820484N8I3 (Histamine); GNR9HML8BA (cesium chloride)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150922
[St] Status:MEDLINE
[do] DOI:10.1111/cns.12451



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