Histamine H2-receptors on single central neurones

Haas, Helmut L.; Bucher, U

doi:10.1038/255634a0

Cited by 72 publications

(22 citation statements)

References 7 publications

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“…In the CNS, H 2 receptor activation can inhibit nerve cells (Haas and Bucher, 1975), but the most intriguing action is a block of the long-lasting after-hyperpolarization and the accommodation of firing, an effect with a remarkably long duration leading to potentiation of excitation in rodent (Haas and Konnerth, 1983) and human brain (Haas and Panula, 2003) (Fig. 8).…”

Section: Functionmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors

et al. 2015

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Section: Functionmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors

et al. 2015

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“…Microiontophoretically applied histamine depresses the firing of feline brain and spinal neurones (Krnjevic & Phillis, 1963;Phillis, Tebecis & York, 1968a,b;Haas, Anders & Hosli, 1973); however, these effects are often non-specifically antagonized by histamine H1-and H2-receptor blockers (Phillis et al, 1968a;Haas & Bucher, 1975;Haas, Wolf & Nussbaumer, 1975). This non-specificity has been tentatively attributed either to a blockade of axonal conduction (i.e.…”

Section: Introductionmentioning

confidence: 99%

Antagonism by Some Antihistamines of the Amino Acid‐evoked Responses Recorded From the Lobster Muscle Fibre and the Frog Spinal Cord

Constanti

Nistri

1976

British J Pharmacology

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I The effects of some antihistamines on the lobster muscle fibre and the frog spinal cord were investigated using intracellular and extracellular recordings, respectively.2 On lobster muscle, histamine Hl-blockers reversibly antagonized responses to bath-applied glutamate, aspartate and quisqualate but not responses to y-aminobutyric acid (GABA). Iontophoretic glutamate potentials were also reduced. Histamine (up to 1 mM) had no effect on this preparation.3 The Hl-antagonists produced a small increase in muscle membrane conductance and a slight hyperpolarization. These effects were largely unchanged in a low Cl-bathing solution. Procaine (1 mM) decreased membrane conductance and did not affect responses to GABA or glutamate. 4 The H2-antagonist burimamide blocked both glutamate and GABA-evoked responses on the lobster muscle without affecting resting potential or conductance. 5 In the frog cord, bath-applied histamine produced ventral root depolarizations and dorsal root hyperpolarizations (sometimes biphasic responses). These effects were reduced by tetrodotoxin (TTX) but not by antazoline (H,-blocker) or burimamide; the latter reversibly antagonized responses to both glutamate and GABA on TTX-treated cords while antazoline was ineffective. 6 It is suggested that antihistamines can act as non-specific amino acid antagonists by interacting at the level of the receptor-coupled ionophores.

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“…and are in accordance with the evidence accumulating in the literature that histamine may be a putative neurotransmitter or modulator in the central nervous system [Taylor and Sny der, 1971;Taylor el al" 1972;Schayer and Reilly, 1974;Garbarg el al" 1974a. b: Baudry et al, 1974Haas and Bucher, 1975;Martres et al. 1975;Rogers et al, 1975;Nowak and Pile, 1977;Vidali and Fregnan, 1979].…”

Section: Resultsmentioning

confidence: 99%

Appearance of Extrapyramidal Symptoms: Interaction between Neuroleptics and Other CNS Active Drugs

Fregnan

Vidali

1982

Pharmacology

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Neuroleptics were able to induce motor incoordination when administered to rats in large amounts. It has been observed that this effect could be antagonized by some CNS active drugs endowed with dopaminergic stimulants, anticholinergic and antihistaminic properties (such as amphetamine, apomorphine, atropine and diphenhydramine), only when evoked by neuroleptics (haloperidol, metoclopramide and LR 511) causing muscle rigidity. Other antihistaminics blocking H i receptors (chlorpheniramine, chlorcyclizine, cyclizine and promethazine), but not those blocking H₂ receptors (cimetidine), were also effective at least on haloperidol-induced incoordination. On the other hand, specific central antiserotoninergic drugs (metergoline and methysergide) and a peripheral anticholinergic agent (isopropamide) did not antagonize but in some cases potentiated haloperidol and LR 511. Chlorpromazine, clozapine and diazepam (a minor tranquilizer), causing motor incoordination only at doses which strongly relaxed the skeletal muscles, were generally not influenced, or at the most slightly potentiated, by any of the above-mentioned drugs. The incoordination induced by pilocarpine (a direct stimulator of the cholinergic receptors of the extrapyramidal system) was selectively inhibited by drugs possessing antimuscarinic properties (such as atropine and cyproheptadine). Thus, the present results indicate that along with the dopaminergic and cholinergic systems, the histaminergic system also plays an important role in modulating the extrapyramidal activity of hypertonic neuroleptics (revealed in rats by the locomotor incoordination) while, in disagreement with some data of the literature, the serotoninergic system should not have any significance.

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Histamine H2-receptors on single central neurones

Cited by 72 publications

References 7 publications

International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors

International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors

Antagonism by Some Antihistamines of the Amino Acid‐evoked Responses Recorded From the Lobster Muscle Fibre and the Frog Spinal Cord

Appearance of Extrapyramidal Symptoms: Interaction between Neuroleptics and Other CNS Active Drugs

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