Subject(s)
Histamine , Allergens , Animals , Basophils/drug effects , Basophils/immunology , Biomedical Research , Cardiovascular System , Circadian Rhythm , Cytokines/biosynthesis , Cytokines/blood , Cytoplasmic Granules/chemistry , Dendritic Cells/immunology , Endothelial Cells/physiology , Eosinophils/physiology , Europe , Food Hypersensitivity , Gastrointestinal Tract , Histamine/genetics , Histamine/immunology , Histamine/physiology , Histamine Antagonists/pharmacology , Humans , Hypersensitivity/immunology , Immunoglobulin G/blood , Immunotherapy , Mast Cells/ultrastructure , Mice , Nervous System , Neurogenesis , Receptors, Histamine/deficiency , Receptors, Histamine/genetics , Receptors, Histamine/physiology , Societies, Medical/organization & administration , SpainSubject(s)
Histamine H1 Antagonists/toxicity , Joint Diseases/chemically induced , Joints/embryology , Abnormalities, Drug-Induced/pathology , Animals , Bone and Bones/embryology , Bone and Bones/pathology , Cleft Palate/chemically induced , Cleft Palate/pathology , Female , Joint Diseases/pathology , Joints/pathology , Pregnancy , RatsSubject(s)
Histamine Agonists/pharmacology , Histamine Antagonists/pharmacology , Receptors, Histamine H2/drug effects , Receptors, Histamine H2/physiology , Seizures/physiopathology , Acoustic Stimulation , Animals , Anticonvulsants/pharmacology , Benzothiazoles , Convulsants/administration & dosage , Dimaprit/administration & dosage , Dimaprit/pharmacology , Female , Male , Mice , Mice, Inbred DBA , Pentylenetetrazole/administration & dosage , Phenoxypropanolamines , Piperidines/pharmacology , Seizures/etiology , Thiazoles/pharmacologySubject(s)
Embryonic and Fetal Development/drug effects , Histamine H2 Antagonists/toxicity , Animals , Cimetidine/pharmacology , Cimetidine/toxicity , Female , Growth/drug effects , Histamine H2 Antagonists/pharmacology , Pregnancy , Ranitidine/pharmacology , Ranitidine/toxicity , Rats , Reflex/drug effects , Reflex, Startle/drug effectsABSTRACT
The first indication that histamine might be important in the functioning of the brain was the finding that the centrally penetrating histamine H1 antagonists had marked sedative properties. Subsequently with the development of more specific compounds and drugs for the H1, H2 and H3 receptors a greater understanding of the neurotransmitter/modulator role of histamine in the CNS has been possible. Histamine is now associated with wakefulness, suppression of seizures, hypothermia and emesis. The histamine H1 antagonists have been shown to potentiate opioid-induced analgesia, and modify eating and drinking patterns as well as endocrine secretions from the pituitary gland. Additionally, clinically useful antidepressants have been shown to inhibit histamine-sensitive adenylate cyclase from the mammalian brain. Recently, a possible role for both histamine H1 and H2 receptors in schizophrenia has been reported. As more specific and centrally-penetrating histaminergic compounds are developed, so the roles of histamine as a neurotransmitter/modulator in the brain will be better understood.
Subject(s)
Central Nervous System/drug effects , Histamine Agents/pharmacology , Animals , Humans , Receptors, Histamine/drug effects , Receptors, Histamine/metabolismSubject(s)
Behavior, Animal/drug effects , Bone Development/drug effects , Bone and Bones/drug effects , Histamine H1 Antagonists/pharmacology , Prenatal Exposure Delayed Effects , Analysis of Variance , Animals , Bone and Bones/embryology , Cell Division/drug effects , Embryonic and Fetal Development/drug effects , Female , Pregnancy , RatsABSTRACT
The effects of compounds active at histamine H3-receptors on morphine-induced antinociception have been investigated in thermal and chemical tests in mice; tail-immersion (50 degrees C) and hot-plate (49 degrees and 55 degrees C) tests and acetic acid-induced writhing. Neither (R)alpha-methylhistamine, a specific agonist, (S)alpha-methylhistamine, a chemical control, nor thioperamide, an antagonist, had any antinociceptive action alone but thioperamide (3 mg kg-1) attenuated the effects of morphine in the tail-immersion test while (R)alpha-methylhistamine (1 mg kg-1), but not the (S) isomer, potentiated its effects in the hot-plate test at 55 degrees C. These results are consistent with the morphine potentiation seen with H1-antagonists and suggest that central histaminergic mechanisms can modulate opioid actions.
Subject(s)
Analgesics/pharmacology , Morphine/pharmacology , Receptors, Histamine H3/drug effects , Animals , Female , Histamine Agonists , Histamine Antagonists , Hot Temperature , Mice , Mice, Neurologic Mutants , Pain/chemically induced , Pain/prevention & control , Pain Measurement/drug effectsABSTRACT
Central histaminergic modulation of H1 rather than H2-receptors has been shown to modify epileptic activity. Compounds acting on the HIC- and H3-receptors were tested against chemically-induced seizures in mice. Compounds antagonising the microsomal and nuclear intracellular receptors (HIC) only modified seizures at doses where toxicity was observed. Antagonists of the histamine H3-receptor (thioperamide and burimamide) only potentiated the severity of clonic convulsions induced by picrotoxin, while impromidine (i.c.v.), an antagonist with H2-agonist activity, inhibited leptazol-induced seizures. The H3-agonist, (R)alpha-methylhistamine, potentiated chemically-induced seizures, but at lower doses there was slight inhibition.
