Erowid References Database
Green JP, Weinstein H, Maayani S.
“Defining the Histamine H2- Receptor in Brain: The Interaction With LSD”.
QUASAR. Quantitative structure activity relationships of analgesics, narcotics, antagonists, and hallucinogens. 1978;22:38-59.
Numerous studies have shown that LSD (D-lysergic acid diethylamide) affects serotonergic, dopaminergic, adrenergic, and tryptaminergic systems ln the central nervous system (see Ilandell and Geyer, 1976; Martin and Sloan 1977; Freedman and Halaris 1978). To this list is now added a histaminergic system. For LSD is a competitive antagonist of the histamine H2-receptor in brain (Green et al. 1977). In describing this action of LSD, we give an account of the estabfished criteria that we followed to define the receptor with which LSD reacts. This definition fostered an analysis of the relationship between the molecular structure of known B2-antagonists and LSD. This results in the correct prediction of a new B2-antagonist. The action of LSD on a histamine receptor in brain may be relevant to the neural effects of LSD. For histamine may be a transitter in brain. Evidence for this function of histamine remains circumstantial but perhaps no more so than that offered for most other biogenic amines that are classified as putative transmitters. In fact, as recently reviewed (Green, Johnson and Weinstein 1978), studies of mammalian brain show that histamine meets most criteria for having transmitter function. It has non-uniform distribution with highest concentration in the hypothalamus. Subcellular fractions of brain containing nerve-endings are rich in histamine. Brain contains the specific enzyme that decarboxylates histidine to form histamine as well as the specific enzyme that metabolizes histamine. After destroying fibers in the median forebrain bundle or the afferent fibers to the hippocampus the activity of .the specific histidine decarboxylase falls in brain regions distal to the lesion. Histamine is released from brain slices by potasslum ions in a process that is dependent on ionic calcium. Histamine turns over rapidly: unlike other aromatic biogenic amines, it is not taken up by presynaptic terminals but is instead metabolized to 3-methylhistamine which is then oxidatively deaminated by monoamine oxidase B. Neurons respond to histamine, a.g., it decreases the firing rate of cerebral cortical and brainstem neurons and increases the firing rate of hypothalamic neurons. Especially provocative is the observation that electrical stimulation of ,
|Notes # : Publ: Barnett G, Trisic M, Willette RE.
NIDA Research Monograph 22
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