Invited Symposium: Neuronal Histamine Systems and Behavior



Sodium Channels

Calcium Channels

Potassium Channels



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Regulation of Histamine Cell Firing

Haas, H.L. (Department of Physiology, Heinrich-Heine-University, Germany)
Stevens, D.R. (Department of Physiology, Heinrich-Heine-University, Germany)

Contact Person: Helmut L Haas (haas@uni-duesseldorf.de)


Histaminergic neurons with long arborizing slowly conducting axons project to virtually the whole CNS and display regular firing related to behavioral state. Whole cell recording in isolated single tuberomammillary (TM) neurons revealed spontaneous firing as an intrinsic property independent of a network. Two transient outward currents prolong the interspike interval and may serve to prevent firing by a brief disturbance during sleep. A hyperpolarisation-activated inward current (IH) could in principle contribute to the pacemaker-like activity of TM-neurons, but blocking this current does not slow their firing. TM neurons exhibit the inactivating low threshold Ca-current and several types of high threshold Ca-currents. Nickel-sensitive, TTX-insensitive prepotentials represent the active process which brings these neurons to threshold and a persistent Na-current contributes to the spontaneous firing. We have observed single sodium channels exhibiting a delayed inactivation. The firing is modulated by a concert of aminergic and peptidergic inputs and histamine (H3-autoreceptor-activation). GABAergic afferents from the ventrolateral preoptic area which is active at the onset of sleep inhibit TM firing (GABAA) and are regulated by GABAB-receptors.

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Presentation Number SAhaas0187

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Haas, H.L.; Stevens, D.R.; (1998). Regulation of Histamine Cell Firing. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/huston/haas0187/index.html
© 1998 Author(s) Hold Copyright