Venom effects on monoaminergic systems

Abstract

The monoamines, dopamine, epinephrine, histamine, norepinephrine, octopamine, serotonin and tyramine serve many functions in animals. Many different venoms have evolved to manipulate monoaminergic systems via a variety of cellular mechanisms, for both offensive and defensive purposes. One common function of monoamines present in venoms is to produce pain. Some monoamines in venoms cause immobilizing hyperexcitation which precedes venom-induced paralysis or hypokinesia. A common function of venom components that affect monoaminergic systems is to facilitate distribution of other venom components by causing vasodilation at the site of injection or by increasing heart rate. Venoms of some scorpions, spiders, fish and jellyfish contain adrenergic agonists or cause massive release of catecholamines with serious effects on the cardiovascular system, including increased heart rate. Other venom components act as agonists, antagonists or modulators at monoaminergic receptors, or affect release, reuptake or synthesis of monoamines. Most arthropod venoms have insect targets, yet, little attention has been paid to possible effects of these venoms on monoaminergic systems in insects. Further research into this area may reveal novel effects of venom components on monoaminergic systems at the cellular, systems and behavioral levels.

Mast cell functions in the innate skin immune system

“…Although MCs have long been thought to promote morbidity and mortality following snake bites and envenomations by other animals (Dutta and Narayanan, 1952;Weisel-Eichler and Libersat, 2004), we have found that in contrast, MCs enhance the resistance against certain venoms (Metz et al, 2006b). Surprisingly, envenomation of the skin with venom from the Western Diamondback rattlesnake induces significantly larger hemorrhagic lesions in MC-deficient Kit W-sh /Kit W-sh than in wildtype mice or in mice that were selectively repaired of their MC-deficiency in the skin.…”

Mast cells – key effector cells in immune responses

“…Indeed, MC-deficient mice were found to be 10-fold more susceptible to the deadly effects of the venom than wildtype mice, and MC-derived carboxypeptidase A was proven to be responsible for enhancing the resistance against the venomous effects [21]. MCs have long been thought to promote the pathology following snake bites, for example by releasing vasoactive mediators such as histamine, which can increase vascular permeability, facilitate both local tissue swelling and the systemic distribution of the venom, and increase its overall toxicity [51,52]. The finding that MCs instead elicit a protective innate response resulting in enhanced resistance to the venom of A. engaddensis was, therefore, unexpected.…”

Mast cell chymase reduces the toxicity of Gila monster venom, scorpion venom, and vasoactive intestinal polypeptide in mice

“…Venoms derived from several animal species other than reptiles and honeybees, including those from scorpions (32), also have been shown to activate mast cells. We therefore also tested venoms from 2 species of medically important scorpions, the deathstalker (yellow) scorpion (Leiurus quinquestriatus hebraeus) (33)(34)(35) and the Arizona bark scorpion (Centruroides exilicauda) (35)(36)(37).…”