Toxins which produce pain

Chahl, Loris A.; Kirk, Elizabeth J.

doi:10.1016/0304-3959(75)90003-2

Cited by 36 publications

(15 citation statements)

References 272 publications

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“…Of the inactive venom components tested, three-hyaluronidase, dopamine, and adrenaline-are reportedly painless, or at least not potently pain-inducing (8,9) The five inactive substances that failed to induce autotomy invariably proved nonlethal to the spiders. But death did not always follow in spiders that retained their leg after injection of active samples.…”

Section: Discussionmentioning

confidence: 99%

“…Three of the four active components-serotonin, phospholipase A2, and histamine-are known to be pain-inducing in humans (7)(8)(9). Whatever the neural basis of their detection in spiders-whether it be comparable to the pain-coupled venomsensing mechanism in humans or not-it is clear that spiders are highly sensitive to these substances and that they respond defensively to them in a manner that prevents their systemic spread.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Spider leg autotomy induced by prey venom injection: An adaptive response to “pain”?

Eisner

Camazine

1983

Proc. Natl. Acad. Sci. U.S.A.

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Field observations showed orb-weaving spiders (Argiope spp.) to undergo leg autotomy if they are stung in a leg by venomous insect prey (Phymatafasciata}. The response occurs within seconds, before the venom can take lethal action by spread to the body of the spiders. Autotomy is induced also by honeybee venom and wasp venom, as well as by several venom components (serotonin, histamine, phospholipase A2, melittin) known to be responsible for the pain characteristically elicited by venom injection in humans. The sensing mechanism by which spiders detect injected harmful chemicals such as venoms therefore may be fundamentally similar to the one in humans that is coupled with the perception of pain.Bee stings hurt. So do wasp stings, scorpion stings, the bites of centipedes, and the venom injections of many other animals, including snakes. To inflict pain is not necessarily to the advantage of an animal that uses its venom strictly for incapacitation of prey. In fact, it may be to its disadvantage because pain may induce increased struggling on the part of the prey. But venoms are also used' defensively, and it is in that context that they may derive their effectiveness largely, if not exclusively, from their pain-inducing qualities. It is principally because venoms are painful that they can function in defense.Pain, in the sense of a consciously perceived experience, remains a subjective notion applicable to humans but untestable with animals. But when defined operationally as a physiological phenomenon induced in an animal by stimuli that are painful to us and resulting in a protective stimulus-avoidance response in that animal, pain is amenable to testing with nonhuman subjects. We here report that' certain chemical venom components that are painful to humans are also responsible for eliciting a natural self-preserving response in spiders: leg autotomy.Leg autotomy had previously been noted to occur in spiders when a leg was pulled or injured. It occurs consistently at the level of the coxa-trochanter joint near the base' of the leg. A special mechanism provides for minimization of bleeding at the site of leg detachment, and spiders can withstand the loss of several legs (1, 2). We found autotomy to occur also when a spider is stung in the leg while attempting to capture venomous insect prey. Here we present evidence that, under such circumstances, the response is adaptive to spiders because it prevents sytemic spread of the poisons and that it is triggered by action of the venom itself rather than by the mechanics of cuticle perforation or fluid injection. Moreover, we show that certain well-known pain-inducing compounds found in venoms are capable of inducing the autotomy response. EXPERIMENTAL PROCEDURES AND OBSERVATIONSOur study was prompted by field observations made while studying prey-capture behavior in orb-weaving spiders of the genus Argiope. A small ambush bug, Phymatafasciata, had just been seen to fly into a web of Argiope aurantia, when the spider pounced upon it in typical fashion, in ant...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Spider leg autotomy induced by prey venom injection: An adaptive response to “pain”?

Eisner

Camazine

1983

Proc. Natl. Acad. Sci. U.S.A.

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“…It has been shown that the oedematous effect induced by PNV in rats involves the generation of kinins and the stimulation of tackykinin receptors. This effect also depends on the histamine, serotonin and polypeptides contained in the venom [5], [6], [7], [8]. Because pain may occur after PNV envenomation even in the absence of oedema, the mechanisms involved in these responses could be distinct.…”

Section: Introductionmentioning

confidence: 99%

“…Because pain may occur after PNV envenomation even in the absence of oedema, the mechanisms involved in these responses could be distinct. Moreover, there are no validated therapies for treating PNV-induced pain, though local anaesthetics, opioids, non-steroidal anti-inflammatory drugs and arachnid antivenin serum have been used empirically [8], [2].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms Involved in the Nociception Triggered by the Venom of the Armed Spider Phoneutria nigriventer

et al. 2013

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Background The frequency of accidental spider bites in Brazil is growing, and poisoning due to bites from the spider genus Phoneutria nigriventer is the second most frequent source of such accidents. Intense local pain is the major symptom reported after bites of P. nigriventer, although the mechanisms involved are still poorly understood. Therefore, the aim of this study was to identify the mechanisms involved in nociception triggered by the venom of Phoneutria nigriventer (PNV).Methodology/Principal Findings Twenty microliters of PNV or PBS was injected into the mouse paw (intraplantar, i.pl.). The time spent licking the injected paw was considered indicative of the level of nociception. I.pl. injection of PNV produced spontaneous nociception, which was reduced by arachnid antivenin (ArAv), local anaesthetics, opioids, acetaminophen and dipyrone, but not indomethacin. Boiling or dialysing the venom reduced the nociception induced by the venom. PNV-induced nociception is not dependent on glutamate or histamine receptors or on mast cell degranulation, but it is mediated by the stimulation of sensory fibres that contain serotonin 4 (5-HT4) and vanilloid receptors (TRPV1). We detected a kallikrein-like kinin-generating enzyme activity in tissue treated with PNV, which also contributes to nociception. Inhibition of enzymatic activity or administration of a receptor antagonist for kinin B2 was able to inhibit the nociception induced by PNV. PNV nociception was also reduced by the blockade of tetrodotoxin-sensitive Na+ channels, acid-sensitive ion channels (ASIC) and TRPV1 receptors.Conclusion/SignificanceResults suggest that both low- and high-molecular-weight toxins of PNV produce spontaneous nociception through direct or indirect action of kinin B2, TRPV1, 5-HT4 or ASIC receptors and voltage-dependent sodium channels present in sensory neurons but not in mast cells. Understanding the mechanisms involved in nociception caused by PNV are of interest not only for better treating poisoning by P. nigriventer but also appreciating the diversity of targets triggered by PNV toxins.

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“…Envenomation can sometimes induce euphoric catalysis or a relatively aloof hemorrhagic state, but more typically, venoms produce pronounced pain and inflammation (Chahl and Kirk, 1975). While in some cases, pain certainly occurs as a side-effect of tissue damage, the existence of toxins that target TRPV1, a receptor found predominantly in nociceptors, suggests that noxiousness is an end in itself for a subset of venom proteins, representing a likely mechanism to avert predation (Siemens et al, 2006).…”

Section: Discussionmentioning

confidence: 99%