The parasitoid wasp envenomates the brain of its host the American cockroach (), thereby making it a behaviorally compliant food supply for its offspring. The target of venom injection is a locomotory command center in the brain called the central complex. In this study, we investigate why stung cockroaches do not respond to injuries incurred during the manipulation process by the wasp. In particular, we examine how envenomation compromises nociceptive signaling pathways in the host. Noxious stimuli applied to the cuticle of stung cockroaches fail to evoke escape responses, even though nociceptive interneurons projecting to the brain respond normally. Hence, while nociceptive signals are carried forward to the brain, they fail to trigger robust nocifensive behavior. Electrophysiological recordings from the central complex of stung animals demonstrate decreases in peak firing rate, total firing, and duration of noxious-evoked activity. The single parameter best correlated with altered noxious-evoked behavioral responses of stung cockroaches is reduced duration of the evoked response in the central complex. Our findings demonstrate how the reproductive strategy of a parasitoid wasp is served by venom-mediated elimination of aversive, nocifensive behavior in its host.
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http://dx.doi.org/10.3389/fphys.2022.907041 | DOI Listing |
Nat Neurosci
January 2025
Department of Physiology, Seoul National University College of Medicine, Seoul, Korea.
The cerebellum is activated by noxious stimuli and pathological pain but its role in noxious information processing remains unknown. Here, we show that in mice, cutaneous noxious electrical stimuli induced noradrenaline (NA) release from locus coeruleus (LC) terminals in the cerebellar cortex. Bergmann glia (BG) accumulated these LC-NA signals by increasing intracellular calcium in an integrative manner ('flares').
View Article and Find Full Text PDFFront Pharmacol
December 2024
Institute of Pharmacology and Clinical Pharmacy, Goethe University Frankfurt, Frankfurt, Germany.
Neurobiol Dis
December 2024
Department of Psychiatry and Behavioral Sciences, Texas A&M University School of Medicine, College Station, TX 77845, USA. Electronic address:
Neuropathic pain presents a significant challenge, with its underlying mechanisms still not fully understood. Here, we investigated the role of GluN2C- and GluN2D-containing NMDA receptors in the development of neuropathic pain induced by cisplatin, a widely used chemotherapeutic agent. Through genetic and pharmacological strategies, we found that GluN2D-containing NMDA receptors play a targeted role in regulating cisplatin-induced neuropathic pain (CINP), while sparing inflammatory or acute pain responses.
View Article and Find Full Text PDFPain
November 2024
Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, MI, United States. Email:
Proc Natl Acad Sci U S A
December 2024
Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, United Kingdom.
Inflammation is associated with localized acidosis, however, attributing physiological and pathological roles to proton-sensitive receptors is challenging due to their diversity and widespread expression. Here, agonists of the proton-sensing GPCR, GPR65, were systematically characterized. The synthetic agonist BTB09089 (BTB) recapitulated many proton-induced signaling events and demonstrated selectivity for GPR65.
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