Chemical communication of predation risk has evolved multiple times in fish species, with conspecific alarm substance (CAS) being the most well understood mechanism. CAS is released after epithelial damage, usually when prey fish are captured by a predator and elicits neurobehavioural adjustments in conspecifics which increase the probability of avoiding predation. As such, CAS is a partial predator stimulus, eliciting risk assessment‐like and avoidance behaviours and disrupting the predation sequence. The present paper reviews the distribution and putative composition of CAS in fish and presents a model for the neural processing of these structures by the olfactory and the brain aversive systems. Applications of CAS in the behavioural neurosciences and neuropharmacology are also presented, exploiting the potential of model fish [e.g., zebrafish Danio rerio, guppies Poecilia reticulata, minnows Phoxinus phoxinus) in neurobehavioural research.
21Chemical communication of predation risk has evolved multiple times in fish species, with the 22 conspecific alarm substance (CAS) contemporaneously being the most well understood mechanism. 23 CAS is released after epithelial damage, usually when prey fish is captured by a predator, and elicits 24 neurobehavioral adjustments in conspecifics which increase the probability of avoiding predation. 25As such, CAS is a partial predator stimulus, eliciting risk assessment-like and avoidance behaviors, 26 and disrupting the predator sequence. The present paper reviews the distribution and putative 27 composition of CAS in fish, and presents a model for the neural processing of these structures by 28 the olfactory and the brain aversive systems. Applications of CAS in the behavioral neurosciences 29 and neuropharmacology are also presented, exploiting the potential of model fish (e.g., zebrafish, 30 guppies, minnows) on neurobehavioral research. 31
Chemical communication of predation risk has evolved multiple times in fish species, with the conspecific alarm substance (CAS) contemporaneously being the most well understood mechanism. CAS is released after epithelial damage, usually when prey fish is captured by a predator, and elicits neurobehavioral adjustments in conspecifics which increase the probability of avoiding predation. As such, CAS is a partial predator stimulus, eliciting risk assessment-like and avoidance behaviors, and disrupting the predator sequence. The present paper reviews the distribution and putative composition of CAS in fish, and presents a model for the neural processing of these structures by the olfactory and the brain aversive systems. Applications of CAS in the behavioral neurosciences and neuropharmacology are also presented, exploiting the potential of model fish (e.g., zebrafish, guppies, minnows) on neurobehavioral research.
20Panic disorder (PD) is characterized by abrupt surges of intense fear and distress. There is evidence 21 for a genetic component in this disorder. We ran a meta-analysis of genome-wide association studies 22 of patients with PD, and found 25 single-nucleotide polymorphisms that were associated with the 23 disorder. Causal gene prediction based on these polymorphisms uncovered 20 hits. Exploratory 24 analyses suggested that these genes formed interactor networks, which was enriched in signaling 25 pathways associated with immune and inflammatory responses, as well as growth factors and other 26 developmental mediators. A subset of genes is enriched in limbic regions of the human brain and in 27 microglia and myelinating oligodendrocytes of mice. While these genes were not associated with 28 relevant neurobehavioral phenotypes in mutant mice, expression levels of several causal genes in 29 the amygdala, prefrontal cortex, hippocampus,, hypothalamus, and adrenal gland of recombinant 30 mouse strains was associated with endophenotypes of fear conditioning. Drug repositioning 31 prediction was unsuccessful, but this does not discard these genes and pathways as targets for 32 investigational drugs. In general, ASB3, EIF2S2, RASGRF2, and TRMT2B (and its coded proteins) 33 emerged as interesting targets for mechanistic research on PD. These exploratory findings point 34 towards hypotheses of pathogenesis and neuropharmacology that need to be further investigated. 35
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