Response of shoaling fish to the threat of aerial predation

Synopsis Many species of shoaling fish are preyed upon by aerial predators. However, to date there has been no analysis of the evasive response of a group of shoaling fish to an aerial threat or attack. The response of a shoal of fish encompasses a suite of behaviors starting with a startle response. Shoals of golden shiner, Notemigonus crysoleucas, responded to the threat of aerial predation from a kingfisher model with a startle response, an increase in shoal depth, an increase in polarity, swimming in the opposite direction under the model predator, shoal compression along the depth axis, and shoal expansion on the plane perpendicular to the depth axis. It was hypothesized that shoal compression along the depth axis serves to increase predator confusion by placing more fish in the predator's visual field. This compression was termed the ‘plane of confusion’.     

Electrophysiological investigation of effect of pulvinar stimulation of caudate nucleus neurons that react to visual stimulation

Responses of caudate neurons to electrical stimulation of the afferent input from thepulvinar thalamic nucleus and to visual stimuli of various orientations were studied extracellularly in awake chronic cats. Activation responses dominated among reactions of these neurons. The response latencies have ranged from 4 to 85 msec for units with primary activation and from 20 to 150 msec for inhibited ones. The values are indicative of both rapidly and slowly conducting afferent pathways. A possibility of monosynaptic transmission in thepulvinarcaudate projections is also revealed.Pulvinar stimulation is found to be efficient for a significant (more than 50 percent) number of caudate neurons responding to visual stimuli, including orientation-selective cells. The mode of influences from other structures of the visual system (optic tract, area 17, the Clare-Bishop area) on caudate neurons responding topulvinar stimulation is described. The data are discussed with respect to the possible role of cortical and subcortical projections of the visual system in the creation of sensory specific responses of the caudate nucleus.A. A. Bogomolets Physiology Institute, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 23, No. 5, pp. 520–529, September–October, 1991.     

Accelerated shedding of prions following damage to the olfactory epithelium

In this study, we investigated the role of damage to the nasal mucosa in the shedding of prions into nasal samples as a pathway for prion transmission. Here, we demonstrate that prions can replicate to high levels in the olfactory sensory epithelium (OSE) in hamsters and that induction of apoptosis in olfactory receptor neurons (ORNs) in the OSE resulted in sloughing off of the OSE from nasal turbinates into the lumen of the nasal airway. In the absence of nasotoxic treatment, olfactory marker protein (OMP), which is specific for ORNs, was not detected in nasal lavage samples. However, after nasotoxic treatment that leads to apoptosis of ORNs, both OMP and prion proteins were present in nasal lavage samples. The cellular debris that was released from the OSE into the lumen of the nasal airway was positive for both OMP and the disease-specific isoform of the prion protein, PrP(Sc). By using the real-time quaking-induced conversion assay to quantify prions, a 100- to 1,000-fold increase in prion seeding activity was observed in nasal lavage samples following nasotoxic treatment. Since neurons replicate prions to higher levels than other cell types and ORNs are the most environmentally exposed neurons, we propose that an increase in ORN apoptosis or damage to the nasal mucosa in a host with a preexisting prion infection of the OSE could lead to a substantial increase in the release of prion infectivity into nasal samples. This mechanism of prion shedding from the olfactory mucosa could contribute to prion transmission.     

Response of host plants to periodical cicada oviposition damage

Insect oviposition on plants is widespread across many systems, but studies on the response of host plants to oviposition damage are lacking. Although patterns of oviposition vary spatially and temporally, ovipositing insects that exhibit outbreak characteristics may have strong effects on host plants during peak abundance. Periodical cicadas (Magicicada spp.), in particular, may reduce the performance of host plants when they synchronously emerge in massive numbers to mate and oviposit on host plants. Here we provide the first experimental manipulation of host plant use by periodical cicadas to evaluate the impact of cicada oviposition on plant performance across a diversity of host species within an ecologically relevant setting. Using a randomized block design, we established a plantation of three native and three exotic host plant species common to the successional forests in which cicadas occur. During the emergence of Brood X in 2004, we employed a highly effective cicada exclusion treatment by netting half of the host plants within each block. We assessed multiple measures of host plant performance, including overall plant growth and the growth and reproduction of individual branches, across three growing seasons. Despite our thorough assessment of potential host plant responses to oviposition damage, cicada oviposition did not generally inhibit host plant performance. Oviposition densities on unnetted host plants were comparable to levels documented in other studies, reinforcing the ecological relevance of our results, which indicate that cicada oviposition damage did not generally reduce the performance of native or exotic host plants.     

Gene expression profiles in Rana pirica tadpoles following exposure to a predation threat

Background

Rana pirica tadpoles show morphological changes in response to a predation threat: larvae of the dragonfly Aeshna nigroflava induce heightened tail depth, whereas larval salamander Hynobius retardatus induce a bulgy morphology with heightened tail depth. Although both predators induce similar tail morphologies, it is possible that there are functional differences between these tail morphs.

Results

Here, we performed a discriminant microarray analysis using Xenopus laevis genome arrays to compare tail tissues of control and predator-exposed tadpoles. We identified 9 genes showing large-scale changes in their expression profile: ELAV-like1, methyltransferase like 7A, dolichyl-phosphate mannosyltransferase, laminin subunit beta-1, gremlin 1, BCL6 corepressor-like 1, and three genes of unknown identity. A further 80 genes showed greater than 5 fold differences in expression after exposure to dragonfly larvae and 81 genes showed altered expression after exposure to larval salamanders. Predation-threat responsive genes were identified by selecting genes that reverted to control levels of expression following removal of the predator. Thirteen genes were induced specifically by dragonfly larvae, nine others were salamander-specific, and sixteen were induced by both. Functional analyses indicated that some of the genes induced by dragonfly larvae caused an increase in laminins necessary for cell adhesion in the extracellular matrix. The higher expression of gremlin 1 and HIF1a genes after exposure to dragonfly larvae indicated an in vivo hypoxic reaction, while down-regulation of syndecan-2 may indicate impairment of angiogenesis. Exposure to larval salamanders caused down-regulation of XCIRP-1, which is known to inhibit expression of adhesion molecules; the tadpoles showed reduced expression of cα(E)-catenin, small muscle protein, dystrophin, and myosin light chain genes.

Conclusion

The connective tissue of tadpoles exposed to larval salamanders may be looser. The differences in gene expression profiles induced by the two predators suggest that there are functional differences between the altered tail tissues of the two groups of tadpoles.

Electronic supplementary material

The online version of this article (doi:10.1186/s12864-015-1389-4) contains supplementary material, which is available to authorized users.     

Response of forest tree seedlings to simulated litterfall damage.

Litterfall is an important cause of seedling mortality in many forests ranging from wet tropical to boreal. However, there is a lack of studies that investigate differences between species in seedling resilience to litterfall damage. We selected seedling pairs of seven tree species and simulated litterfall damage by pinning one of each pair to the ground. The mortality and growth rates varied significantly between species for pinned individuals, but were similar for unpinned seedlings. The mortality of pinned Nestegis cunninghamii and Prumnopitys ferruginea was significantly greater than that of unpinned individuals (P < 0.05). However, contrary to expectations, the growth rates of pinned Hedycarya arborea and Nothofagus menziesii were much greater than for those left unpinned (P < 0.05). In general, seedling resilience to the bending damage differed substantially between species. N. cunninghamii and P. ferruginea suffered high mortalities and did not increase growth rates in response to damage, whereas, H. arborea and N. menziesii suffered few mortalities and regained height quickly. Other study species demonstrated intermediate resilience. This study demonstrates that some species are more likely to survive in high-risk litterfall regimes than are others. Given that litterfall risk can vary greatly between microsites, these results suggest that litterfall can contribute to regeneration niche differentiation. This revised version was published online in August 2006 with corrections to the Cover Date.     

Hypothalamic S-Nitrosylation Contributes to the Counter-Regulatory Response Impairment following Recurrent Hypoglycemia

Aims

Hypoglycemia is a severe side effect of intensive insulin therapy. Recurrent hypoglycemia (RH) impairs the counter-regulatory response (CRR) which restores euglycemia. During hypoglycemia, ventromedial hypothalamus (VMH) production of nitric oxide (NO) and activation of its receptor soluble guanylyl cyclase (sGC) are critical for the CRR. Hypoglycemia also increases brain reactive oxygen species (ROS) production. NO production in the presence of ROS causes protein S-nitrosylation. S-nitrosylation of sGC impairs its function and induces desensitization to NO. We hypothesized that during hypoglycemia, the interaction between NO and ROS increases VMH sGC S-nitrosylation levels and impairs the CRR to subsequent episodes of hypoglycemia. VMH ROS production and S-nitrosylation were quantified following three consecutive daily episodes of insulin-hypoglycemia (RH model). The CRR was evaluated in rats in response to acute insulin-induced hypoglycemia or via hypoglycemic-hyperinsulinemic clamps. Pretreatment with the anti-oxidant N-acetyl-cysteine (NAC) was used to prevent increased VMH S-nitrosylation.

Results

Acute insulin-hypoglycemia increased VMH ROS levels by 49±6.3%. RH increased VMH sGC S-nitrosylation. Increasing VMH S-nitrosylation with intracerebroventricular injection of the nitrosylating agent S-nitroso-L-cysteine (CSNO) was associated with decreased glucagon secretion during hypoglycemic clamp. Finally, in RH rats pre-treated with NAC (0.5% in drinking water for 9 days) hypoglycemia-induced VMH ROS production was prevented and glucagon and epinephrine production was not blunted in response to subsequent insulin-hypoglycemia.

Conclusion

These data suggest that NAC may be clinically useful in preventing impaired CRR in patients undergoing intensive-insulin therapy.     

Tecto-thalamo-telencephalic interrelationships following visual deafferentation

21-23 months after uni- and bilateral enucleation of the eyes, the turtles Emys orbicularis and Testudo horsfieldi exhibited atrophy, gliosis and residual degenerative changes in the visual nerves and tracts and in the two upper layers of the optic tectum, as well as a reduced density of fibres in the tecto-thalamic tract on the deafferentated side. Electrophysiological experiments on the turtles have shown that tectal impulses en route to the general cortex of the forebrain are relayed in the n. rotundus. Conduction of impulses along the tecto-geniculo-cortical path, found in intact animals, ceases, which is apparently due to transsynaptic changes in the surface layers of the optic tectum.     

Proteins in the nutrient-sensing and DNA damage checkpoint pathways cooperate to restrain mitotic progression following DNA damage

Checkpoint pathways regulate genomic integrity in part by blocking anaphase until all chromosomes have been completely replicated, repaired, and correctly aligned on the spindle. In Saccharomyces cerevisiae, DNA damage and mono-oriented or unattached kinetochores trigger checkpoint pathways that bifurcate to regulate both the metaphase to anaphase transition and mitotic exit. The sensor-associated kinase, Mec1, phosphorylates two downstream kinases, Chk1 and Rad53. Activation of Chk1 and Rad53 prevents anaphase and causes inhibition of the mitotic exit network. We have previously shown that the PKA pathway plays a role in blocking securin and Clb2 destruction following DNA damage. Here we show that the Mec1 DNA damage checkpoint regulates phosphorylation of the regulatory (R) subunit of PKA following DNA damage and that the phosphorylated R subunit has a role in restraining mitosis following DNA damage. In addition we found that proteins known to regulate PKA in response to nutrients and stress either by phosphorylation of the R subunit or regulating levels of cAMP are required for the role of PKA in the DNA damage checkpoint. Our data indicate that there is cross-talk between the DNA damage checkpoint and the proteins that integrate nutrient and stress signals to regulate PKA.     

Changes in the behavior of laboratory-reared rhesus monkeys following the threat of separation

Four heterosexual pairs of three-year-old rhesus monkeys were either repeatedly separated from each other for 30-min or not separated. Prior to each separation, a transfer cage was displayed at the front of the cage to serve as a cue that the pair would be separated. After only a few trials, the animals displayed disturbance, particularly in the form of stereotyped pacingprior to the separation. Practical considerations related to laboratory methodology, a theoretical discussion concerning the fear of separation in monkeys and man, and the need for attention to individual differences in response to separation were emphasized.Supported by NIH grants MH22253, HD04335, and RR00169, to Dr.Gary Mitchell; whose assistance is gratefully acknowledged.     

Countermeasures to the bioterrorist threat of smallpox

Variola, the agent of smallpox, is a bioterrorist threat, as is monkeypox virus, which also occurs naturally in Africa. Development of countermeasures, in the form of improved vaccines, antiviral drugs, and other therapeutic strategies are a high priority. Recent advances in molecular biology and in animal model development have provided fresh insight into the virulence determinants for smallpox and the pathophysiology of disease. The complex replication cycle for orthopoxviruses, and the pivotal role for viral-specific immunomodulatory proteins which contribute to escape from immunologic surveillance, provide many unique targets for therapeutic intervention. The "toxemia" of smallpox has been elucidated in part by variola-infected primate studies which revealed the central role of apoptosis and the evolution of a cytokine storm leading to hemorrhagic diathesis, resembling fulminent "black" smallpox. This suggests a potential role for therapeutic strategies developed for septic shock, in treatment of smallpox. Drugs licensed for other viruses which share molecular targets with orthopoxviruses (e.g. Cidofovir) or cancer drugs (e.g. Gleevec and other tyrosine kinase inhibitors) have immediate application for treatment of smallpox and monkeypox and provide leads for second generation drugs with higher therapeutic indices. Recent advances in identification of virulence determinants and immune evasion genes facilitate the design of alternative vaccines to replace live vaccinia strains that are unsuitable for a large proportion of individuals in a mass immunization campaign.