Social and environmental regulation of signal plasticity and signal reliability in the electric fish Brachyhypopomus gauderio

The balance between the costs and benefits of conspicuous signals ensures that the expression of those signals is related to the quality of the bearer. Plastic signals could enable males to maximize conspicuous traits to impress mates and competitors, but reduce the expression of those traits to minimize signaling costs, potentially compromising the information conveyed by the signals. ^ I investigated the effect of signal enhancement on the information coded by the biphasic electric signal pulse of the gymnotiform fish Brachyhypopomus gauderio. Increases in population density drive males to enhance the amplitude of their signals. I found that signal amplitude enhancement improves the information about the signaler's size. Furthermore, I found that the elongation of the signal's second phase conveys information about androgen levels in both sexes, gonad size in males and estrogen levels in females. Androgens link the duration of the signal's second phase to other androgen-mediated traits making the signal an honest indicator of reproductive state and aggressive motivation. ^ Signal amplitude enhancement facilitates the assessment of the signaler's resource holding potential, important for male-male interactions, while signal duration provides information about aggressive motivation to same-sex competitors and reproductive state to the opposite sex. Moreover, I found that female signals also change in accordance to the social environment. Females also increase the amplitude of their signal when population density increases and elongate the duration of their signal's second phase when the sex ratio becomes female-biased. Indicating that some degree of sexual selection operates in females. ^ I studied whether male B. gauderio use signal plasticity to reduce the cost of reproductive signaling when energy is limited. Surprisingly, I found that food limitation promotes the investment in reproduction manifested as signal enhancement and elevated androgen levels. The short lifespan and single breeding season of B. gauderio diminishes the advantage of energy savings and gives priority to sustaining reproduction. I conclude that the electric signal of B. gauderio provides reliable information about the signaler, the quality of this information is reinforced rather than degraded with signal enhancement.^

Human Synaptic Plasticity Gene Expression Profile and Dendritic Spine Density Changes in HIV-Infected Human CNS Cells: Role in HIV-Associated Neurocognitive Disorders (HAND)

HIV-associated neurocognitive disorders (HAND) is characterized by development of cognitive, behavioral and motor abnormalities, and occur in approximately 50% of HIV infected individuals. Our current understanding of HAND emanates mainly from HIV-1 subtype B (clade B), which is prevalent in USA and Western countries. However very little information is available on neuropathogenesis of HIV-1 subtype C (clade C) that exists in Sub-Saharan Africa and Asia. Therefore, studies to identify specific neuropathogenic mechanisms associated with HAND are worth pursuing to dissect the mechanisms underlying this modulation and to prevent HAND particularly in clade B infection. In this study, we have investigated 84 key human synaptic plasticity genes differential expression profile in clade B and clade C infected primary human astrocytes by using RT2 Profile PCR Array human Synaptic Plasticity kit. Among these, 31 and 21 synaptic genes were significantly (≥3 fold) down-regulated and 5 genes were significantly (≥3 fold) up-regulated in clade B and clade C infected cells, respectively compared to the uninfected control astrocytes. In flow-cytometry analysis, down-regulation of postsynaptic density and dendrite spine morphology regulatory proteins (ARC, NMDAR1 and GRM1) was confirmed in both clade B and C infected primary human astrocytes and SK-N-MC neuroblastoma cells. Further, spine density and dendrite morphology changes by confocal microscopic analysis indicates significantly decreased spine density, loss of spines and decreased dendrite diameter, total dendrite and spine area in clade B infected SK-N-MC neuroblastoma cells compared to uninfected and clade C infected cells. We have also observed that, in clade B infected astrocytes, induction of apoptosis was significantly higher than in the clade C infected astrocytes. In conclusion, this study suggests that down-regulation of synaptic plasticity genes, decreased dendritic spine density and induction of apoptosis in astrocytes may contribute to the severe neuropathogenesis in clade B infection.