State-Dependent Plasticity of Neural Responses to 70dB Clicks Along Central, Primary, Auditory Transmission Pathways

Author(s):  
Charles D. Woody
Author(s):  
Giacomo Zilio ◽  
Louise Solveig Noergaard ◽  
Giovanni Petrucci ◽  
Nathalie Zeballos ◽  
Claire Gougat-Barbera ◽  
...  

Dispersal plays a main role in determining spatial dynamics, and both theory and empirical evidence indicate that evolutionary optima exist for constitutive or plastic dispersal behaviour. Plasticity in dispersal can be influenced by factors both internal (state-dependent) or external (context-dependent) to individuals. Parasitism is interesting in this context, as it can influence both types of host dispersal plasticity: individuals can disperse in response to internal infection status but might also respond to the presence of infected individuals around them. We still know little about the driving evolutionary forces of host dispersal plasticity, but a first requirement is the presence of a genetic basis on which natural selection can act. In this study, we used microcosm dispersal mazes to investigate plastic dispersal of 20 strains of the freshwater protist Paramecium caudatum in response to the bacterial parasite Holospora undulata. We additionally quantified the genetic component of the plastic responses, i.e. the heritability of state- and context-depended dispersal. We found that infection by the parasite can either increase or decrease dispersal of individual strains relative to the uninfected (state-dependent plasticity), and this to be heritable. We also found strain-specific change of dispersal of uninfected Paramecium when exposed to variable infection prevalence (context-dependent plasticity) with very low level of heritability. To our knowledge, this is the first explicit empirical demonstration and quantification of genetic variation of plastic dispersal in a host-parasite system, which could have important implications for meta-population and epidemiological dynamics. We discuss some of the underlying mechanisms of this variation and link our results to the existing theoretical models.


2018 ◽  
Vol 115 (15) ◽  
pp. E3559-E3568 ◽  
Author(s):  
Meng-chin A. Lin ◽  
Stephen C. Cannon ◽  
Diane M. Papazian

A de novo mutation in the KCND2 gene, which encodes the Kv4.2 K+ channel, was identified in twin boys with intractable, infant-onset epilepsy and autism. Kv4.2 channels undergo closed-state inactivation (CSI), a mechanism by which channels inactivate without opening during subthreshold depolarizations. CSI dynamically modulates neuronal excitability and action potential back propagation in response to excitatory synaptic input, controlling Ca2+ influx into dendrites and regulating spike timing-dependent plasticity. Here, we show that the V404M mutation specifically affects the mechanism of CSI, enhancing the inactivation of channels that have not opened while dramatically impairing the inactivation of channels that have opened. The mutation gives rise to these opposing effects by increasing the stability of the inactivated state and in parallel, profoundly slowing the closure of open channels, which according to our data, is required for CSI. The larger volume of methionine compared with valine is a major factor underlying altered inactivation gating. Our results suggest that V404M increases the strength of the physical interaction between the pore gate and the voltage sensor regardless of whether the gate is open or closed. Furthermore, in contrast to previous proposals, our data strongly suggest that physical coupling between the voltage sensor and the pore gate is maintained in the inactivated state. The state-dependent effects of V404M on CSI are expected to disturb the regulation of neuronal excitability and the induction of spike timing-dependent plasticity. Our results strongly support a role for altered CSI gating in the etiology of epilepsy and autism in the affected twins.


2010 ◽  
Vol 103 (4) ◽  
pp. 1785-1797 ◽  
Author(s):  
Jason V. Thompson ◽  
Timothy Q. Gentner

Learning typically increases the strength of responses and the number of neurons that respond to training stimuli. Few studies have explored representational plasticity using natural stimuli, however, leaving unknown the changes that accompany learning under more realistic conditions. Here, we examine experience-dependent plasticity in European starlings, a songbird with rich acoustic communication signals tied to robust, natural recognition behaviors. We trained starlings to recognize conspecific songs and recorded the extracellular spiking activity of single neurons in the caudomedial nidopallium (NCM), a secondary auditory forebrain region analogous to mammalian auditory cortex. Training induced a stimulus-specific weakening of the neural responses (lower spike rates) to the learned songs, whereas the population continued to respond robustly to unfamiliar songs. Additional experiments rule out stimulus-specific adaptation and general biases for novel stimuli as explanations of these effects. Instead, the results indicate that associative learning leads to single neuron responses in which both irrelevant and unfamiliar stimuli elicit more robust responses than behaviorally relevant natural stimuli. Detailed analyses of these effects at a finer temporal scale point to changes in the number of motifs eliciting excitatory responses above a neuron's spontaneous discharge rate. These results show a novel form of experience-dependent plasticity in the auditory forebrain that is tied to associative learning and in which the overall strength of responses is inversely related to learned behavioral significance.


Parasitology ◽  
2017 ◽  
Vol 144 (11) ◽  
pp. 1468-1475 ◽  
Author(s):  
LIEN T. LUONG ◽  
TAYLOR BROPHY ◽  
EMILY STOLZ ◽  
SOLOMON J. CHAN

SUMMARYParasites can evolve phenotypically plastic strategies for transmission such that a single genotype can give rise to a range of phenotypes depending on the environmental condition. State-dependent plasticity in particular can arise from individual differences in the parasite's internal state or the condition of the host. Facultative parasites serve as ideal model systems for investigating state-dependent plasticity because individuals can exhibit two life history strategies (free-living or parasitic) depending on the environment. Here, we experimentally show that the ectoparasitic mite Macrocheles subbadius is more likely to parasitize a fruit fly host if the female mite is mated; furthermore, the propensity to infect increased with the level of starvation experienced by the mite. Host condition also played an important role; hosts infected with moderate mite loads were more likely to gain additional infections in pairwise choice tests than uninfected flies. We also found that mites preferentially infected flies subjected to mechanical injury over uninjured flies. These results suggest that a facultative parasite's propensity to infect a host (i.e. switch from a free-living strategy) depends on both the parasite's internal state and host condition. Parasites often live in highly variable and changing environments, an infection strategy that is plastic is likely to be adaptive.


2019 ◽  
Vol 114 ◽  
pp. 104539 ◽  
Author(s):  
Julie M. Butler ◽  
Sarah M. Whitlow ◽  
Loranzie S. Rogers ◽  
Rosalyn L. Putland ◽  
Allen F. Mensinger ◽  
...  

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