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Biology subjects

Kremer, C.

Publications and source records attributed to Kremer, C..

4 recordsLinked to original sources

Influence of natural enemy specificity and functional response on victim coexistence

Natural enemies are thought to promote coexistence of competing victim species. Although existing theory suggests victim coexistence increases with enemy specialization, the dynamics and potential extinction of enemies is generally discounted. Where enemy dynamics have been considered, empirically atypical linear functional responses have been studied. These limitations could over-simplify inferences about enemy-mediated coexistence. We studied the dynamics of two competing victim species and two enemy species with a deterministic model. We derived equilibrium points, and used linear stability analysis, numerical simulations and Floquet theory to determine the influence of enemy specificity and non-linear functional responses on coexistence in this victim-enemy community. We found greater specificity could drive enemy equilibrium points to infeasible values. We found only accelerating enemy functional responses result in stable equilibrium point coexistence of otherwise equivalent competitor victims, in which case greater specificity results in greater stability. Linear and saturating responses produce complex dynamics (neutral or limit cycles, chaos) or extinction, with limit cycle stability highest at intermediate specificity. Our results indicate strict specificity may not maximize coexistence, and enemy functional response critically influences whether enemies promote victim coexistence. They highlight the need to incorporate enemy dynamics into the growing body of theory regarding enemy-mediated diversity maintenance.

ecology↗

Cortical determinants of loudness perception and auditory hypersensitivity

Parvalbumin-expressing inhibitory neurons (PVNs) stabilize cortical network activity, generate gamma rhythms, and regulate experience-dependent plasticity. Here, we observed that activation or inactivation of PVNs functioned like a volume knob in the mouse auditory cortex (ACtx), turning neural and behavioral classification of sound level up or down over a 20dB range. PVN loudness adjustments were "sticky", such that a single bout of 40Hz PVN stimulation sustainably suppressed ACtx sound responsiveness, potentiated feedforward inhibition, and behaviorally desensitized mice to loudness. Sensory sensitivity is a cardinal feature of autism, aging, and peripheral neuropathy, prompting us to ask whether PVN stimulation can persistently desensitize mice with ACtx hyperactivity, PVN hypofunction, and loudness hypersensitivity triggered by cochlear sensorineural damage. We found that a single 16-minute bout of 40Hz PVN stimulation session restored normal loudness perception for one week, showing that perceptual deficits triggered by irreversible peripheral injuries can be reversed through targeted cortical circuit interventions.

neuroscience↗

Cortical contributions to the perception of loudness and hyperacusis

Sound perception is closely linked to the spatiotemporal patterning of neural activity in the auditory cortex (ACtx). Inhibitory interneurons sculpt the patterns of excitatory ACtx pyramidal neuron activity, and thus play a central role in sculpting the perception of sound. Reduced inhibition from parvalbumin-expressing (PV) inhibitory interneurons and the associated increased gain of sound-evoked pyramidal neuron spike rates are well-established consequences of aging and sensorineural hearing loss. Here, we reasoned that changes in PV-mediated inhibition would directly impact the perception of loudness. We hypothesized that ACtx PV activity could function as a perceptual volume knob, where reduced or elevated PV activity would increase or decrease the perceived loudness of sound, respectively. To test these hypotheses, we developed a two-alternative forced-choice loudness classification task for head-fixed mice and demonstrated that noise-induced sensorineural hearing loss directly caused a [~]10 dB loudness hyperacusis that begins hours after noise-induced sensorineural hearing loss and persists for at least several weeks. Conversely, sounds were perceived as [~]10 dB softer during optogenetic activation of ACtx PV neurons without having any effect on the overall detectability of sound. These data suggest that ACtx PV neurons can bi-directionally control the perceived loudness of sound, presumably via the strength of their inhibition onto local pyramidal neurons. Further, these data identify cortical PV neurons as a target for hyperacusis therapies and demonstrate a direct link between acquired sensorineural hearing loss and loudness hyperacusis.

neuroscience↗

Genetic rescue without genomic swamping in wild populations

Gene flow is an enigmatic evolutionary force because it can limit adaptation but can also help populations escape inbreeding depression. Manipulating gene flow for conservation purposes is a controversial, but potentially powerful management strategy. We use multigenerational pedigrees and genomics to test demographic and evolutionary consequences of manipulating gene flow in two isolated wild Trinidadian guppy populations. We found that on average, hybrids lived longer and reproduced more. Despite overall genome-wide homogenization, alleles potentially associated with local adaptation were not entirely swamped by gene flow. Our results suggest that combining new genomic variation from immigrants with potentially adaptive variation from the recipient population resulted in highly fit hybrids and subsequent increases in population size. Contrary to the prevailing view that gene flow constrains adaptation, our study shows that immigration can produce long-term fitness benefits in small populations without swamping locally adaptive variation.

evolutionary biology↗