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Callen, A.

Publications and source records attributed to Callen, A..

3 recordsLinked to original sources

Chytridiomycosis infection and heat compromises sperm quality in a threatened frog

Environmental change is reshaping wildlife reproduction through increasing temperatures and the spread of emerging infectious diseases, yet the physiological consequences of managing these stressors remain poorly understood. Amphibians are particularly vulnerable due to their ectothermy and high susceptibility to chytridiomycosis, caused by Batrachochytrium dendrobatidis (Bd). Here, we examine how Bd infection and thermal treatment interact to influence sperm quality and reproductive investment in male green and golden bell frogs (Ranoidea aurea), a species that has suffered severe population declines. Moderate Bd infection was associated with elevated sperm concentration relative to uninfected and heavily infected males, consistent with increased short-term reproductive investment under elevated mortality risk. However, severe infection led to pronounced reductions in sperm concentration and motility. Thermal treatment successfully eliminated Bd infection but imposed substantial reproductive costs: sperm concentration declined following treatment and remained significantly reduced six months later, despite partial recovery of sperm motility and membrane integrity. These results indicate persistent impairment of spermatogenic capacity rather than transient suppression. Our findings reveal that disease and thermal stress jointly shape amphibian reproductive outcomes through context-dependent trade-offs between immune defence and gamete production. While mild infection may trigger short-lived increases in reproductive output, both severe infection and pathogen clearance via thermal exposure impose lasting constraints on fertility. These results highlight an underappreciated cost of disease mitigation and suggest that increasing thermal extremes associated with climate change may further limit amphibian reproductive resilience, with important implications for conservation management and population persistence.

physiology↗

Heightened Sensitivity to Voice Loudness Changes in Parkinson's Disease

Parkinsons disease (PD) affects voice and speech production, often resulting in reduced vocal intensity and monotonous speech. Recent studies have suggested that these changes can be partially explained by altered sensory feedback processing when producing speech. Individuals with PD (IwPD) may fail to monitor sensory feedback from their own voice, impairing their ability to adjust voice and speech when sensory input differs from expectations. In this study, we investigated sensory feedback processing in PD by looking at the sensory attenuation typically observed in event-related responses (ERP) to the self-generated voice. When sensory feedback processing is intact, the P50, N100, and P200 ERP responses to the self-generated voice are more attenuated than to an externally-generated voice. Twenty-three IwPD and 23 healthy controls (HCs) participated in a voice playback study that comprised three conditions: self-generated voice (auditory-motor condition; AMC), externally-generated voice (auditory-only condition; AOC), and motor-only. The AMC and AOC conditions also included an amplitude modulation of the voice (0/+15dB). Linear mixed models assessed group differences in ERP morphology. While groups did not differ in their P50 and P200 responses, there was a significant group-condition- loudness interaction for the N100. Follow-up analyses showed that IwPD displayed much larger N100 error responses for unexpected loudness modulations as compared to HC. This observation suggests that IwPD may process voice modulations differently than HC. The hypersensitivity to loudness changes may underlie IwPDs difficulties in processing and adapting their voice acoustics.

neuroscience↗

The Secondary Somatosensory Cortex Gates Mechanical and Thermal Sensitivity

The cerebral cortex is vital for the perception and processing of sensory stimuli. In the somatosensory axis, information is received by two distinct regions, the primary (S1) and secondary (S2) somatosensory cortices. Top-down circuits stemming from S1 can modulate mechanical and cooling but not heat stimuli such that circuit inhibition causes blunted mechanical and cooling perception. Using optogenetics and chemogenetics, we find that in contrast to S1, an inhibition of S2 output increases mechanical and heat, but not cooling sensitivity. Combining 2-photon anatomical reconstruction with chemogenetic inhibition of specific S2 circuits, we discover that S2 projections to the secondary motor cortex (M2) govern mechanical and thermal sensitivity without affecting motor or cognitive function. This suggests that while S2, like S1, encodes specific sensory information, that S2 operates through quite distinct neural substrates to modulate responsiveness to particular somatosensory stimuli and that somatosensory cortical encoding occurs in a largely parallel fashion.

neuroscience↗