Defining management units for European captive aardvarks.

The Aardvark (Orycteropus afer) is a very unique, but relatively widespread African mammal. Although some morphological variation has been observed between forest and savannah populations and among different African regions, they are all considered as a single species. However, no modern taxonomic revision is available. All captive aardvarks in Europe are believed to stem from wild born animals from Namibia, but recently several new wild-caught aardvarks from Tanzania have been integrated into the captive population. This raises the question, whether these specimens should be interbred with the existing captive population or whether there is a risk of outbreeding depression. We studied the genetic structure of the captive populations by sequencing two mitochondrial genes (cytochrome b and 16S rRNA) to assess the degree of genetic differentiation between the two source regions. Our data suggest that the aardvarks kept in European zoos belong to the same phylogenetic (mitochondrial) lineage as the differentiation in the two studied mitochondrial markers was extremely low. A more comprehensive analysis of a larger sample with well documented origin (covering the complete geographic range) and with more sensitive genetic markers is needed to infer any final conclusions concerning the aardvark's taxonomy and identification of suitable aardvark management units.

Noise-induced cochlear synaptopathy in C57BL/6 N mice as a function of trauma strength: ribbons are more vulnerable than postsynapses.

Noise-induced cochlear synaptopathy is characterized by irreversible loss of synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) despite normal hearing thresholds. We analyzed hearing performance and cochlear structure in C57BL/6 N mice exposed to 100, 106, or 112 dB SPL broadband noise (8-16 kHz) for 2 h. Auditory brainstem responses (ABRs) were assessed before, directly after, and up to 28 days post-trauma. Finally, the number, size, and pairing of IHC presynaptic (CtBP2-positive) ribbons and postsynaptic AMPA receptor scaffold (Homer1-positive) clusters were analyzed along the cochlea. Four weeks after the 100 dB SPL trauma, a permanent threshold shift (PTS) was observed at 45 kHz, which after the higher traumata extended toward middle to low frequencies. Loss in ABR wave I amplitudes scaled with trauma strength indicating loss of functional IHC synaptic connections. Latencies of wave I mostly increased with trauma strength. No trauma-related OHC loss was found. The number of synaptic pairs was reduced in the midbasal and basal cochlear region in all trauma conditions, with ribbon loss amounting up to 46% of control. Ribbons surviving the trauma were paired, whereas 4-6 unpaired postsynapses/IHC were found in the medial, midbasal, and basal regions irrespective of trauma strength, contrasting findings in CBA/CaJ mice. Our data confirm the susceptibility of ribbon synapses and ABR wave I amplitudes to a noise trauma of 100 dB SPL or larger. Notably, peripheral dendrites bearing IHC postsynapses were less vulnerable than presynaptic ribbons in C57BL/6 N mice.