Hearing thresholds of small native Australian mammals : red-tailed phascogale (Phascogale calura), kultarr (Antechinomys laniger) and spinifex hopping-mouse (Notomys alexis)

Hearing is essential for communication, to locate prey and to avoid predators. We addressed the paucity of information regarding hearing in Australian native mammals by specifically assessing the hearing range and sensitivity of the red-tailed phascogale (Phascogale calura), the kultarr (Antechinomys laniger) and the spinifex hopping-mouse (Notomys alexis). Auditory brainstem response (ABR) audiograms were used to estimate hearing thresholds within the range of 1–84 kHz, over a dynamic range of 0–80 dB sound pressure level (SPL). Phascogales had a hearing range of 1–40 kHz, kultarrs 1–35 kHz and hopping-mice 1–35 kHz, with a dynamic range of 17–59 dB SPL, 20–80 dB SPL and 30–73 dB SPL, respectively. Hearing for all species was most sensitive at 8 kHz. Age showed no influence on optimal hearing, but younger animals had more diverse optimal hearing frequencies. There was a relationship between males and their optimal hearing frequency, and greater interaural distances of individual males may be related to optimal hearing frequency. Because nocturnal animals use high-range hearing for prey or predator detection, our study suggests this may also be the case for the species examined in this study. Future studies should investigate their vocalizations and behaviour in their natural environments, and by exposing them to different auditory stimuli

Tracking the expression of GABAA receptor subunit a1, Glutamic-Acid Decarboxylase-67, N-Methyl-D-Aspartate receptor subunit 2A in rat auditory pathway following noise-induced hearing loss

Excessive exposure to loud noise or a mechanical insult results in damage to the cochlea, which can lead to a range of neuronal changes in key nuclei in the auditory pathway. Neuronal changes that have been observed include plasticity of tonotopic organisation, changes in the pattern of spontaneous activity and in the balance of excitatory and inhibitory transmitter systems. Moreover, a cochlear hearing loss is strongly associated with tinnitus in humans. This suggests that one or more of these neuronal changes may be involved in generating tinnitus, although the mechanisms and site remain unknown. In an attempt to determine which area(s) may be involved in the generation of tinnitus, we are investigating neuronal changes at a number of levels of the auditory pathway (auditory cortex (AC), inferior colliculus (IC) and dorsal cochlear nucleus (DCN)), primarily focusing on the balance of excitatory and inhibitory transmitter systems. In this study we examined the time-course of changes in the expression of the GABAA receptor subunit a1(GABAARa1), Glutamic-Acid Decarboxylase-67 (GAD-67), N-Methyl-D-Aspartate receptor subunit 2A (NMDAR2A) in AC, IC and DCN up to 32 days following exposure to a 16kHz band pass (1/10th octave noise (115 dB SPL))

Tracking the expression of GABAA receptor subunit α1 in rat auditory cortex, inferior colliculus and dorsal cochlear nucleus following noise-induced hearing loss

Damage to the cochlea, produced by exposure to a loud noise or a mechanical insult results in a range of changes in key auditory nuclei in the auditory pathway. Neuronal changes observed include plasticity of tonotopic representation, changes in the pattern of spontaneous activity and changes in the balance of excitatory and inhibitory transmitter systems. Moreover, damage to the cochlea frequently results in tinnitus. This suggests that one or more of these neuronal changes may be involved in tinnitus generation, although the mechanism remains to be elucidated. In an attempt to determine which area(s) may be involved in the generation of tinnitus, we are investigating neuronal changes at different levels of the auditory system (brainstem, midbrain and cortex). In this study we examine the timecourse of changes in the expression of the GABAA receptor in cochlear nucleus, inferior colliculus and auditory cortex up to 32 days following exposure to a 16 kHz bandpass (1/10th octave noise (115 dB SPL)). Male Long Evans rats (n = 10) were unilaterally exposed to the damaging noise for 1hour. At 0, 4, 8, 16 or 32 days rats were euthanased, their brains were removed and processed for immunohistochemistry to identify GABAARα1 subunit expression, which was subsequently quantified in the cochlear nucleus, inferior colliculus and auditory cortex. Over the course of the study period we saw significant changes in GABAARα1 expression. In auditory cortex these changes were evident from 4 days to 32 days where we saw a progressive increase in GABAARα1 up to twofold by 32 days. These increases may reflect an attempt to balance excitatory transmission, which is known to increase following noiseinduced hearing loss

Tracking tonotopic changes in the auditory system following noise-induced hearing loss

Unilateral noiseinduced hearing loss results in significant changes throughout the auditory system, but the manifestation of these changes depends on the nuclei under study. For instance, significant changes in the distribution of characteristic frequencies are observed in the inferior colliculus and primary auditory cortex following noiseinduced hearing loss, but only in the auditory cortex are these changes thought to be due to plastic reorganisation. Determining how these changes develop at different levels of the auditory pathway may shed light on the mechanisms responsible for the cortical plastic effects. Moreover, a growing body of evidence suggests that hearing loss and its accompanying neuronal changes are also involved in tinnitus. Thus, understanding the development of neuronal changes following noiseinduced hearing loss may aid us in our understanding of the neural basis of tinnitus. Accordingly, we examined neuronal changes at three different levels of the auditory pathway and at different time points up to 6 months following exposure to a damaging narrow band noise. Male Long Evans rats (n = 16) were unilaterally exposed to a 115 dB SPL 16 kHz 1/10th octave bandpass noise for 1hour. Principally, we were interested in the frequency representation and spontaneous activity of neurons in cochlear nucleus, inferior colliculus and auditory cortex. We recorded simultaneously from each of these structures using multichannel electrodes. Six unexposed rats served as controls. Hearing was assessed before and after the noise trauma procedure using auditory brainstem response (ABR) audiograms. Tone pips (144 kHz, 50 ms duration, 080 dB SPL, 1 Hz presentation rate) were used to obtain frequency tuning curves. At 30 days following the noise treatment the majority of multiunit clusters recorded in auditory cortex had two peaks in their frequency tuning curves (912 kHz and 3035 kHz), which bordered the spectral range of the noisetrauma stimulus. Similar changes were also evident when we recorded from animals 6 months after noise trauma. Less pronounced tonotopic changes were observed in the IC. The only reliable effect shown in the cochlear nucleus was an absence of neuronal activity in response to 16 kHz stimulation. In summary, the pattern of tonotopic changes is evident in the first month following noise exposure and remains unchanged for up to 6 months

Tracking neuronal changes in the auditory system following noise-induced hearing loss

Noise-induced hearing loss results in significant changes throughout the auditory system. Significant changes in the distribution of characteristic frequencies are observed in the inferior colliculus (IC), medial geniculate nucleus (MG) and primary auditory cortex (A1), but only in A1 and MG are these changes thought to be due to plastic reorganisation. A growing body of evidence suggests that hearing loss and its accompanying neuronal changes are also involved in tinnitus. Thus, understanding the development of neuronal changes following noise-induced hearing loss may aid us in understanding the neural basis of tinnitus. We examined neuronal changes at three different levels of the auditory pathway and at different time-periods up to 7 months following exposure to a damaging, narrow band noise

Alpha Lipoic Acid and noise induced hearing loss : a prevention and treatment trial

There are currently no effective treatments for Noise-Induced Hearing Loss (NIHL), however, recent studies have shown that certain antioxidants can, to some extent, protect against NIHL. There is some evidence to suggest a link between NIHL and oxidative stress, and antioxidants may play a role in reducing the damaging effects of reactive oxygen species within the peripheral auditory system. Our study measured changes in hearing thresholds following acoustic trauma in animals given Alpha Lipoic Acid (ALA), a potent antioxidant, either before or after the acoustic trauma

Soluble lipoprotein receptor-related protein immunoreactive species in cell culture media and serum replacement supplements

The low-density lipoprotein receptor-related protein (LRP) is a large multifunctional cell surface membrane receptor capable of binding over 50 ligands. These include molecules important in Alzheimer's disease such as the amyloid beta-protein precursor (A beta PP), the beta-amyloid (A beta) peptide and apolipoprotein E (ApoE). Full length LRP consists of a 515 kDa extracellular ligand binding alpha-chain and an 85 kDa membrane spanning beta-chain. A soluble form of LRP (sLRP) present in human plasma retains the ability to bind ligands, including A beta. This soluble form is an ectodomain fragment generated from the membrane bound form of the receptor by proteolytic cleavage. Here we report data demonstrating that some commercial 'serum-free' supplements and 'serum-free' media contain unlisted sLRP immunoreactive species that may reflect the presence of undefined serum protein extracts in these 'serum-free' preparations. This has the potential to interfere with experimental results and interpretation in a range of cell culture studies involving LRP or any of its ligands and possibly also other serum proteins