Functional laminar architecture of rat primary auditory cortex following acoustic trauma

• Main Author: Khodai, Tansi Jamshed
• Published: University of Strathclyde 2014
• Subjects: 610
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.658933

Exposure to loud sound can cause a series of hearing problems, the most common being tinnitus or hearing loss (temporary or permanent). Furthermore, tinnitus caused due to acoustic trauma may be observed with or without hearing loss, making it harder for tinnitus researchers to understand the pathology of this condition. Despite extensive studies in both animal and human subjects, it is still not fully understood how acoustic trauma can change neuronal activity in the auditory cortex. Several animal studies suggest changes in auditory tuning properties and increase in spontaneous activity after exposure to acoustic trauma. However, there are several discrepancies in observed changes. One possible explanation for this could be that these findings represent an average response across cortical depths which could mask the layer specific alteration in neural activity following acoustic trauma because previous studies have shown laminar specific evoked and spontaneous activity. In this study we tested the hypothesis that acoustic trauma alters neural activity in a layer-specific manner. Rats were anesthetised with urethane anaesthesia and recordings were obtained using multichannel linear silicon probes inserted vertically into the primary auditory cortex. The animals were exposed (bilaterally) to one octave white noise centred at 16 kHz, at 110 dB SPL for 1 hour. Spontaneous and auditory-evoked activity was measured before trauma and then one and two hour time-points after the acoustic trauma. We quantified laminar specific and average changes in different tuning curve parameters such as threshold, characteristic frequency, bandwidth, sparseness, spontaneous firing rate and burst like activity after trauma exposure in three different frequency regions of primary auditory cortex. We observed laminar-specific changes in auditory tuning properties such as increase in threshold and spontaneous activity mainly in layer V of the primary auditory cortex following acoustic trauma. Furthermore, we also observed increase in burst-like spiking in the superficial layers. These findings support the hypothesis that acute effects of acoustic trauma on auditory cortical population activity is laminar-specific. These findings provide essential information regarding the changes in circuit mechanisms that develop following acoustic trauma which are critical for enhancing our knowledge about the pathology of these conditions and also to identify new potential targets to treat them.