Abstract
In the adult auditory system, loss of input resulting from peripheral deafferentation is well known to lead to plasticity in the central nervous system, manifested as reorganization of cortical maps and altered activity throughout the central auditory pathways. The auditory system also has strong afferent and efferent connections with cortico-limbic circuitry including the prefrontal cortex and the question arises whether this circuitry is also affected by loss of peripheral input. Recent studies in our laboratory showed that PFC activation can modulate activity of the auditory thalamus or medial geniculate nucleus (MGN) in normal hearing rats. In addition, we have shown in rats that cochlear trauma resulted in altered spontaneous burst firing in MGN. However, whether the PFC influence on MGN is changed after cochlear trauma is unknown. We investigated the effects of electrical stimulation of PFC on single neuron activity in the MGN in anaesthetized Wistar rats 2 weeks after acoustic trauma or sham surgery. Electrical stimulation of PFC showed a variety of effects in MGN neurons both in sham and acoustic trauma groups but inhibitory responses were significantly larger in the acoustic trauma animals. These results suggest an alteration in functional connectivity between PFC and MGN after cochlear trauma. This change may be a compensatory mechanism increasing sensory gating after the development of altered spontaneous activity in MGN, to prevent altered activity reaching the cortex and conscious perception.
Highlights
Loss of input from peripheral deafferentation in adult sensory systems is well known to lead to plasticity in the central nervous system, leading to reorganization of cortical maps [1,2,3,4,5] and increases in cortical spontaneous activity [6,7]
This paper provides the first evidence in an animal model for altered functional connectivity between prefrontal cortex (PFC) and medial geniculate nucleus (MGN) after cochlear trauma
Electrical stimulation of PFC resulted in diverse changes to the firing rate of individual MGN neurons in agreement with our previously published data in animals without exposure to an acoustic trauma (AT) [34]
Summary
Loss of input from peripheral deafferentation in adult sensory systems is well known to lead to plasticity in the central nervous system, leading to reorganization of cortical maps [1,2,3,4,5] and increases in cortical spontaneous activity [6,7]. We have developed a rat model of cochlear trauma that results in a temporary hearing loss and the development of tinnitus in about 50% of animals In this model, we have shown plastic changes in MGN burst firing parameters in all animals independent of whether they developed tinnitus [10]. We have shown plastic changes in MGN burst firing parameters in all animals independent of whether they developed tinnitus [10] These plastic changes are most likely to be due to the cochlear trauma and subsequent loss of peripheral input even in the absence of a shift in peripheral thresholds (so-called hidden hearing loss [32,33]). We have already demonstrated functional connectivity between PFC and MGN in rats, using single neuron recordings in MGN whilst electrically stimulating the PFC [34]
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