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There is considerable capacity for plasticity in the mature auditory brain stem and plastic changes can be evoked by the change in activity resulting from profound deafness. There are deafness related changes in transmitters and receptors with resulting changes in inhibition and activity that can effect auditory processing. An understanding of the underlying mechanisms of plasticity, with gene microarray results pointing to a number of regulatory pathways, could help in development of interventions to influence plasticity. Such interventions should be helpful to provide the best circumstances for return of hearing with cochlear prostheses following deafness as well as for management of clinical problems resulting from the plasticity of partial deafness and central tinnitus.

The results of the present study document that a significant low-frequency hearing loss occurrs as early as in one-month-old F344 rats and results in a lack of recordable TEOAEs and in the absence of DPOAEs at low frequencies. The low-frequency defect, which preceeds the later occurring high-frequency hearing loss, is probably not connected with the degeneration of hair cells or specific age-related hearing loss genes, but can be related to more general genetic mutations present in this rat strain.

c-Fos immunocytochemistry is used for labelling activated neurons in studies of auditory cortical processing of communication sounds in mice. Activation of the primary auditory fields AI and AAF does not discriminate between sounds of high or low behavioural significance. Labelling related to call recognition occurs in the second auditory field AIL Activation in another auditory field of higher order, the dorsoposterior field DP, seems to be related to an integration of call recognition with the emotional/motivational background of the animals. A left-hemisphere advantage of activation in this field is associated with higher levels of maternal emotions. These data on auditory cortical activation fit excellently to perception data of communication calls in mice.

Accurate speech-sound encoding and perception depends on precise timing of neural events. A deficit in speech-sound perception may be cognitive in origin, but in many instances, imprecise afferent encoding is its source. It has been demonstrated that physiological responses signalling the proper encoding of speech are measurable, and deficits have been discerned in both the auditory cortex and in subcortical regions.

Importantly, this preconscious encoding of sound is plastic. Auditory training has long been used to improve perception. With physiological recording, it is possible to track where neural reorganization has occurred, providing us with insight into the nature of auditory system plasticity as well as an unbiased gauge of training success.

Training and stimulus cue enhancement’s impact on optimising neural timing to acoustic sound structure leads to speculation about their impact on learning other types of sounds. The malleability of encoding of sound within the auditory pathway suggests approaches that could be applied more generally in other instances where improved perception of sound is desirable, such as learning music or foreign languages.

There is considerable capacity for plasticity in the mature auditory brain stem and plastic changes can be evoked by the change in activity resulting from profound deafness. There are deafness related changes in transmitters and receptors with resulting changes in inhibition and activity that can effect auditory processing. An understanding of the underlying mechanisms of plasticity, with gene microarray results pointing to a number of regulatory pathways, could help in development of interventions to influence plasticity. Such interventions should be helpful to provide the best circumstances for return of hearing with cochlear prostheses following deafness as well as for management of clinical problems resulting from the plasticity of partial deafness and central tinnitus.

The results of the present study document that a significant low-frequency hearing loss occurrs as early as in one-month-old F344 rats and results in a lack of recordable TEOAEs and in the absence of DPOAEs at low frequencies. The low-frequency defect, which preceeds the later occurring high-frequency hearing loss, is probably not connected with the degeneration of hair cells or specific age-related hearing loss genes, but can be related to more general genetic mutations present in this rat strain.

Since negotiators are decision-makers, understanding a negotiation requires a deep understanding of the negotiators’ decisions. As Hayek suggests, the theoretical foundations in this chapter address decision-making and preferences from the viewpoint of different disciplines. The origin of preferences and their stability over time varies widely across fields: Economists, for example, usually assume preferences to be an underlying property of any individual and to be stable over time. If an agent’s choice changes over time, then either the production technology available or the information at hand have changed—preferences do not. This widely used perspective is most notably vindicated by Stigler and Becker (1977) in a seminal paper arguing against the assumption of changing preferences and it is outlined in several microeconomic textbooks, e.g. Kreps (1990), Varian (1992), Mas-Colell, Whinston, and Green (1995).

The present study indicates that the neuro-specific co-transporter KCC2 is expressed abundantly throughout the IC. The postnatal expression pattern of KCC2 is upregulated in the IC as well as that in the neocortex, the hippocampus and the cerebellum. Considering the importance of this co-transporter on controlling auditory function, further studies are needed in all aspects including the neuronal maturation and the switching mechanisms.

Presented results show that in adult congenitally deaf cats there is: a local desynchronization of inputs within adjacent synapses, an interlayer desynchronization of inputs to different layers in cortex, and possibly also a decreased inhibition in layer IV and III.

Although switching a monaurally presented sound from one ear to the other evoked much larger negative difference potentials, we concluded that lateralization change in MMN studies must be made by altering the binaural cues, either by changing interaural time and/or level disparities under dichotic conditions, or by using loudspeakers. This was because our results indicated a significant role of different states of refractoriness for the responses to standard and deviant monaural stimuli, which is a clear violation of conditions for a genuine, memory comparison based MMN.