linguistic:voice_change
Plasticity of auditory critical period

The auditory critical period of rats, which lasts from postnatal day 11 (P11) to P13 can be extended through deprivation experiments such as white noise-rearing. It has been shown that subsets of the tonotopic map in A1 can be held in a plastic state indefinitely by exposing the rats to white noise consisting of frequencies within a particular range determined by the experimenter. For example, exposing a rat during auditory critical period to white noise that includes tone frequencies between 7 kHz and 10 kHz will keep the corresponding neurons in a plastic state far past the typical critical period–one study has retained this plastic state until the rats were 90 days old. Recent studies have also found that release of the neurotransmitter norepinephrine is required for critical period plasticity in the auditory cortex, however intrinsic tonotopic patterning of the auditory cortical circuitry occurs independently from norepinephrine release. A recent toxicity study showed that in-utero and postnatal exposure to polychlorinated biphenyl (PCB) altered overall primary auditory cortex (A1) organization, including tonotopy and A1 topography. Early PCB exposure also changed the balance of excitatory and inhibitory inputs, which altered the ability of the auditory cortex to plastically reorganize after changes in the acoustic environment, thereby altering the critical period of auditory plasticity.