During hair cell death ‘scars’ develop, which prevent potassium rich fluid of the endolymph from mixing with the fluid on the basal domain. The potassium rich fluid is toxic to the neuronal endings and can damage hearing of the entire ear. If the endolymph fluid mixes with the fluid on the basal domain the neurons become depolarized, causing complete hearing loss. In addition to complete hearing loss, if the area is not sealed and leakage continues further tissue damage will occur. The ‘scars’ that form to replace the damaged hair cell are caused by supporting hair cells undergoing apoptosis and sealing the reticular lamina, which prevents fluid leakage. The cell death of two supporting hair cells rapidly expands their apical domain, which compresses the hair cell beneath its apical domain. Recent studies have investigated additional mechanisms of NIHL involving delayed or disabled electrochemical transmission of nerve impulses from the hair cell to and along the auditory nerve. In cases of extreme acute acoustic trauma, a portion of the postsynaptic dendrite (where the hair cell transfers electrochemical signals to the auditory nerve) can rupture from overstimulation, temporarily stopping all transmission of auditory input to the auditory nerve. This is known as excitotoxicity. Usually, this sort of rupture heals within about five days, resulting in functional recovery of that synapse. While healing, an over-expression of glutamate receptors can result in temporary tinnitus, or ringing in the ears. Repeated ruptures at the same synapse may eventually fail to heal, leading to permanent hearing loss. Prolonged exposure to high intensity noise has also been linked to the disruption of ribbon synapses located in the synaptic cleft between inner hair cells and spiral ganglion nerve fibers, leading to a disorder referred to as cochlear synaptopathy or hidden hearing loss. This disorder is cumulative and over time, leads to degeneration of the spiral ganglion cells of the inner ear and overall dysfunction in the neural transmission between auditory nerve fibers and the central auditory pathway. The most common symptom of cochlear synaptopathy is difficulty understanding speech, especially in the presence of competing noise. However, this type of hearing impairment is often undetectable by conventional pure tone audiometry, thus the name "hidden" hearing loss. Acoustic over-exposure can also result in decreased myelination at specific points on the auditory nerve. Myelin, an insulating sheath surrounding nerve axons, expedites electrical impulses along nerves throughout the nervous system.