text: Acoustic trauma evokes hyperactivity and changes in gene expression in guinea-pig auditory brainstem.
  Hearing loss from acoustic trauma is a risk factor for tinnitus. Animal models using acoustic trauma have demonstrated hyperactivity in central auditory pathways, which has been suggested as a substrate for tinnitus. We used a guinea-pig model of unilateral acoustic trauma. Within the same animals, measurements of peripheral hearing loss, spontaneous activity of single neurons in the inferior colliculus and gene expression in cochlear nucleus and inferior colliculus were combined, acutely and after recovery from acoustic trauma. Genes investigated related to inhibitory (GABA-A receptor subunit alpha 1; glycine receptor subunit alpha 1) and excitatory neurotransmission (glutamate decarboxylase 1; glutamate receptor AMPA subunit alpha 2; glutamate receptor NMDA subunit 1), regulation of transmitter release (member of RAB family of small GTPase; RAB3 GTPase activating protein subunit 1) and neuronal excitability (potassium channel subfamily K member 15). Acoustic trauma resulted in unilateral hearing loss and hyperactivity bilaterally in inferior colliculus. Changes in expression of different mRNAs were observed in ipsilateral cochlear nucleus and in ipsi- and contralateral inferior colliculus, immediately after acoustic trauma, and after 2 and 4 weeks' recovery. Gene expression was generally reduced immediately after trauma, followed by a return to near normal levels or over-expression as recovery time increased. Different mechanisms appear to underlie the spontaneous hyperactivity observed. There is evidence of down-regulation of genes associated with neuronal inhibition in the contralateral inferior colliculus, whereas in ipsilateral cochlear nucleus, competing actions of inhibitory and excitatory systems seem to play a major role in determining overall excitability.
  
entities.text: ['brainstem']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T1
entities.text: ['neurons']
entities.type: Cell
entities.entity_id: PMID-20525074_T2
entities.text: ['cochlear nucleus']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T3
entities.text: ['inferior colliculus']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T4
entities.text: ['inferior colliculus']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T5
entities.text: ['neuronal']
entities.type: Cell
entities.entity_id: PMID-20525074_T6
entities.text: ['inferior colliculus']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T7
entities.text: ['cochlear nucleus']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T8
entities.text: ['inferior colliculus']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T9
entities.text: ['neuronal']
entities.type: Cell
entities.entity_id: PMID-20525074_T10
entities.text: ['inferior colliculus']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T11
entities.text: ['cochlear nucleus']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20525074_T12