Ensemble spontaneous activity in the guinea-pig cochlear nerve.
Spectral analysis of electrical noise recorded from the round window (RW) of the cochlea is referred to as the ensemble spontaneous activity (ESA) of the cochlear nerve. The ESA is considered to represent the summed spontaneous activity of single fibers of the auditory nerve and changes in the spectral characteristics of the ESA have been observed in humans with tinnitus. Experiments were undertaken to determine the relationship of the ESA to auditory neurotransmission. The ESA consisted of energy centered at approximately 900 Hz, similar to the spectral peak of single auditory neuron discharges. The amplitude of the ESA was correlated with good auditory sensitivity in the 12-30 kHz region of the cochlea. Constant pure tones of 12-22 kHz suppressed the ESA reducing its amplitude in a frequency and intensity dependent manner implying that the ESA recorded at the RW is generated or dominated by neurons in the basal region of the cochlea. The ESA was significantly suppressed by round window perfusion of the P2X receptor agonist adenosine 5'-O-(3-thiotriphosphate) (ATPgammaS) (10 mM) the glutamate receptor antagonist 6-7-dinitroquinoxaline-2,3-dione (DNQX) (1 mM), and the sodium channel antagonist tetrodotoxin (TTX) (20 microM). Following intravenous furosemide injection (40 mg/kg) reduction and recovery of the ESA correlated with similar changes in the endocochlear potential (EP). Following DNQX and ATPgammaS an additional spectral peak at 200 Hz was often observed. This peak has been postulated to be a correlate of tinnitus in humans but had not previously been observed in a guinea-pig model of tinnitus. These data confirm the spectral characteristics of the ESA in guinea-pigs and show it is dependent on the sensitivity of the auditory nerve and intact auditory neurotransmission. In addition these experiments support the view that the ESA represents summed spontaneous neural activity in the cochlea and provide a platform for studies of the influence of ototoxic compounds on the spontaneous neural outflow of the cochlea as a model of tinnitus.
Searchfield
G D
GD
Discipline of Audiology and Division of Physiology, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, New Zealand. g.searchfield@auckland.ac.nz
Muñoz
D J B
DJ
Thorne
P R
PR
D000161:Acoustic Stimulation; D000255:Adenosine Triphosphate / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D003056:Cochlear Nerve / Q000187:drug effects / Q000502:physiology*; D004195:Disease Models, Animal; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D006168:Guinea Pigs; D006801:Humans; D008297:Male; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology; D058910:Purinergic P2 Receptor Agonists; D011810:Quinoxalines / Q000494:pharmacology; D058469:Receptors, Purinergic P2X; D026941:Sodium Channel Blockers / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects; D013779:Tetrodotoxin / Q000494:pharmacology; D014012:Tinnitus / Q000503:physiopathology
D018691:Excitatory Amino Acid Antagonists; D058910:Purinergic P2 Receptor Agonists; D011810:Quinoxalines; D058469:Receptors, Purinergic P2X; D026941:Sodium Channel Blockers; C022571:adenosine 5'-O-(3-thiotriphosphate); D013779:Tetrodotoxin; C056723:FG 9041; D005665:Furosemide; D000255:Adenosine Triphosphate