Inhibitory inputs modulate discharge rate within frequency receptive fields of anteroventral cochlear nucleus neurons.
1. The amino acid neurotransmitters gamma-aminobutyric acid (GABA) and glycine function as inhibitory neurotransmitters associated with nonprimary inputs onto spherical bushy and stellate cells, two principal cell types located in the anteroventral cochlear nucleus (AVCN). These neurons are characterized by primary-like (including phase-locked) and chopper temporal response patterns, respectively. 2. Inhibition directly adjacent to the excitatory response area has been hypothesized to sharpen or limit the breadth of the tonal frequency receptive field. This study was undertaken to test whether GABA and glycine circuits function primarily to sharpen the lateral edges of the tonal excitatory response area or to modulate discharge rate within central portions of the excitatory response area of AVCN neurons. 3. To test this, iontophoretic application of the glycineI antagonist, strychnine, or the GABAA antagonist, bicuculline, was used to block inhibitory inputs after obtaining control families of isointensity contours (response areas) from extracellularly recorded AVCN neurons. 4. Blockade of GABA and/or glycine inputs was found to increase discharge rate primarily within the excitatory response area of neurons displaying chopper and primary-like temporal responses with little or no change in bandwidth or in off-characteristic frequency (CF) discharge rate. 5. The principal sources of inhibitory inputs onto AVCN neurons are cells located in the dorsal cochlear nucleus and superior olivary complex, which appear to be tonotopically matched to their targets. In agreement with these morphological studies, the data presented in this paper suggest that most GABA and/or glycine inhibition is tonotopically aligned with excitatory inputs. 6. These findings support models that suggest that GABA and/or glycine inputs onto AVCN neurons are involved in circuits that adjust gain to enable the detection of signals in noise by enhancing signal relative to background.
Caspary
D M
DM
Southern Illinois University School of Medicine, Department of Pharmacology, Springfield 62794-9230.
Backoff
P M
PM
Finlayson
P G
PG
Palombi
P S
PS
D000818:Animals; D001288:Attention / Q000502:physiology; D001306:Auditory Pathways / Q000502:physiology; D001931:Brain Mapping; D002682:Chinchilla; D003056:Cochlear Nerve / Q000502:physiology; D017626:Cochlear Nucleus / Q000502:physiology*; D005072:Evoked Potentials, Auditory / Q000502:physiology; D005998:Glycine / Q000502:physiology*; D009415:Nerve Net / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology*; D010898:Pitch Perception / Q000502:physiology*; D013018:Sound Spectrography; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D005680:gamma-Aminobutyric Acid; D005998:Glycine