GABAA receptor antagonist bicuculline alters response properties of posteroventral cochlear nucleus neurons

Abstract

1. The role of GABAergic inhibitory inputs onto posteroventral cochlear nucleus (PVCN) neurons in the anesthetized chinchilla was investigated through iontophoretic application of the GABAA receptor agonist muscimol and the GABAA receptor antagonist bicuculline. The majority of the neurons studied displayed phasic temporal response patterns. 2. All the neurons were sensitive to bicuculline and displayed an increase in discharge rate, which was greatest during the post-onset portion of the response. Most of the tested neurons were also sensitive to muscimol, which appeared to mimic the putative effect of endogenous GABA. 3. Bicuculline reduced the average first-spike latency and the average variability of the first-spike latency. Muscimol had the opposite effect. 4. Bicuculline did not significantly alter the threshold but rather increased discharge rate at suprathreshold intensities. 5. The width of the excitatory response area was not significantly increased by application of bicuculline. The increase in discharge rate occurred within the units' excitatory response areas. 6. The shape of the rate-intensity functions was not altered by bicuculline application. 7. We conclude that GABAergic inhibitory inputs control the post-onset discharge rate of some PVCN neurons. They may suppress tonic activity, resulting in more phasic discharge patterns.

Spectral integration in auditory cortex: Mechanisms and modulation

“…Moreover, there is some evidence that spectral integration in ACx is more extensive than in subcortical auditory regions. For example, whereas blockade of local inhibition in ACx expands frequency receptive Welds (see above), similar manipulations in the cochlear nucleus or inferior colliculus produce lesser or no expansion (Caspary et al, 1994;LeBeau et al, 2001;Palombi and Caspary, 1992). However, this result may only indicate that cortical and subcortical receptive Welds are not similarly regulated by inhibition; direct measurement of subthreshold receptive Welds at cortical and subcortical levels (in particular, at the thalamic level) will be needed to resolve this issue fully.…”

GABA- and glycine-immunoreactive projections from the superior olivary complex to the cochlear nucleus in guinea pig

“…For example, Evans and Zhao (1993) have shown that side-band inhibition, important for spectral contrasts and dynamic range, is probably mediated by glycine in the DCN. Glycine affects the ongoing discharge rates within the excitatory response areas of many neuronal types in the ventral CN, including PVCN phasic-firing neurons and AVCN neurons with chopper and primarylike response patterns (Palombi and Caspary, 1992;Caspary et al, 1993Caspary et al, , 1994. This has been hypothesized to act either to control dynamic range and/or detection of signals in noise.…”

“…Intracellular recordings have shown inhibitory potentials in response to tones and auditory nerve stimulation Rhode 1987, 1989;Wickesberg and Oertel, 1990;Feng et al, 1994). Pharmacological manipulations also reveal ongoing inhibitory effects on the responses of cells in the CN (Palombi and Caspary, 1992;Caspary et al, 1993Caspary et al, , 1994. Inhibitory effects on some cell types in the dorsal cochlear nucleus (DCN) are evoked by contralateral acoustic stimulation (Young and Brownell, 1976).…”

Morphology and spatial distribution of GABAergic neurons in cat primary auditory cortex (AI)

“…These include, but are not limited to, rate-level functions and aurality (Pollak and Park, 19931, interaural frequency-intensity disparities (Park and Pollak, 19931, frequency modulation (Mendelson, 1992), echo suppression (Wickesberg and Oertel, 19901, and disinhibition (Adams and Mugnaini, 1990), to name just a few. Not all aspects of receptive field fine structure, however, at least in the auditory hindbrain, are under GABAergic modulation (Palombi and Caspary, 1992). In other instances it has proved difficult to define precisely the interlaminar substrates for phenomena such as end inhibition, despite the readily demonstrable pathways that might subserve it (Grieve and Sillito, 1991).…”