Varieties of inhibition in the processing and control of processing in the mammalian cochlear nucleus.
Seven-barrel micropipettes were used to apply drugs microiontophoretically to single units in the dorsal cochlear nucleus (DCN) in chloralose-anaesthetised guinea-pigs. While both agonists and antagonists of putative neurotransmitters in the cochlear nucleus have been investigated in these experiments, the main thrust has been to explore the influence of specific antagonists on cells' spectral and temporal properties, thus elucidating the effects of naturally occurring inhibitory transmitters. At least five types of inhibition appear to be pharmacologically/physiologically separable: (1) Stimulus-evoked tonic "lateral/sideband" inhibition: glycinergic; (blocked by strychnine); responsible for the lateral inhibition of dorsal cochlear nucleus (DCN) type III and IV cells. Strychnine has its predominant effect on sustained (lateral) inhibition compared with the more transient forms of inhibition. Subtraction of receptive field maps enables us to visualise the extent of the inhibitory receptive field. It extends virtually throughout the unit's response field for both these classes but is generally, especially in type IV cells, maximal at the characteristic frequency (CF). This type of inhibition will primarily be responsible for enhancing spectral contrasts in the way that, in the visual system, surround inhibition enhances visual contrast. Furthermore, lateral inhibitory sidebands can "bias" the "working point" of a cell's response so that the dynamic range of effective stimuli and response can be extended. (2) "Background" tonic inhibition: GABAAergic; (blocked by bicuculline). Blocking this inhibition generally results in an increase in the background (i.e., spontaneous) activity. This inhibition is probably responsible for adjusting excitatory-inhibitory contrasts in both spectral and temporal domains. (3) Stimulus-related off-inhibition appears to be neither glycinergic nor GABAAergic. Blocking these receptors actually enhances off-inhibition. Nicotinic cholinergic blockers may have a small effect on off-inhibition, but so far we have not been able to block it entirely. This off-inhibition is important for enhancing temporal contrast. This inhibition must, therefore, be mediated by other transmitters, yet undetermined, or by a local feedback circuit or, less likely, be a membrane-based after-effect of stimulation. (4) Pre-synaptic inhibition, mediated by GABAB receptors presumed to act on primary afferent terminals, thus controlling afferent input to DCN principal cells. (5) Short-latency contralateral inhibition, mediated by glycine.
Evans
E F
EF
Department of Communication and Neuroscience, University of Keele, Staffs., U.K.
Zhao
W
W
D000818:Animals; D017626:Cochlear Nucleus / Q000502:physiology*; D005998:Glycine / Q000378:metabolism; D006168:Guinea Pigs; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism / Q000494:pharmacology*; D018733:Nicotinic Antagonists; D011978:Receptors, Nicotinic / Q000502:physiology; D013331:Strychnine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018377:Neurotransmitter Agents; D018733:Nicotinic Antagonists; D011978:Receptors, Nicotinic; D005680:gamma-Aminobutyric Acid; D013331:Strychnine; D005998:Glycine