Somatosensory effects on neurons in dorsal cochlear nucleus.
1. Single units and evoked potentials were recorded in dorsal cochlear nucleus (DCN) in response to electrical stimulation of the somatosensory dorsal column and spinal trigeminal nuclei (together called MSN for medullary somatosensory nuclei) and for tactile somatosensory stimuli. Recordings were from paralyzed decerebrate cats. 2. DCN principal cells (type IV units) were strongly inhibited by electrical stimulation (single 50-microA bipolar pulse) in MSN or by somatosensory stimulation. Units recorded in the fusiform cell and deep layers of DCN were inhibited, suggesting that the inhibition affects both types of principal cells (i.e., both fusiform and giant cells). 3. Interneurons (type II units) that inhibit principal cells were only weakly inhibited by electrical stimulation and were never excited, demonstrating that the inhibitory effect on principal cells does not pass through the type II circuit. In the vicinity of the DCN/PVCN (posteroventral cochlear nucleus) boundary, units were encountered that were excited by electrical stimulation in MSN; some of these neurons responded to sound, and some did not. Their response properties are consistent with the hypothesis that they are deep-layer inhibitory interneurons conveying somatosensory information to the DCN. 4. Analysis of the evoked potentials produced by electrical stimulation in MSN suggests that the somatosensory inputs activate the granule cell system of the DCN molecular layer. A model based on previous work by Klee and Rall was used to show that the distribution of evoked potentials in DCN can be explained as resulting from radial currents produced in the DCN molecular and fusiform-cell layers by synchronous activation of granule cells inputs to fusiform and cartwheel cells. Current-source density analysis of the evoked potentials is consistent with this model. Thus molecular layer interneurons (cartwheel and stellate cells) are a second possible source of inhibition to principal cells. 5. With lower stimulus levels (20 microA) and pulse-pair stimuli (50- to 100-ms interstimulus interval), three components of the inhibitory response can be recognized in both fusiform cell layer and deep layer type IV units: a short-latency inhibition that begins before the start of the evoked potential; a longer-latency inhibition whose timing corresponds to the evoked potential; and an excitatory component that occurs on the rising phase of the evoked potential. The excitatory component is usually overwhelmed by the inhibitory components and could be derived from granule cell inputs; the long-latency inhibitory component could be derived from cartwheel cells or the hypothesized deep-layer inhibitory interneurons.(ABSTRACT TRUNCATED AT 400 WORDS)
Young
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Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland 21205, USA.
Nelken
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Conley
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D000818:Animals; D002415:Cats; D017626:Cochlear Nucleus / Q000166:cytology / Q000502:physiology*; D004558:Electric Stimulation; D005071:Evoked Potentials; D008959:Models, Neurological; D009433:Neural Inhibition; D009474:Neurons / Q000502:physiology*; D010812:Physical Stimulation; D011930:Reaction Time; D012677:Sensation / Q000502:physiology*; D013116:Spinal Cord / Q000502:physiology*; D014110:Touch / Q000502:physiology; D014279:Trigeminal Nucleus, Spinal / Q000502:physiology*