Michael S. Jones

Sensory-evoked high-frequency (γ-band) oscillating potentials in somatosensory cortex of the unanesthetized rat

A 64-channel epipial electrode array was used to investigate high-frequency (gamma-band) oscillations in somatosensory cortex of the unanesthetized and unrestrained rat. Oscillations were evoked by manual stimulation of the vibrissae and mystacial pad. Stimulation of the contralateral vibrissae resulted in a significant increase in gamma-power during 128-ms epochs taken just following stimulus onset compared to the prestimulus baseline. Stimulation of the ipsilateral vibrissae was completely ineffective in evoking gamma-oscillations in any animals. Sensory evoked gamma-oscillations were constrained to primary (SI) and secondary (SII) somatosensory cortex. When averaged to an arbitrary reference of peak times in one of the channels, these oscillations exhibited a systematic temporal organization, propagating from the rostral portion of SI to the barrel field proper, and finally to SII. These spatiotemporal characteristics were probably produced by intracortical pathways within rodent somatosensory cortex. The rostrocaudal propagation of gamma-oscillations within the barrel field may also reflect whisking patterns observed when the vibrissae are used as a sensory array, suggesting that synchronized gamma-oscillations may play a role in assembling punctate afferent information provided by the vibrissae into a coherent representation of a somatosensory stimulus.

Bilateral processing of vestibular responses revealed by injecting lidocaine into the eighth cranial nerve in vitro.

Extracellular unit responses were recorded from the vestibular nucleus (VN) and medial longitudinal fasciculus during horizontal head rotation of an in vitro turtle brainstem in which the temporal bones remained attached. Units were characterized as type I or type II based on the responses to ipsiversive or contraversive rotation, respectively. Lidocaine injections (0.5-2 microl of 0.5%) into the root of the eighth cranial nerve within the cranium caused rapid effects on unit responses to head rotation. Responses of type I units were reduced by ipsilateral injection but enhanced following contralateral injection. On the other hand, type II units had their responses increased by ipsilateral injections yet decreased by contralateral injections. In approximately half of the type II cells, decrease of the contraversive response was accompanied by the appearance of latent ipsiversive activity. Our findings not only confirm that each eighth nerve has afferents that drive ipsiversive excitation of both vestibular nuclei but also suggest that both nerves compete to dominate a central neurons vestibular response. These results may be inconsistent with the push-pull vestibular model in which each nerve drives the central neuron with a complementary response that enhances the vestibular output. An alternate model is described in which vestibular neurons receive bilateral excitation, and that excitatory input is antagonized by crossed inhibition during contraversive motion.