My Ph.D. work with Eric Young ( and Paul Manis at JHU focussed on understanding the Dorsal Cochlear Nucleus (DCN, review). The DCN is one of the first central stations in the ascending auditory pathway and receives direct input from the cochlea. The DCN is very special in that it also receives non-auditory inputs. I performed both in vivo and in vitro studies revealing the origin of the somatosensory input and the specific cellular specializations in the DCN that enabled somatosensory-auditory integration.

Pioneering studies by Dr. Young had shown that the DCN receives input from the medullary somatosensory nuclei (esp. the cuneate and spinal triageminal nucleus) but it was unknown where in the periphery these inputs originated and what information they were conveying. I showed that the cervical nerve C2 and the mandibular branch of the spinal trigeminal nerve provided the dominant input to the DCN. Moreover, I found that these inputs conveyed proprioceptive information from the muscles moving the ear (this was in cats which can move their ears). In other experiments I showed that stimulating the somatosensory input could lead to altered auditory responses in the DCN, even if the somatosensory input came quite a bit before the sound. Thus there was some kind of memory in the system. This work has been replicated in other species and pairing somatosensory and sound stimulation has led to the design of devices to reduce tinnitus (see here and here).

My work with Dr. Manis focussed on understanding how DCN pyramidal cells worked. I found experimentally using patch clamp recordings that these cells have certain inactivating potassium channels that enabled them to have interesting firing patterns and validated this with a computational model. I also showed that these channels enabled DCN pyramidal cells to encode both excitatory and inhibitory inputs in their spiking patterns and esp. inhibitory inputs that occurred before excitation. Thus, these channels enable a form of cellular memory.