RT Journal Article
SR Electronic
T1 Thalamic Burst Firing Propensity: A Comparison of the Dorsal Lateral Geniculate and Pulvinar Nuclei in the Tree Shrew
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 17287
OP 17299
DO 10.1523/JNEUROSCI.6431-10.2011
VO 31
IS 47
A1 Haiyang Wei
A1 Maxime Bonjean
A1 Heywood M. Petry
A1 Terrence J. Sejnowski
A1 Martha E. Bickford
YR 2011
UL http://www.jneurosci.org/content/31/47/17287.abstract
AB Relay neurons in dorsal thalamic nuclei can fire high-frequency bursts of action potentials that ride the crest of voltage-dependent transient (T-type) calcium currents [low-threshold spike (LTS)]. To explore potential nucleus-specific burst features, we compared the membrane properties of dorsal lateral geniculate nucleus (dLGN) and pulvinar nucleus relay neurons using in vitro whole-cell recording in juvenile and adult tree shrew (Tupaia) tissue slices. We injected current ramps of variable slope into neurons that were sufficiently hyperpolarized to de-inactivate T-type calcium channels. In a small percentage of juvenile pulvinar and dLGN neurons, an LTS could not be evoked. In the remaining juvenile neurons and in all adult dLGN neurons, a single LTS could be evoked by current ramps. However, in the adult pulvinar, current ramps evoked multiple LTSs in >70% of recorded neurons. Using immunohistochemistry, Western blot techniques, unbiased stereology, and confocal and electron microscopy, we found that pulvinar neurons expressed more T-type calcium channels (Cav 3.2) and more small conductance potassium channels (SK2) than dLGN neurons and that the pulvinar nucleus contained a higher glia-to-neuron ratio than the dLGN. Hodgkin–Huxley-type compartmental models revealed that the distinct firing modes could be replicated by manipulating T-type calcium and SK2 channel density, distribution, and kinetics. The intrinsic properties of pulvinar neurons that promote burst firing in the adult may be relevant to the treatment of conditions that involve the adult onset of aberrant thalamocortical interactions.