Biophysical mechanism for neural spiking dynamics
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Description
In the honey bee antennal lobe, uniglomerular projection neurons (uPNs) transiently spike to odor sensory stimuli with odor-specific response latencies, i.e., delays to first spike after odor
stimulation onset. Recent calcium imaging studies show that the spatio-temporal response profile of the activated uPNs are dynamic and changes as a result
of associative conditioning, facilitating odor-detection of learned odors.
Moreover, odor-representation in the antennal lobe undergo reward-mediated plasticity processes that increase response delay variations
in the activated ensemble of uniglomerular projection neurons. Octopamine is necessarily involved in these plasticity processes. Yet, the cellular mechanisms are not
well understood. I hypothesize that octopamine modulates cholinergic transmission to uPNs by triggering translation
and upregulation of nicotinic receptors, which are more permeable to calcium. Consequently, this increased calcium-influx signals transcription factors that upregulate potassium
channels in the dendritic cortex of glomeruli, similar to synaptic plasticity mechanisms recently
shown in various insect species. A biophysical model of the antennal lobe circuit is developed in order to test the hypothesis that increased potassium channel expression in uPNs mediate response delays to first
spike, dynamically tuning odor-representations to facilitate odor-detection of learned odors.
stimulation onset. Recent calcium imaging studies show that the spatio-temporal response profile of the activated uPNs are dynamic and changes as a result
of associative conditioning, facilitating odor-detection of learned odors.
Moreover, odor-representation in the antennal lobe undergo reward-mediated plasticity processes that increase response delay variations
in the activated ensemble of uniglomerular projection neurons. Octopamine is necessarily involved in these plasticity processes. Yet, the cellular mechanisms are not
well understood. I hypothesize that octopamine modulates cholinergic transmission to uPNs by triggering translation
and upregulation of nicotinic receptors, which are more permeable to calcium. Consequently, this increased calcium-influx signals transcription factors that upregulate potassium
channels in the dendritic cortex of glomeruli, similar to synaptic plasticity mechanisms recently
shown in various insect species. A biophysical model of the antennal lobe circuit is developed in order to test the hypothesis that increased potassium channel expression in uPNs mediate response delays to first
spike, dynamically tuning odor-representations to facilitate odor-detection of learned odors.