Comparison of Transmission at Synapses of Layers 2/3 Input onto Layer 5 Pyramidal and GABAergic Neurons in Rostral Agranular Insular Cortex
Date Issued
2016
Date
2016
Author(s)
Chang, Ting-Hsuan Daniel
Abstract
It has been shown that inhibition or lesion of the rostral agranular insular cortex (RAIC) results in analgesia, it suggests that RAIC tonically produces hyperalgesia signal. RAIC is a cortical area where nociceptive output originates, and it has been reported to activate in chronic pain perception. It’s believed that chronic pain is associated with the long-term change in synaptic plasticity. Moreover, the imbalance of excitatory and inhibitory (E/I) synaptic signaling in neural circuits is responsible to modulate synaptic plasticity in certain behavior disorders. In our lab, previous study had reported that the induction of chronic pain induced differential activation in pyramidal cells and GABAergic neurons in RAIC. We propose here that E/I imbalance in RAIC may contribute to the increased cortical output of nociceptive signal in chronic pain. To test this possibility, we compared synaptic transmission of layers 2/3 (L2/3) inputs onto layer 5 (L5) pyramidal cells (PC), which are the descending projection neurons, and onto local GABAergic interneurons (IntN) in RAIC. We performed dual-patch recording from a paired IntN-PC in layer 5, and elicited EPSC by putting an electrode in layer 2/3. We found functional connectivity in 34.2% of all recorded IntN-PC pairs. There was no significant difference in data sampled from IntN-PC pairs with and without functional connectivity, and all data were pooled. Our data showed no significant difference in paring-pulse ratio between transmission at L2/3-PC synapses and at L2/3-IntN synapses. L2/3-IntN seemed to have higher releasing probability than L2/3-PC synapse in quantum study. The ratio of NMDA and non-NMDA EPSCs component was larger at L2/3-PC synapses than at L2/3-IntN synapses. Furthermore, the rising and decay of EPSCs were much faster at L2/3-IntN synapse than at L2/3-PC synapse. We further examined the modulation of pERK on IntN-PC pairs by applying PKC activator Phorbol 12,13- diacetate (PDA). PDA enhanced the postsynaptic currents at L2/3-PC synapses and L2/3- IntN synapses. The further issue of chronic pain model is under studying.
Subjects
rostral agranular insular cortex (RAIC)
E-I ratio
pain
pERK
whole-cell patch clamp
Type
thesis
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