Insulin facilitates synaptic transmission via gap junctions between fast-spiking interneurons in the rat insular cortex

Satoshi Kosukegawa, Yuka Nakaya, Satomi Kobayashi, Kohei Kitano, Sachie Matsumura, Shohei Ogisawa, Manabu Zama, Mitsuru Motoyoshi, Masayuki Kobayashi

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)


Purpose: Inhibitory synaptic currents from fast-spiking neurons (FSNs), a typical gamma-aminobutyric acid (GABA)ergic interneuron in the cerebral cortex, to pyramidal neurons are facilitated by insulin. FSNs frequently show electrical synapses to FSNs, however, the effect of insulin on these electrical synapses is unknown. The aim of this study was to evaluate effects of insulin on electrical synaptic potentials between FSNs. Methods: Electrical synaptic potentials via gap junctions between FSNs were recorded to examine how insulin modulates these potentials in the rat insular cortex (IC). Results: Bath application of insulin (10 nM), which increases the spike firing rate of pyramidal neurons and unitary inhibitory postsynaptic currents recorded from FSN to pyramidal neuron connections, slightly but significantly increased electrical synaptic currents. The mean ratio of electrical synapses, the coupling coefficient that is obtained by postsynaptic voltage responses divided by presynaptic voltage amplitude, was 8.3 ± 1.1% in control and 9.2 ± 1.1% (n = 14) during 10 nM insulin application. Input resistance and voltage responses to large hyperpolarizing currents (−140 pA) were not changed by insulin. Conclusion: These results suggest that insulin facilitates spike synchro-nization by increasing electrical synaptic currents via gap junctions of GABAergic FSNs in the IC.

Original languageEnglish
Pages (from-to)77-80
Number of pages4
JournalJournal of Oral Science
Issue number2
Publication statusPublished - Apr 2023


  • GABAergic neuron
  • coupling coefficient
  • electrical synapse
  • hormone
  • inhibitory neurons


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