Abstract
The insular cortex plays pivotal roles in taste learning. As cellular mechanisms of taste learning, long-term potentiation (LTP) at glutamatergic synapses is well studied. However, little is known about long-term changes of synaptic efficacy at GABAergic synapses in the insular cortex. Here, we examined the synaptic mechanisms of long-term plasticity at GABAergic synapses in layer V pyramidal neurons of the mouse insular cortex. In response to a prolonged high-frequency stimulation (HFS), GABAergic synapses displayed endocannabinod (eCB)-mediated long-term depression (LTDGABA). When cannabinoid 1 receptors (CB1Rs) were blocked by a CB1R antagonist, the same stimuli caused LTP at GABAergic synapses (LTPGABA) which was mediated by production of nitric oxide (NO) via activation of NMDA receptors. Intriguingly, NO signaling was necessary for the induction of LTDGABA. In the presence of leptin which blocks CB1 signaling, the prolonged HFS caused LTPGABA which was mediated by NO signaling. These results indicate that long-term plasticity at GABAergic synapses in the insular cortex can be modulated by combined effects of eCB and NO signaling. These forms of GABAergic synaptic plasticity in the insular cortex may be crucial synaptic mechanisms in taste learning.
Highlights
The insular cortex plays pivotal roles in taste learning
We examined whether evoked postsynaptic currents are solely mediated by GABAergic inputs onto layer V pyramidal neurons
The prolonged high-frequency stimulation (HFS) induced long-term depression (LTD) of GABAergic synapses (LTDGABA) in layer V pyramidal neurons of the insular cortex (72 ± 5% of baseline responses, n = 13; paired t-test: t(12) = −5.03, p < 0.001) (Fig. 1,d and 2f)
Summary
The insular cortex plays pivotal roles in taste learning. As cellular mechanisms of taste learning, long-term potentiation (LTP) at glutamatergic synapses is well studied. We examined the synaptic mechanisms of long-term plasticity at GABAergic synapses in layer V pyramidal neurons of the mouse insular cortex. In the presence of leptin which blocks CB1 signaling, the prolonged HFS caused LTPGABA which was mediated by NO signaling These results indicate that long-term plasticity at GABAergic synapses in the insular cortex can be modulated by combined effects of eCB and NO signaling. These forms of GABAergic synaptic plasticity in the insular cortex may be crucial synaptic mechanisms in taste learning. In the presence of leptin which blocks eCB signaling, the prolonged HFS causes LTPGABA
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