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We suggest presynaptic inhibition as a candidate that rapidly provides stability by compensating recurrent excitation induced by Hebbian changes. Computational work suggests that in recurrent networks, the homeostatic mechanisms observed in experiments are too slow to compensate instabilities arising from Hebbian plasticity and need to be complemented by rapid compensatory processes. Because this constitutes an unstable positive feedback loop, it requires additional homeostatic control. Hebbian plasticity, a mechanism believed to be the substrate of learning and memory, detects and further enhances correlated neural activity. Overall, our results reveal a novel mechanism that SOM‐INs activation‐induced synaptic depression is partially mediated by the activation of astrocytic GABABRs. In turn, adenosine inhibits excitatory synaptic transmission by activating presynaptic adenosine A1 receptors (A1Rs). SOM‐INs depress excitatory neurotransmission by activating presynaptic GABABRs and astrocytic GABABRs, the latter inducing the release of ATP/adenosine. We found that optogenetic stimulation of SOM‐INs increases astrocyte Ca2+ signaling via the activation of astrocytic GABABRs and GAT‐3. To address this issue, we combined whole‐cell recordings, optogenetics, calcium imaging, and pharmacological approaches to specifically activate hippocampal somatostatin‐expressing interneurons (SOM‐INs), a type of interneuron that targets pyramidal cell dendrites, while monitoring excitatory synaptic transmission in CA1 pyramidal cells. However, little is known about whether astrocytic GABABRs regulate excitatory synaptic transmission mediated by GABAergic network activity. It is well documented that astrocytes express GABABRs and respond to GABAergic network activity. Extensive studies have corroborated that GABAergic network activity regulates excitatory synaptic networks by activating presynaptic GABAB receptors (GABABRs). GABAergic network activity has been established to be involved in numerous physiological processes and pathological conditions.

Because Sst interneuron activity has been shown to be regulated by sensory and motor input, these results suggest a mechanism by which functional connectivity and synaptic plasticity could be gated in a state-dependent manner.Ĭopyright © 2015 Elsevier Ltd. This is an unanticipated role for Sst interneurons, which have been assigned a role only in fast GABAa-mediated inhibition.

These data indicate that Sst interneurons can rapidly and reversibly silence excitatory synaptic connections through the regulation of presynaptic release. Optogenetic suppression of Sst neuron firing was sufficient to enhance EPSP amplitude and reduce failure rates, effects that were fully reversible and occluded by GABAb antagonists. This suppression is mediated by tonic activation of presynaptic GABAb receptors gated by the spontaneous activity of somatostatin-expressing (Sst) interneurons. Paired-cell recordings from pyramidal neurons in acute brain slices of mouse somatosensory cortex show that excitatory synaptic transmission is markedly suppressed during spontaneous network activity: EPSP amplitudes are 2-fold smaller and failure rates are greater than 50%. The range of synaptic function in the presence of inhibitory and excitatory activity within the neocortical circuit is unknown. Excitatory synaptic transmission is typically studied under optimized conditions, when background activity in the network is low. Understanding the dynamic range for excitatory transmission is a critical component of building a functional circuit diagram for the mammalian brain.

Expectations multipatch receiving blanket