Circuit firing homeostasis following synaptic perturbation ensures robust behavior

Abstract

AbstractHomeostatic regulation of excitability and synaptic transmission ensures stable neural circuit output under changing conditions. We find that pre- or postsynaptic weakening of motor neuron (MN) to muscle glutamatergic transmission inDrosophilalarva has little impact on locomotion, suggesting non-synaptic compensatory mechanisms.In vivoimaging of MN to muscle synaptic transmission and MN activity both show that synaptic weakeningincreasesactivity in tonic type Ib MNs, but not in the phasic type Is MN that innervate the same muscles. Additionally, an inhibitory class of pre-MNs that innervates type Ib—but not Is—MNsdecreasesactivity. Our experiments suggest that weakening of MN evoked synaptic release onto the muscle is compensated for by an increase in MN firing due to a combined cell-autonomous increase in excitability and decreased inhibitory central drive. Selectivity for type Ib MNs may serve to restore tonic drive while absence of firing adjustment in the convergent Is MN can maintain the contraction wave dynamics needed for locomotion.