Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability.

Weakening of synaptic transmission at the larval neuromuscular junction triggers two forms of homeostatic compensation, one that increases the probability of glutamate release per action potential () and another that increases motoneuron (MN) activity. We investigated the molecular changes in MNs that underlie the increase in MN activity. RNA sequencing (RNA-seq) analysis on MNs whose glutamate release is weakened by knockdown of components of the MN transmitter release machinery reveals a reduction in expression of a group of genes that encode potassium channels and their positive modulators.

Balanced synapse-to-synapse short-term plasticity ensures constant transmitter release.

Synaptic strength can vary greatly between synapses. Optical quantal analysis at Drosophila glutamatergic motor neuron synapses shows that short-term plasticity also varies greatly between synapses, even those made by an individual motor neuron. Strong and weak synapses are randomly distributed in the motor neuron nerve terminal, as are facilitating and depressing synapses.

Synapse-specific catecholaminergic modulation of neuronal glutamate release.

Norepinephrine in vertebrates and its invertebrate analog, octopamine, regulate the activity of neural circuits. We find that, when hungry, larvae switch activity in type II octopaminergic motor neurons (MNs) to high-frequency bursts, which coincide with locomotion-driving bursts in type I glutamatergic MNs that converge on the same muscles. Optical quantal analysis across hundreds of synapses simultaneously reveals that octopamine potentiates glutamate release by tonic type Ib MNs, but not phasic type Is MNs, and occurs via the G-coupled octopamine receptor (OAMB).

Synapse-to-synapse plasticity variability balanced to generate input-wide constancy of transmitter release.

Basal synaptic strength can vary greatly between synapses formed by an individual neuron because of diverse probabilities of action potential (AP) evoked transmitter release ( ). Optical quantal analysis on large numbers of identified larval glutamatergic synapses shows that short-term plasticity (STP) also varies greatly between synapses made by an individual type I motor neuron (MN) onto a single body wall muscle. Synapses with high and low and different forms and level of STP have a random spatial distribution in the MN nerve terminal, and ones with very different properties can be located within 200 nm of one other.

Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability.

Weakening of synaptic transmission at the Drosophila larval neuromuscular junction triggers two forms of homeostatic compensation, one that increases the probability of glutamate release per action potential (Pr) and another that increases motoneuron (MN) activity. We investigated the molecular changes in MNs that underlie the increase in MN activity. RNA-seq analysis on MNs whose glutamate release is weakened by knockdown of components of the MN transmitter release machinery reveals a reduction in expression of a group of genes that encode potassium channels and their positive modulators.