Topic: short-term depression

One of the most fundamental tenets in neuroscience is that information is stored in the strength of synapses, and that learning relies on changes in synaptic strength. Here we aim to extend this tenet into the temporal domain by proposing that synapses not only learn to strengthen or weaken, but can learn when to be weak or strong on the subsecond scale. It has been known for more than half a century that synapses exhibit short-term synaptic plasticity (STP): a form of presynaptic, use-dependent, plasticity in which consecutive spikes can elicit progressively depressing (short-term depression/

Glycinergic synapses between the medial nucleus of the trapezoid body (MNTB) and the lateral superior olive (LSO) are involved in sound source localization. These synapses can reliably transmit inhibitory signals, even during minutes of high-frequency activation. Glycine transporter 2 (GlyT2) is involved in glycine reuptake from the synaptic cleft into MNTB axon terminals. Loss of GlyT2 reduces the synaptic transmission but does not lead to a complete failure (Brill et al 2021). The resilience suggests the presence of another glycine source. Here we investigated the contribution of Asc1, a hig

Striatal dopamine (DA) and acetylcholine (ACh) play key roles in reward prediction signalling and goal-directed behaviour. Midbrain DA neurons increase their firing in response to unexpected rewards or reward-predicting cues, while striatal cholinergic interneurons exhibit coincident burst-pause activity. Striatal DA and ACh also reciprocally regulate each other’s release with ACh modulating DA release through axonal nicotinic acetylcholine receptors (nAChRs). Activation of nAChRs can drive DA release but also generate strong short-term depression (STD) of subsequent DA release, not arising fr

Short-term plasticity (STP) is the neuronal substrate for modification of the efficiency of synaptic transmission in the timescale of milliseconds to seconds. STP renders synapses the ability to process and integrate inputs which in-turn controls information flow and processing in networks. Our work explored the diversity in STP of hippocampal CA1 synapses and the summation of multiple inputs during STP in a CA1 neuron with balanced excitation and inhibition. We performed invitro experiments on the CA3-CA1 network in acute hippocampal slices from mice expressing channelrhodopsin specifically i