# Postsynaptic spiking determines anti-Hebbian LTD in visual cortex basket cells

## TL;DR

The study shows that postsynaptic spiking in visual cortex basket cells influences anti-Hebbian long-term depression at specific synapses.

## Contribution

The paper reveals that postsynaptic spiking drives anti-Hebbian LTD in PC→BC synapses of the visual cortex.

## Key findings

- Postsynaptic APs cause supralinear Ca2+ responses in BC dendrites for pre-before-postsynaptic pairing.
- Pre-before-postsynaptic pairing leads to anti-Hebbian LTD at PC→BC synapses.
- Dendritic Ca2+ nonlinearities and plasticity are modulated by somatic spiking in V1 BCs.

## Abstract

Long-term plasticity at pyramidal cell to basket cell (PC → BC) synapses is important for the functioning of cortical microcircuits. It is well known that at neocortical PC → PC synapses, dendritic calcium (Ca2+) dynamics signal coincident pre-and postsynaptic spiking which in turn triggers long-term potentiation (LTP). However, the link between dendritic Ca2+ dynamics and long-term plasticity at PC → BC synapses of primary visual cortex (V1) is not as well known. Here, we explored if PC → BC synaptic plasticity in developing V1 is sensitive to postsynaptic spiking. Two-photon (2P) Ca2+ imaging revealed that action potentials (APs) in dendrites of V1 layer-5 (L5) BCs back-propagated decrementally but actively to the location of PC → BC putative synaptic contacts. Pairing excitatory inputs with postsynaptic APs elicited dendritic Ca2+ supralinearities for pre-before-postsynaptic but not post-before-presynaptic temporal ordering, suggesting that APs could impact synaptic plasticity. In agreement, extracellular stimulation as well as high-throughput 2P optogenetic mapping of plasticity both revealed that pre-before-postsynaptic but not post-before-presynaptic pairing resulted in anti-Hebbian long-term depression (LTD). Our results demonstrate that V1 BC dendritic Ca2+ nonlinearities and synaptic plasticity at PC → BC connections are both sensitive to somatic spiking.