CB₁-receptor-mediated inhibitory long-term depression (LTD) relies on both protein synthesis and ubiquitination to elicit structural changes that underlie long-term reduction of GABA release.

Electrophysiological and optical analysis of neurotransmitter release at central synapses reveals that glutamate signalling is not required for the long-term potentiation (LTP) of presynaptic function, and instead only promotes presynaptic long-term depression (LTD).

Vulnerability to cocaine addiction during adolescence depends on translational control.

Non-invasive optogenetic induction of synaptic plasticity revealed that long-term potentiation and long-term depression alter the chances of a synapse to survive the next seven days.

Motor training decreased the unit synaptic response and suppressed induction of long-term depression at parallel fiber to Purkinje cell synapses in the cerebellum, supporting involvement of long-term depression in motor learning.

There are at least two separate pathways for AMPA receptor recycling, which are regulated by synaptic activity.

Taking advantage of awell-established learning paradigm, conditioned taste aversion (CTA), change of hedonic value of a palatable tastant revealed the neural mechanisms encoding this learning process.

Behavioral and pharmaceutical interventions reverse defects associated with increased cerebellar long-term depression in a mouse model of Fragile X syndrome.

The molecular mechanisms beyond the bidirectionality (tTLP and tLTD) of endocanabinoid spike-timing dependent synaptic plasticity have been identified.

Patients with DYT1 dystonia show aberrant risk-aversion in a simple decision-making task, in accordance with predictions of a reinforcement learning model of corticostriatal trial-and-error learning.