The α₁-adrenergic receptor augments the activity of the L-type Ca²⁺ channel Ca_V1.2 through PKC and the tyrosine kinases Pyk2 and Src and thereby synaptic plasticity.

Group III metabotropic glutamate receptor inhibition facilitates synaptic plasticity in the plasticity-resistant synapses of hippocampal area CA2, a brain region critical for social memory.

Mouse models with specific presynaptic knockout demonstrate that Rim1α is subjected to threonine phosphorylation by a novel EPAC-PKCε module, which is essential to presynaptic transmitter release, required for the induction of presynaptic LTP, and critical for motor learning.

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).

A novel mechanism of local plasticity in the distal dendrites of hippocampal granule cells.

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.

At distal synapses onto hippocampal CA1 pyramidal neurons, synaptic plasticity is dependent on dendritically initiated sodium spikes, thus establishing a new role for voltage-gated sodium channels in the dendrites that may have important implications for how learning rules are implemented.

Lrp4 mutant mice display profound deficits in cognitive tasks that assess learning and memory with disruptions in the subcellular organization of synaptic inputs and synaptic plasticity in the hippocampus.

Despite being the key element of the classic model for excitatory synaptic plasticity, the cytoplasmic AMPA receptor C-tail is not required for hippocampal LTP.

Physiology studies demonstrate that CaMKII is a molecular storage device.