Induction of LTP mechanisms in dually innervated dendritic spines.

Dendritic spines are the postsynaptic compartments of excitatory synapses, however, a substantial subset of spines additionally receives inhibitory input. In such dually innervated spines (DiSs), excitatory long-term potentiation (LTP) mechanisms are suppressed, but can be enabled by blocking tonic inhibitory GABA receptor signaling. Here we show that LTP mechanisms at DiSs are also enabled by two other excitatory LTP stimuli.

LTP induction by structural rather than enzymatic functions of CaMKII.

Learning and memory are thought to require hippocampal long-term potentiation (LTP), and one of the few central dogmas of molecular neuroscience that has stood undisputed for more than three decades is that LTP induction requires enzymatic activity of the Ca/calmodulin-dependent protein kinase II (CaMKII). However, as we delineate here, the experimental evidence is surprisingly far from conclusive. All previous interventions inhibiting enzymatic CaMKII activity and LTP also interfere with structural CaMKII roles, in particular binding to the NMDA-type glutamate receptor subunit GluN2B.

Tumor talk: A descriptive study of communication about tumor board meetings.

Tumor board meetings are behind-the-scenes settings where communication about health and strategizing about healthcare delivery take place. Despite their wide use in hospitals and cancer centers, there is a dearth of information about the communication practices in this context. Drawing upon six weeks of observations, this study investigated communication during tumor board meetings at a tertiary cancer center in the Southeastern United States.

Distinct synaptic pools of DAPK1 differentially regulate activity-dependent synaptic CaMKII accumulation.

The death-associated protein kinase 1 (DAPK1) regulates the synaptic movement of the Ca/calmodulin (CaM)-dependent protein kinase II (CaMKII). Synaptic CaMKII accumulation is mediated via binding to the NMDA-receptor subunit GluN2B and is required for long-term potentiation (LTP). By contrast, long-term depression (LTD) instead requires specific suppression of this movement, which is mediated by competitive DAPK1 binding to GluN2B.