Nucleolar integrity is required for the maintenance of long-term synaptic plasticity.

Long-term memory (LTM) formation requires new protein synthesis and new gene expression. Based on our work in Aplysia, we hypothesized that the rRNA genes, stimulation-dependent targets of the enzyme Poly(ADP-ribose) polymerase-1 (PARP-1), are primary effectors of the activity-dependent changes in synaptic function that maintain synaptic plasticity and memory. Using electrophysiology, immunohistochemistry, pharmacology and molecular biology techniques, we show here, for the first time, that the maintenance of forskolin-induced late-phase long-term potentiation (L-LTP) in mouse hippocampal slices requires nucleolar integrity and the expression of new rRNAs.

An in vitro model to study brain tissue recovery.

Brain tissue slices can be maintained within metabolically stable conditions for long periods of time (hours). This experimental setting has been productive for investigating long-term neural function in vitro. Here, we utilize this experimental approach to describe the recovery of functional connectivity in slices from the mouse hippocampus.

Synaptic instability in a neuronal population as an element of encoding information.

An unexpected and novel finding is described and discussed here concerning the synaptic physiology of hippocampal slices during the period of recovery after brain dissection. Contrary to the common notion that the amplitude of synaptic responses recovers in a single exponential rising fashion, we found that synaptic response amplitude displayed an oscillatory pattern. The period of oscillation was of 6h and its frequency depended on the input frequency of stimulation.