Prions

A neuronal isoform of the Aplysia CPEB has prion-like properties. Si, K. et al. Cell 115, 879–891 (2003)

A neuronal isoform of CPEB regulates local protein synthesis and stabilizes synapse-specific long-term facilitation in Aplysia. Si, K. et al. Cell 115, 893–904 (2003)

Prions are notorious for their role in the pathogenesis of spongiform encephalopathies, but it is unclear whether they play a part in normal neuronal function. In these two papers, Si et al. identify a neuronal isoform of the Aplysia cytoplasmic polyadenylation element binding protein (CPEB) that has prion-like properties and is required for long-term facilitation at the synapse. They found that CPEB contains a structural motif that, when expressed in yeast, can induce other CPEB molecules to adopt a prion-like conformation and form aggregates. CPEB was previously shown to stimulate local protein translation by activating dormant mRNAs, and the authors propose that synaptic activity promotes its conversion to a prion-like state, which enables it to activate local protein synthesis and also stably mark the synapse for future long-term changes in efficacy.

Neural development

Foxg1 suppresses early cortical cell fate. Hanashima, C. et al. Science 303, 56–59 (2004)

During development, neuronal progenitors give rise to specific types of neuron in a particular order. At later time points, they are unable to produce cell types that are characteristic of earlier developmental points. Hanashima et al. find that a transcription factor called Foxg1 is responsible for suppressing an early cell fate in cortical progenitors. In Foxg1-null mice, there is an excess of the earliest-born neuron — the Cajal–Retzius cell. Conditional inactivation of Foxg1 in cortical progenitors also enables them to produce Cajal–Retzius cells.

Behavioural neuroscience

Selective deficits in appetitive conditioning as a consequence of ethanol withdrawal. Ripley, T. L. et al. Eur. J. Neurosci. (in the press)

Chronic treatment with, and withdrawal from, ethanol is known to cause behavioural deficits that are similar in some respects to those produced by amygdala lesions. Ripley et al. investigated the effects of chronic ethanol treatment and withdrawal on behavioural tasks that are sensitive to lesions of specific nuclei within the amygdala. They found that conditioned reinforcement and reinforcer devaluation, which depend on the basolateral amygdala, were unaffected by ethanol withdrawal, but that Pavlovial-to-instrumental transfer, which depends on the central nucleus of the amygdala, was impaired. Chronic ethanol treatment and withdrawal therefore produces deficits that resemble those resulting from lesions of the central nucleus but not the basolateral amygdala.