Development

The boundary cap: a source of neural crest stem cells that generate multiple sensory neuron subtypes. Hjerling-Leffler, J. et al. Development 132, 2623–2632 (2005)

The boundary cap is a group of neural crest-derived cells that gives rise to neurons and glia in the dorsal root ganglion. Ernfors and colleagues have now shown that these cells can self-renew and that their fate as neurons or glia depends on the stage of embryonic development. After neuronal differentiation, single boundary cap stem cells can spontaneously generate various subtypes of nociceptive and thermoreceptive neuron that are present only in the spinal and cranial nerve ganglia. These findings identify boundary cap cells as a source of truly multipotent neural crest stem cells that can give rise to several subtypes of functional peripheral sensory neuron.

Sleep

The neural substrates of infant sleep in rats. Karlsson, K. Æ. et al. PLoS Biol. 3, 891–901 (2005)

Unlike adults, sleeping infants do not show clear state-dependent changes in cortical electroencephalographic activity. This has led to proposals that sleep in infants is more primitive than adult sleep, and that it depends on diffuse activation in the CNS rather than the more specific circuits that mediate adult sleep. However, Karlsson and colleagues have now shown that sleep in infant rats is characterized by periods of muscle atonia and myoclonic twitching that resemble those seen during adult sleep, and that the medullary inhibitory area that is required for the expression of atonia is part of a circuit that includes the subcoeruleus, pontis oralis and dorsolateral pontine tegmentum. Neurons in these areas show patterns of state-dependent activity that are similar to the neural basis of sleep in adults.

Neurotransmitter receptors

G protein-dependent presynaptic inhibition mediated by AMPA receptors at the calyx of Held. Takago, H. et al. Proc. Natl Acad. Sci. USA 102, 7368–7373 (2005)

AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)-type glutamate receptors (AMPARs) mediate ionotropic excitatory synaptic transmission in the mammalian CNS. However, these receptors can also interact with secondary messenger signalling pathways in neurons. Takago and colleagues use patch-clamp recordings at the giant nerve terminal of the calyx of Held to show that AMPARs are expressed presynaptically at this site and mediate metabotropic presynaptic inhibition by interacting with specific G proteins. The G-protein activation reduces glutamatergic transmission by inhibiting voltage-gated Ca2+ currents in the nerve terminal. AMPARs have also been reported to be expressed presynaptically at several other types of nerve terminal, and might, therefore, regulate presynaptic glutamate release at other sites.