Andrew & Patrick’s Neuroblog

In a 2000 publication, Huh et al. (http://www.ncbi.nlm.nih.gov/pubmed/11118151) demonstrated a novel role for immune molecules (MHCI, major histocompatibility complex class I) in the nervous system. In mice lacking the proper molecules for stable cell surface expression of MHCI molecules, retinogeniculate refinement is incomplete, LTP is enhanced, and LTD is absent. This was the first demonstration that MHCI molecules are important for activity-dependent development and refinement of neural circuits, and in synaptic plasticity.

Syken et al. extends this work by identifying that PirB, an MHCI receptor in the immune system, is also a neuronal receptor. They lay the groundwork, showing that PirB is present at synapses and binds to neurons in an MHCI-level-dependent manner. In an ocular dominance plasticity assay, PirB-/- mice exhibit expanded OD columns relative to wildtype following monocular enucleation - this suggests that PirB, along with associated MHCI molecules, restricts the extent of plasticity and perhaps acts to stabilize circuit

• http://www.ncbi.nlm.nih.gov/pubmed/16917027

Much neuroscience research is dedicated to the question of speech and language in humans. But a more basic question is the evolutionary origin of the neural networks responsible for vocalizations in vertebrates. Many birds, mammals, amphibians, and fish produce vocal signals for territorial and courtship purposes. Humans and birds produce sound with a specialized organ (larynx in humans, syrinx in birds) to vibrate expelled air from the lungs. Fish do it differently, with a neural circuit that governs contraction of swim bladder muscles.

It’s tempting to think that these diverse vocalization may have evolved separately several times, but Bass et al., studying the vocal neurons of the highly vocal toadfish, showed that they are localized to a specific developmental compartment that is consistent with the placement in amphibians, mammals, and birds. They propose that all these vertebrates share a common ancestral neural circuit for vocalization, an amazing example of the conserved vertebrate body plan.

• http://www.sciencemag.org/cgi/content/abstract/321/5887/417

When we have a conversation, our brain needs to differentiate between self-produced speech and vocalization from the external environment and monitoring feedback from one’s own voice seems to be essential in doing so. Yet, when we’re speaking, our brains suppress signals from the auditory cortex. Johns Hopkins professor Xiaoqing Wang, who studies neural mechanisms underlying auditory communication and sound perception, is the senior author on a recent Nature paper investigating the effect of vocal feedback and cortical suppression in the sensitivity of auditory cortex neurons in marmoset monkeys.

With chronically implanted electrode arrays, the researchers recorded from single neurons during vocalizations self-induced by the monkeys and discovered cortical suppression increased neural sensitivity to vocal feedback. This enhanced self-monitoring of vocal feedback helps monkeys discriminate between sounds and play roles in effective vocal production and communication.

• http://www.nature.com/nature/journal/v453/n7198/full/nature06910.html

Rockefeller scientists led by Shai Shaham found C. elegans neurons survive in the absence of glia, albeit with highly abnormal morphologies. They observed in a recent Development paper that dendrites were severely shortened and axon guidance/branching were impaired, implicating glia in brain development.

GIia removal was performed by mutating mls-2 and vab-3, genes involved in glia differentiation and expression, or by using laser microbeams to ablate glial precursors. Crucially, C. elegans glia do not exhibit trophic support of neurons and resemble vertebrate glia both morphologically and functionally, making possible in vivo studies of neural-glial roles in both the development and function of the nervous system.

• http://www.ncbi.nlm.nih.gov/pubmed/18508862

John Ngai at Berkeley’s Helen Wills Neuroscience Institute recently reported in Neuron a role for insulin-like growth factor (Igf) in the neural development of olfaction – IGF was previously established mainly as a hormone that stimulated cell proliferation.

By studying Igf1 and Igf2 mutant mice, Ngai and colleagues in China and Columbia found the disruption of IGF signaling pathways during neural development disrupted the mirror symmetry of the olfactory bulb’s sensory innervation map. Furthermore, axons targeted for the lateral olfactory bulb were misrouted to ectopic sites, suggesting a role for Igf in axon guidance. Igf was also shown, through primary neuronal cultures, to be a chemoattractant for axon growth cones; this is a new role for Igf in development and is currently being investigated further.

For further reading, see:

• http://www.ncbi.nlm.nih.gov/pubmed/18367086