Author Correction: Sema7A/PlxnCl signaling triggers activity-dependent olfactory synapse formation.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Sema7A/PlxnCl signaling triggers activity-dependent olfactory synapse formation.

In mammals, neural circuits are formed based on a genetic program and further refined by neuronal activity during the neonatal period. We report that in the mouse olfactory system, the glomerular map is not merely refined but newly connected to second-order neurons by odorant-receptor-derived neuronal activity. Here, we analyzed a pair of molecules, Sema7A, expressed in olfactory sensory neurons (OSNs) in an activity-dependent manner, and PlxnC1, localized to dendrites of mitral/tufted (M/T) cells in the first week after birth.

Tbr2 deficiency in mitral and tufted cells disrupts excitatory-inhibitory balance of neural circuitry in the mouse olfactory bulb.

The olfactory bulb (OB) is the first relay station in the brain where odor information from the olfactory epithelium is integrated, processed through its intrinsic neural circuitry, and conveyed to higher olfactory centers. Compared with profound mechanistic insights into olfactory axon wiring from the nose to the OB, little is known about the molecular mechanisms underlying the formation of functional neural circuitry among various types of neurons inside the OB. T-box transcription factor Tbr2 is expressed in various types of glutamatergic excitatory neurons in the brain including the OB projection neurons, mitral and tufted cells.

5T4 glycoprotein regulates the sensory input-dependent development of a specific subtype of newborn interneurons in the mouse olfactory bulb.

Sensory input has been shown to regulate development in a variety of species and in various structures, including the retina, cortex, and olfactory bulb (OB). Within the mammalian OB specifically, the development of dendrites in mitral/tufted cells is well known to be odor-evoked activity dependent. However, little is known about the developmental role of sensory input in the other major OB population of the GABAgenic interneurons, such as granule cells and periglomerular cells.

Characterization of nestin expression in the spinal cord of GFP transgenic mice after peripheral nerve injury.

Many studies have shown that activation and increase in the number of astrocytes and microglia in the spinal cord participate in the initiation and maintenance of neuropathic pain, but little attention has been paid to the responses of neural progenitor cells to peripheral nerve injury. Nestin, a class VI intermediate filament protein, is expressed both in neuronal and glial progenitors as well as in their common precursors; and nestin-positive cells appear in the brain and spinal cord following various forms of damage to these regions. To clarify the responses of neural progenitor cells to nerve injury, we applied L5 spinal nerve transection (L5-SNT) to nestin-promoter GFP (pNestin-GFP) transgenic mice to narrow the target to them.