Cellular/Molecular
The Brain's Salt Sensor
Takeshi Y. Hiyama, Eiji Watanabe, Haruo Okado, and Masaharu Noda
(see pages 9276-9281)
Maintenance of proper sodium and water balance, critical to survival, appears to involve both osmosensors and sodium sensors in the brain. A putative sodium sensor was identified recently as a member of a subfamily of voltage-gated sodium channels. This channel, Nax, a product of the SCN7A gene, is expressed in a few areas in the CNS, particularly the subfornical organ, a specialized structure situated in the midline wall of the ventricles. Mice lacking Nax continue to ingest salt even when serum sodium is increased by dehydration. Hiyama et al. extend their recent work to locate the sodium sensor. Unlike Nax-deficient mice, normal mice increased their water intake and avoided salt when hypertonic saline was infused into the ventricles. Adenoviral-mediated expression of Nax in Nax knock-out mice only rescued salt-avoiding behavior when the expression included the subfornical organ. Thus the subfornical organ appears to be a prime locus for this salt sensor.
Development/Plasticity/Repair
Using Fibronectin as Your Guide
Veronica J. Tom, Catherine M. Doller, Alfred T. Malouf, and Jerry Silver
(see pages 9282-9290)
Astroglia provide a permissive environment for pioneering axons during development, whereas CNS myelin in the adult generally inhibits axonal regeneration. However, the adult environment can support neurite outgrowth of transplanted sensory neurons. This week, Tom et al. examine possible factors from adult astroglia that support such neurite regeneration. Using an in situ slice culture of adult (postnatal day 35) rat corpus callosum, they seeded slices with cortical or dorsal root ganglion (DRG) neurons from green fluorescent protein (GFP)-expressing mice and then watched neurite outgrowth. The DRG neurons extended long axonal processes along the astrocyte-rich corpus callosum, but cortical neurons did not. Fibronectin was highly expressed in the corpus callosum and tightly associated with astrocytes, whereas laminin, another putative extracellular matrix growth-promoting factor, was detected only along blood vessels. Fibronectin function-blocking antibodies stunted neurite outgrowth. Because CNS neurons do not grow well on fibronectin, the authors speculate that fibronectin may actually inhibit CNS neuronal outgrowth while supporting the outgrowth of sensory neurons.
Regenerating GFP-positive neurites (green) generally followed host GFAP-positive astrocytic processes (red) and grew longitudinally (arrowhead). However, there were instances during which neurites wandered and jumped from one astrocytic process to another (asterisk). See the article by Tom et al. for details.
Behavioral/Systems/Cognitive
Remembering the Second Time Around
Sevil Duvarci and Karim Nader
(see pages 9269-9275)
Protein synthesis is required for the formation of long-term memories. Interestingly, reactivation of such memories is followed by a period in which storage is once again dependent on protein synthesis. One prevailing idea is that memories must be reconsolidated. Alternatively, protein synthesis inhibition could be equivalent to extinction, or memory retrieval could be blocked? This week Duvarci and Nader explore these possibilities by injecting anisomycin into the rat lateral amygdala immediately after retrieval of consolidated fear memories. Extinction requires new memory formation; thus the authors argue that facilitation of extinction cannot underlie anisomycin block of reactivated consolidated memory. In addition, extinction is context dependent, so a memory extinguished in one setting should resurface in another. However, when rats were tested in a neutral environment after blocking protein synthesis, the memories were still inaccessible. Two tests of retrieval deficiency also failed, suggesting that the reactivated memories do indeed require reconsolidation.
Neurobiology of Disease
A Consequence of Prenatal Nicotine in the Rat
Robert A. Neff, Samuel J. Simmens, Cory Evans, and David Mendelowitz
(see pages 9261-9268)
If any additional reasons were needed to avoid smoking during pregnancy, Neff et al. deliver them in this week's Journal. Sudden infant death syndrome (SIDS) has been linked to prenatal nicotine exposure and may result from an exaggerated response to hypoxia. Cardioinhibitory vagal neurons (CVNs) in the brainstem regulate the heart rate via the vagus nerve, and thus could be involved in such changes. These neurons are inhibited by GABAergic and glycinergic inputs that caused biphasic changes in activity during hypoxia. The frequency of IPSCs first increases and then decreases, thus speeding and then slowing respiration and heart rate to adjust metabolic demand. The authors recorded from fluorescent-labeled CVNs in rat brainstem slices. After exposure to prenatal nicotine, GABAergic inputs showed a marked decrease in activity. The authors suggest that the subsequent disinhibition of CVNs could cause excessive slowing of the heart rate and thus contribute to the pathophysiology of SIDS.
