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The Journal of Neuroscience, September 21, 2005, 25(38)

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This Week in the Journal

Cellular/Molecular

Painful to a T

Michael T. Nelson, Pavle M. Joksovic, Edward Perez-Reyes, and Slobodan M. Todorovic

(see pages 8766–8775)

T-type calcium channels are activated near the resting membrane potential and thus are poised to influence cell excitability. This week, Nelson et al. report a role for T-channels in a subset of nociceptors. The authors recorded from rat dorsal root ganglion neurons in the intact ganglia or after dissociation. Small, capsaicin-sensitive, nonpeptidergic neurons expressed a preponderance of T-type calcium currents. Isolectin B4 also labeled the "T-rich" cells. These nociceptors terminate in lamina II in the spinal cord and contribute to chronic pain after nerve injury. L-Cysteine, an endogenous reducing agent, augmented T-type currents, increased the T-channel-mediated after depolarization, and substantially increased action potential firing. Nociceptor responses to noxious stimuli can be increased by central or peripherally expressed molecules; thus modulation of T-channels may be one of the mechanisms of sensitization to painful stimuli after nerve injury.

Development/Plasticity/Repair

TGF1 and Cell-Cycle Exit in the Ventricular Zone

Julie A. Siegenthaler and Michael W. Miller

(see pages 8627–8636)

Cyclin/cyclin-dependent kinase (cdk) complexes guide cells through the cell cycle, whereas cdk inhibitors (CKIs) facilitate their exit. Transforming growth factor 1 (TGF1) can affect proliferation of non-neuronal cells by suppressing the transcription of cyclins and upregulating CKIs. This week, Siegenthaler and Miller report that TGF1 also modulates cell-cycle exit in the cortical ventricular zone (VZ) by affecting expression of cell-cycle proteins. In organotypic slice cultures of the cerebral wall, 24 h of treatment with exogenous TGF1 increased the fraction of cells exiting the cell cycle, but the cell-cycle length remained constant. Treated cells that exited the cell cycle expressed high levels of the CKI p21, suggesting that p21 mediated the action of TGF1. Although these studies examined only exogenous TGF1, endogenous TGF1 is strategically expressed in the VZ.

Behavioral/Systems/Cognitive

Sensory Regulation of a Rhythmic Motor Circuit

Mark P. Beenhakker, Nicholas D. DeLong, Shari R. Saideman, Farzan Nadim, and Michael P. Nusbaum

(see pages 8794–8806)

Sensory inputs strongly influence central pattern generators. This week, Beenhakker et al. map the modulatory action of proprioceptive input on rhythmic muscle activity in the crab stomatogastric nervous system. The gastropyloric muscle stretch receptor (GPR) regulates the gastric mill, or chewing, motor rhythm. Alternating activity of teeth protractor and retractor neurons drives the movement, whereas the GPR consists of pairs of neurons activated by stretch of the gastric mill protractor muscles. The authors used in vitro stimulation to evoke the mill rhythm and concurrently stimulated the GPR during retraction. GPR activation slowed the rhythm by prolonging the retractor phase. The GPR modulated the motor rhythm by two parallel actions: presynaptic inhibition of modulatory commissural neuron 1, thereby reducing the drive to all gastric mill neurons, and direct excitation of retractor phase neurons. The latter effect serves to compensate for the presynaptic inhibition of the retractors. Chew, stretch, chew, stretch: so it goes.

View larger version (20K): [in this window] [in a new window]   GPR stimulation prolongs the retractor phase of the gastric mill rhythm. The top trace shows intracellular recording of the protractor neuron [lateral gastric (LG) neuron]; the bottom trace shows extracellular recording of the dorsal gastric nerve (dgn) with the retractor neuron [dorsal gastric (DG) neuron] activity. See the article by Beenhakker et al. for details.

 
Neurobiology of Disease

Another Reason to Drink Green Tea?

Kavon Rezai-Zadeh, Doug Shytle, Nan Sun, Takashi Mori, Huayan Hou, Deborah Jeanniton, Jared Ehrhart, Kirk Townsend, Jin Zeng, David Morgan, John Hardy, Terrence Town, and Jun Tan

(see pages 8807–8814)

If only it were so easy; it tastes good and it's good for you. This week, Rezai-Zadeh et al. report that a component of green tea modulated amyloid precursor protein (APP) processing in a mouse model of Alzheimer's disease in vitro and in vivo. Epigallocatechin-3-gallate (EGCG), the main polyphenolic component of green tea, reduced -amyloid (A) production in neurons cultured from APP-overexpressing mice (Tg APP_SW). Notably, EGCG was more effective than whole green tea extract. -secretase and -secretase process APP by parallel amyloidogenic and nonamyloidogenic pathways, respectively. EGCG boosted activity of the latter pathway, indicated by increased -C-terminal fragment and soluble APP-. Tumor necrosis factor (TNF)- converting enzyme (TACE), a candidate -secretase, increased after EGCG treatment, and -secretase activity was reduced by TNF- protease inhibitor-1 (TAPI-1), a selective TACE inhibitor. Treatment of Tg APP_SW mice at 12 months of age with EGCG (provided as intraperitoneal injections, not by teacup) also promoted -secretase activity. After 2 months of treatment, A-containing plaques were significantly reduced.

This Article Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content

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