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The Journal of Neuroscience, September 24, 2003, 23(25)
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This Week in the Journal
Cellular/Molecular
An Inhibitory Module in the Dorsal Horn
A Specific Inhibitory Pathway between Substantia Gelatinosa Neurons Receiving Direct C-Fiber Input
Yan Lu and Edward R. Perl
(see pages 8752-8758)
Neurons of the substantia gelatinosa (SG), lamina II, of the dorsal horn, receive input from unmyelinated C fibers and thinly myelinated A
afferents that carry nociceptive information. Thus the SG is often considered as a first processing stage for painful stimuli, yet we have relatively little knowledge of the intrinsic circuitry within lamina II. Lu and Perl approached this problem in a straightforward but technically challenging way. They made simultaneous recordings from 248 cell pairs of SG neurons in rat spinal cord slices. It was not easy: only 11% of the pairs were synaptically coupled. Postsynaptic responses were approximately split between excitatory and inhibitory responses. They focused on monosynaptic inhibitory synapses between "islet cells" and "transient central" neurons. The cell classification was based on their recent combined morphological-functional criteria for SG neurons but was consistent with the observations of Ramon y Cajal. What is the function of these inhibitory synapses? The SG also contains some C and A
Development/Plasticity/Repair
Altered Migration in Lis1-Less Neurons
Disregulated RhoGTPases and Actin Cytoskeleton Contribute to the Migration Defect in Lis1-Deficient Neurons
Stanislav S. Kholmanskikh, Joseph S. Dobrin, Anthony Wynshaw-Boris, Paul C. Letourneau, and M. Elizabeth Ross
(see pages 8673-8681)
Lissencephaly is a severe human brain malformation associated with a smooth cortical surface lacking sulci or gyri. Several causative genes have been identified, including Lis1, a highly conserved gene involved in cell motility. In rodents, loss of Lis1 results in embryonic death, whereas haploinsufficiency results in disrupted neuronal migration. Several hypotheses for the Lis1-less phenotype have been proposed. Kholmanskikh et al. noticed that cultured Lis1+/- neurons had abnormal motility, and thus wondered whether actin-based motility might be affected. Using time-lapse video microscopy of Lis1+/- neurons, they observed reduced F-actin in the "leading edge" and a reduction in filpodia. The abnormal motility was associated with altered activity of the Rho family of small GTPases that regulate actin polymerization, and the motility abnormalities were rescued when RhoA was inhibited. Investigation of this "disease" gene may provide additional insights into the coordinated regulation of the cytoskeleton.
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Cultured cerebellar neurons were stained with rhodamine-phalloidin, which labels actin (red) and III-tubulin (green). Lis1+/- neurons had a smaller leading edge (l.e.) with fewer filopodia as well as increased F-actin in the soma. See Figure 3 of Kholmanskikh et al. for details.
Behavioral/Systems/Cognitive
Conditioned Responses and the Central Amygdala
Central Amygdala Lesions Block Ultrasonic Vocalization and Freezing as Conditional But Not Unconditional Responses
June-Seek Choi and Thomas H. Brown
(see pages 8713-8721)
Defensive reactions to threatening stimuli ("fear responses") are usually considered to involve circuits within the amygdala. For example, "freezing" and 22 kHz ultrasonic vocalizations (USV), common measures of fear-related conditioned responses (CRs) in rodents, are absent after lesions of the amygdala. Although this has been called a "fear memory" deficit, others have postulated that it simply reflects a motor deficit. In this week's Journal, Choi and Brown examine these two possibilities by taking advantage of the fact that both freezing and USV also occur in male rats after sexual activity [i.e., a nonaversive, unconditioned stimulus (US)]. They reasoned that if rats with amygdala lesions still exhibited freezing and USV after the nonaversive stimulus, then the amygdala must be selectively required for conditioned stimulus (CS)-CR learning pathways. They found that lesions of the central nucleus of the amygdala did not prevent freezing and USV production after sexual activity; however, both were impaired after fear conditioning. Rejecting the "motor-deficit" hypothesis, the authors propose parallel CS-CR and US-unconditioned response (UR) neural pathways with only the conditioned circuitry involving the central nucleus of the amygdala.
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