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The Journal of Neuroscience, April 12, 2006, 26(15)
This Week in The Journal
This Week in The Journal
Cellular/Molecular
Wiring up for Color
Patricia R. Jusuf, Paul R. Martin, and Ulrike Grünert
(see pages 3908–3917)
The primate midget-parvocellular (PC) visual system contributes to red–green color detection. In this week’s Journal, Jusuf et al. sought to determine whether selective wiring of the pathway connects red–green-sensitive cells with one another. The PC pathway successively involves cone photoreceptors, midget bipolar cells, midget ganglion cells, PC relay cells in the lateral geniculate nucleus, and finally the visual cortex. To determine whether color selectivity arises from cone-selective contacts, the authors examined the OFF pathway of the peripheral retina in dichromatic (red–green color blind) and trichromatic (color normal) marmosets. They identified OFF midget bipolar cells immunohistochemically and retrogradely labeled OFF midget ganglion cells. The authors found a loose convergence pattern of connections between these populations that was not related to red–green color vision. Thus, the function of the PC pathway in the peripheral retina does not depend on recognition between individual members of bipolar–ganglion cell mosaics.
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A reconstructed OFF-midget ganglion cell (black) is superimposed on the corresponding flat midget bipolar axon terminal fields (gray) in a dichromatic animal. See the article by Jusuf et al. for details.
Development/Plasticity/Repair
BDNF and Thermostatic Control
Adi Katz and Noam Meiri
(see pages 3899–3907)
We generally take our internal body thermostat for granted, but this week, Katz and Meiri provide evidence that this system is sensitive to early experience. The authors examined the developmental plasticity of this hypothalamic controller during the critical period. In the chick, heat- and cold-sensitive neurons are located in the preoptic/anterior hypothalamus (PO/AH). The authors report that brain-derived neurotrophic factor (BDNF) is a key regulator in the PO/AH. Chicks that were heat-conditioned (37.5°C for 24 h) on postnatal day 3 had increases in BDNF but not nerve growth factor or neurotrophin-3. Cold conditioning also induced BDNF transcription, whereas cold acclimation in older chicks did not. Both heat- and cold-induced BDNF expression was limited to the PO/AH. Chicks whose BDNF was knocked down by antisense treatment during the critical period had persistent difficulty in regulating body temperature, and chicks that received heat conditioning during the critical period fared worse than those that did not.
Behavioral/Systems/Cognitive
Retinal Gain Control
Felice A. Dunn, Thuy Doan, Alapakkam P. Sampath, and Fred Rieke
(see pages 3959–3970)
Sensory systems do an impressive job of maintaining sensitivity across a broad range of stimulus intensities. This requires a balancing act between the amplification needed for high sensitivity and the gain controls needed to avoid saturation. This week, Dunn et al measured responses to brief light flashes at different background light levels to examine the location of gain controls among the bipolar, amacrine, and ganglion cells of the inner retina. Using isolated retina preparations from both mice and primates, the authors first concluded that the rod bipolar-to-AII amacrine synapses control the gain of rod-mediated signals at low background intensities. Interestingly, current noise in AII amacrine and ganglion cells (i.e. after the gain controls) was independent of background light levels, suggesting that the synaptic response encodes signal-to-noise rather than flash strength. Thus, at low sensitivity, the substantial noise in the circuitry limits the response of ganglion cells and maintains these output cells within their dynamic spiking range.
Neurobiology of Disease
Memantine Revisited
Catherine Creeley, David F. Wozniak, Joanne Labruyere, George T. Taylor, and John W. Olney
(see pages 3923–3932)
It seemed simple. Excess glutamate kills neurons; thus, blocking glutamate receptors should have benefit in disorders that involve a component of excitotoxic neuronal injury or cell death. However, clinical trials of NMDA receptor antagonists were disappointing because of cognitive side effects such as hallucinations. Recently, a low-affinity NMDA receptor channel blocker, memantine, has come into use in Alzheimer’s disease, seemingly because it does not cause side effects. This was puzzling to some because memantine acts similarly to ketamine, which causes significant cognitive side effects. This week, Creeley et al. examined seizure-related brain damage in adult rats treated with kainic acid. As expected, memantine provided some neuroprotection, but at the same dose, it produced side effects on each of eight behavioral tests. Lower doses also resulted in sensorimotor and memory deficits. At least in rodents and for these tasks, memantine behaved predictably as an NMDA receptor antagonist.
DOI:
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