The use of human embryonic stem cells (hESCs) in research is of course highly controversial, raising ethical questions that for many people amount to serious dilemmas. In our April editorial we didn’t address the moral questions at all, but criticized recent efforts to discredit hESC research.

We’ve received two letters chiding us for the editorial. Though we can’t publish these letters in Nature Neuroscience, we are happy to discuss the matter on Action Potential. We invite the authors of the two letters to join us on the blog, and everyone else of course is also welcome to chip in.

Here are the links to the editorial, and the two pieces we discussed as examples for the new trick of spinning stem cell science against stem cell science. All are available for free:

Nature Neuroscience April 2007 editorial

Maureen L. Condic, “What We Know About Embryonic Stem Cells”, First Things, January 2007

The White House Domestic Policy Council, “Advancing Stem Cell Science Without Destroying Human Life”, January 2007

As the news out of Blacksburg, Virginia continues to unfold, it is difficult not to reflect on the importance of mental health services for young adults. In a sad coincidence, a meta-analysis published today in JAMA suggests that despite earlier reports of increased suicide risk, the benefits of antidepressant treatment in children and young adults outweigh the risks. Bridge et al. report that antidepressants helped young people with major depressive disorder, obsessive compulsive disorder and anxiety and increased their risk of suicidal thoughts or attempts by less than 1%. Improved treatment protocols specific for children and teenagers will hopefully help young adults in need. Unfortunately, we all know that treatments can only help those who seek them.

Just a few weeks can separate a splash from a quiet ripple. On 5 April, Neuron and Nature both published articles reporting genetically targeted silencing of mammalian neurons. In Neuron, Lerchner et al. detailed drug-induced hyperpolarization of neurons expressing a C. elegans chloride channel within hours of treatment. In Nature, Zhang et al. reported light-induced hyperpolarization of neurons expressing an archaea opsin within milliseconds of illumination. The media took note of Zhang’s article, but not Lerchner’s.

To be fair, the two articles are quite different in scope. Zhang et al. reported not just inducible neuron silencing, but a neuron on/off switch. In the same neuron, the authors induced firing with a blue light-activated cation channel and inhibited endogenous firing with a yellow-light induced chloride pump. They turned behaviors on and off with blue and yellow light, respectively, in C. elegans expressing both the cation channel and the chloride pump. The ability to control neuron function is nothing short of stunning and will undoubtedly impact both bench and bedside.

Although their scope was much smaller, Lerchner et al. approached neuronal silencing cleverly. Ivermectin is a chloride channel agonist in C. elegans, but not mammals, making it a potent antiparasitic agent that literally puts worms to sleep, sparing mammalian hosts. The authors silenced mammalian neurons expressing the C. elegans ivermectin-gated chloride channel and suppressed behavior with systemic treatment of ivermectin.

Systemic drug treatment is virtually guaranteed to take longer than illumination to achieve inhibition. And an off switch alone can’t compare to the deluxe on/off model. But I can’t help wondering if I’d be more excited about Lerchner’s article if it came out a few weeks earlier.

There is one interesting postscript to Zhang’s amazing achievement. Han and Boyden reported an identical yellow-light induced chloride pump earlier in the month in PLoS ONE. They examined the properties of blue and yellow light-induced excitation and inhibition in cultured hippocampal neurons. Although Han and Boyden don’t show any in vivo data, their study technically preceded Zhang et al. So, in the grand scheme of things, who will be credited with the discovery? Maybe timing isn’t everything.