Every week I look back at what caught my eye in the neuro world. This is for those of you who hate/are scared of/don’t understand/can’t be bothered by/had a bad experience with/never heard of/simply avoid reading my feed (please circle only one) on Twitter, because these stories were all listed there. If you are coming from Twitter, consider this a refresher on the tweets that got away.
(cont.)

ADHD drugs no longer effective after 24 months
The chronically interesting Furious Seasons blog discussed a study and a debate described in the Washington Post regarding the use of ADHD drugs. New work suggests that these drugs do not have the same efficacy after 24 months, but the mechanism underlying this tolerance is unknown. This important information since children tend to remain on these drugs for many years. If they are not effective, get them off. And a scary statistic that also came out of the long-term study: researchers noted that children who remained on these drugs for 36 months tended to be 1 inch shorter and 6 pounds lighter than their undrugged classmates. Can we please re-assess our over-medicating society?

US government investigates human research protections
Not neuroscience, but of course this has ringing implications for neuroscience research done in humans. The Great Beyond blog details recent tests and sting operations targeting for-profit IRBs with lax standards. Some of the faux studies used to target the rogue IRBs are downright funny, but this accountability office has uncovered some pretty unnerving practices. I was surprised that this story didn’t make a bigger splash (although it was discussed in the WSJ).

Hyperbaric treatment improves autistic symptoms
Autistic children who received oxygen chamber treatment exhibited significant improvements in overall functioning, receptive language, social interaction, and eye contact. But this reaction was much stronger in those children over 5 as compared to younger children. The researchers discuss the evidence that autistic subjects may suffer from cerebral hypoperfusion, leading to hypoxia. Therefore, the increase in oxygen levels by hyperbaric treatment may aleviate this problem, allowing for improved function. This study was broken down on the Autism Research Blog

Early parental depression and child language development
I was unaware of the concept of paternal postpartum depression, but apparently it exists and it is almost as high as the prevalence seen in new moms (10% paternal vs. 14% maternal). In a study of language development and expression, paternal PPD was predictive of more stunted language development later. Maternal PPD did not induce the same ill effects. This may be because it is more rare for a mom with PPD to pull away from her child completely, whereas it is much more common for dad to do exactly that. When the latter happens, BAM! It is the equivalent of a 1-parent home, bringing with it all of the language deficit risks that potentially come from reduced adult interaction. We know that 2 adults are better than 1 in the house during development, so when dad wusses out from PPD, the kids suffer. Dad doesn’t play a more important role in language development than mom, it’s just that depressed moms (mostly) still interact with their children.

Neonatal desensitization allows long-term survival of xenotransplants without immunosuppression
There are plenty of labs out there working on neural transplants that could potentially be used to replace the cells lost from various neurodegenerative disorders. However, as with any transplantation, immune responses and rejection are the main obstacles. This new study finds that early exposure, during development, to foreign neural stem cells and tissue actually desensitizes rats to later transplantation of similar tissue as an adult. The adults no longer needed immune suppression therapy to thwart rejection. Now although this is exciting, this is still the rat immune system that we are talking about here and there is evidence that our system is more active and potent than that of the rodent.

Nicotine increases the signal-to-noise relationship along dopamine afferents
This is an interesting study that examines the differential effect nicotine has on the striatum. Essentially, the researchers found that although nicotine decreased tonic dopamine release in different parts of the striatum, the increased ratio of phasic bursts relative to tonic firing boosted the basal dopamine concentration predominantly in the NAc shell. Thus, the signal-to-noise ratio of dopamine signaling was enhanced. This is intriguing since it is well-known that over 90% of psychiatric patients smoke. And since there is evidence for aberrant dopamine signaling in various psychiatric illnesses, one could speculate that smoking (getting the nicotine into one’s system) actually “normalizes” dopamine signaling, allowing the patient to function a little better.