Thursday, October 20, 2011

Hot off the presses! Nov 01 Nat Rev Neurosci

The Nov 01 issue of the Nat Rev Neurosci is now up on Pubget (About Nat Rev Neurosci): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

  • - Nat Rev Neurosci 12(11):613 (2011)
  • Neurodevelopmental disorders: Mice that mirror autism | PDF (197 KB)
    - Nat Rev Neurosci 12(11):615 (2011)
    Understanding the pathophysiology of autism, and ultimately the development of treatments for impairments associated with the condition, is greatly dependent on reliable animal models. As described in a paper published in Cell, mice lacking contactin-associated protein-like 2 (Cntnap2) recapitulate the three core symptoms of autism, two of which are normalized by treatment with the antipsychotic drug risperidone.
  • Neural development: Neurogenesis ends near the beginning | PDF (248 KB)
    - Nat Rev Neurosci 12(11):616 (2011)
    In rodent mammals, substantial numbers of new neurons that are destined for the olfactory bulb are produced in the subventricular zone (SVZ), but whether this occurs in adult humans remains controversial. Sanai et al.
  • Learning and memory: Small molecule, big hindrance to memory | PDF (222 KB)
    - Nat Rev Neurosci 12(11):617 (2011)
    There is growing evidence of the importance of microRNA-regulated gene expression in the nervous system. These small non-coding RNAs have been implicated in synaptic plasticity and neurogenesis, as well as in neurodegeneration and psychiatric diseases.
  • Synaptic plasticity: Transporting memories | PDF (265 KB)
    - Nat Rev Neurosci 12(11):617 (2011)
    In humans, polymorphisms in the gene encoding KIBRA have been linked to variation in memory performance; however, the neural function of this protein has been unclear. Now, Huganir and colleagues report that KIBRA regulates AMPA receptor (AMPAR) trafficking and synaptic plasticity.
  • Sensory systems: Charting vomeronasal receptor function | PDF (230 KB)
    - Nat Rev Neurosci 12(11):618 (2011)
    Vomeronasal receptors detect sex- and species-specific chemical cues, such as those found in urine and saliva, and this enables the recognition of predators, competitors and potential mates. However, the specific cues that activate each of the hundreds of vomeronasal receptors that have been identified so far are mostly unknown.
  • Pain: A prickly solution? | PDF (201 KB)
    - Nat Rev Neurosci 12(11):618 (2011)
    The Hedgehog (HH) signalling pathway is best known for its roles in development. Now, a study by Galko and colleagues reveals that this protein is also involved in pain signalling.
  • Neuropharmacology: Pain, pain, go away | PDF (106 KB)
    - Nat Rev Neurosci 12(11):616 (2011)
    Placebo responses to painful stimuli are mediated by both opioid and non-opioid mechanisms, and the latter are poorly understood. Here, Benedetti and colleagues examined the role of the endocannabinoid system in such responses.

  • - Nat Rev Neurosci 12(11):616 (2011)

  • - Nat Rev Neurosci 12(11):616 (2011)
  • Addiction: from mechanisms to treatment
    - Nat Rev Neurosci 12(11):621 (2011)
    It needs no explanation that addiction is an extremely serious problem, considering its impact on both health and society. Unsurprisingly, addiction is a major focus of neuroscience research, and the molecular, cellular and circuit mechanisms underlying addiction are slowly beginning to be understood. Despite these research efforts, few effective treatments exist, highlighting the need for continuing investigation. This Focus on Addiction brings together five articles that review the current state of the field and that point to potential new treatment opportunities.
  • Transcriptional and epigenetic mechanisms of addiction
    - Nat Rev Neurosci 12(11):623 (2011)
    Investigations of long-term changes in brain structure and function that accompany chronic exposure to drugs of abuse suggest that alterations in gene regulation contribute substantially to the addictive phenotype. Here, we review multiple mechanisms by which drugs alter the transcriptional potential of genes. These mechanisms range from the mobilization or repression of the transcriptional machinery — including the transcription factors Î"FOSB, cyclic AMP-responsive element binding protein (CREB) and nuclear factor-κB (NF-κB) — to epigenetics — including alterations in the accessibility of genes within their native chromatin structure induced by histone tail modifications and DNA methylation, and the regulation of gene expression by non-coding RNAs. Increasing evidence implicates these various mechanisms of gene regulation in the lasting changes that drugs of abuse induce in the brain, and offers novel inroads for addiction therapy.
  • Opiate versus psychostimulant addiction: the differences do matter
    - Nat Rev Neurosci 12(11):685 (2011)
    The publication of the psychomotor stimulant theory of addiction in 1987 and the finding that addictive drugs increase dopamine concentrations in the rat mesolimbic system in 1988 have led to a predominance of psychobiological theories that consider addiction to opiates and addiction to psychostimulants as essentially identical phenomena. Indeed, current theories of addiction — hedonic allostasis, incentive sensitization, aberrant learning and frontostriatal dysfunction — all argue for a unitary account of drug addiction. This view is challenged by behavioural, cognitive and neurobiological findings in laboratory animals and humans. Here, we argue that opiate addiction and psychostimulant addiction are behaviourally and neurobiologically distinct and that the differences have important implications for addiction treatment, addiction theories and future research.
  • Correspondence: The regional specificity of rapid actions of cocaine
    - Nat Rev Neurosci 12(11):700 (2011)
    In their recent Perspective article, Roy Wise and Eugene Kiyatkin conclude that, "the primary, unconditioned rewarding effects of cocaine in naive animals involves the blockade of dopamine reuptake rather than stimulation of dopamine release" (Differentiating the rapid actions of cocaine. Nature Rev. Neurosci. 12, 479–484 (2011)

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