Thursday, December 23, 2010

Hot off the presses! Jan 01 Nat Rev Neurosci

The Jan 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(1):1 (2011)
  • Fear: A frightful circuit | PDF (199 KB)
    - Nat Rev Neurosci 12(1):2 (2011)
    The amygdala is central to the learning and expression of fear, but the circuits and neuron types within the amygdala that mediate these aspects of fear conditioning are poorly understood. In two new papers, Lüthi and colleagues and Anderson and colleagues use various pharmacological and cutting-edge molecular genetics techniques to identify an inhibitory microcircuit within the central nucleus of the amygdala, of which the lateral (CEl) and medial (CEm) subdivisions mediate the acquisition and expression of conditioned fear, respectively, in mice.
  • Cancer: Tumour stem cells generate vasculature | PDF (198 KB)
    - Nat Rev Neurosci 12(1):3 (2011)
    Glioblastoma is a highly angiogenic tumour and, although it is known that neural stem cells closely interact with the vascular niche, the origins of the endothelial cells in this malignancy are poorly understood. Two new papers show that stem-like cells in the tumour can differentiate into endothelial cells, thereby generating the tumour vasculature.
  • Motor control: A sense of movement | PDF (126 KB)
    - Nat Rev Neurosci 12(1):3 (2011)
    Neuroscience textbooks tell us that the motor cortex controls movement. But now, Carl Petersen and colleagues show that sensory cortex may have an equally important role in motor control.
  • Addiction: A sobering thought | PDF (194 KB)
    - Nat Rev Neurosci 12(1):4 (2011)
    Drugs of abuse, including alcohol, can promote maladaptive synaptic plasticity mechanisms in the brain's reward system, but the underlying molecular pathways are not well characterized. Now, Ron and colleagues highlight a key role of the serine/threonine kinase complex mammalian target of rapamycin complex 1 (mTORC1) in the nucleus accumbens (NAc) in mediating synaptic changes that accompany alcohol addiction.
  • Neuroplasticity: Functional recovery after stroke | PDF (178 KB)
    - Nat Rev Neurosci 12(1):4 (2011)
    There is no pharmacological therapy available to promote recovery after stroke. The brain region next to that suffering stroke damage — the peri-infarct zone — has some capacity for increased neuroplasticity that can aid functional recovery.
  • Synaptic plasticity: A new partnership | PDF (125 KB)
    - Nat Rev Neurosci 12(1):5 (2011)
    The endocannabinoid anandamide inhibits neurotransmitter release through presynaptic cannabinoid receptor 1 (CB1) receptors. Anandamide also binds transient receptor potential vanilloid 1 (TRPV1), but the physiological relevance of this binding has not been established.
  • Neurodegenerative disease | Development | Olfaction | Synaptic transmission | PDF (138 KB)
    - Nat Rev Neurosci 12(1):5 (2011)
    Reversing EphB2 depletion rescues cognitive functions in Alzheimer model Cissé, al. Nature28 Nov 2010 (doi:10.1038/nature09635)
  • Plasticity: Don't get too excited! | PDF (212 KB)
    - Nat Rev Neurosci 12(1):6 (2011)
    To keep the brain working efficiently, neuronal activity has to be maintained around an optimum level. However, various types of plasticity occur across a network or in individual neurons, resulting in changes in synaptic strength and neuronal firing.
  • Neurodegenerative disease: SNc neurons' Achilles heel | PDF (196 KB)
    - Nat Rev Neurosci 12(1):6 (2011)
    In Parkinson's disease, degeneration of dopamine neurons in the substantia nigra pars compacta (SNc) is thought to result from oxidative stress. However, why SNc neurons are particularly vulnerable to degeneration has been a long-standing conundrum.
  • Sensory Processing: Scratching an itch with VGLUT2 | PDF (128 KB)
    - Nat Rev Neurosci 12(1):7 (2011)
    'Don't scratch it, you'll make it worse!' But our automatic response to an itch is to scratch it, and scratching does — at least temporarily — relieve the sensation of itching.
  • How does PKMζ maintain long-term memory?
    - Nat Rev Neurosci 12(1):9 (2011)
    Most of the molecular mechanisms contributing to long-term memory have been found to consolidate information within a brief time window after learning, but not to maintain information during memory storage. However, with the discovery that synaptic long-term potentiation is maintained by the persistently active protein kinase, protein kinase Mζ (PKMζ), a possible mechanism of memory storage has been identified. Recent research shows how PKMζ might perpetuate information both at synapses and during long-term memory.
  • Making memories last: the synaptic tagging and capture hypothesis
    - Nat Rev Neurosci 12(1):17 (2011)
    The synaptic tagging and capture hypothesis of protein synthesis-dependent long-term potentiation asserts that the induction of synaptic potentiation creates only the potential for a lasting change in synaptic efficacy, but not the commitment to such a change. Other neural activity, before or after induction, can also determine whether persistent change occurs. Recent findings, leading us to revise the original hypothesis, indicate that the induction of a local, synapse-specific 'tagged' state and the expression of long-term potentiation are dissociable. Additional observations suggest that there are major differences in the mechanisms of functional and structural plasticity. These advances call for a revised theory that incorporates the specific molecular and structural processes involved. Addressing the physiological relevance of previous in vitro findings, new behavioural studies have experimentally translated the hypothesis to learning and the consolidation of newl! y formed memories.
  • Hereditary spastic paraplegias: membrane traffic and the motor pathway
    - Nat Rev Neurosci 12(1):31 (2011)
    Voluntary movement is a fundamental way in which animals respond to, and interact with, their environment. In mammals, the main CNS pathway controlling voluntary movement is the corticospinal tract, which encompasses connections between the cerebral motor cortex and the spinal cord. Hereditary spastic paraplegias (HSPs) are a group of genetic disorders that lead to a length-dependent, distal axonopathy of fibres of the corticospinal tract, causing lower limb spasticity and weakness. Recent work aimed at elucidating the molecular cell biology underlying the HSPs has revealed the importance of basic cellular processes — especially membrane trafficking and organelle morphogenesis and distribution — in axonal maintenance and degeneration.
  • Emerging concepts for the dynamical organization of resting-state activity in the brain
    - Nat Rev Neurosci 12(1):43 (2011)
    A broad body of experimental work has demonstrated that apparently spontaneous brain activity is not random. At the level of large-scale neural systems, as measured with functional MRI (fMRI), this ongoing activity reflects the organization of a series of highly coherent functional networks. These so-called resting-state networks (RSNs) closely relate to the underlying anatomical connectivity but cannot be understood in those terms alone. Here we review three large-scale neural system models of primate neocortex that emphasize the key contributions of local dynamics, signal transmission delays and noise to the emerging RSNs. We propose that the formation and dissolution of resting-state patterns reflects the exploration of possible functional network configurations around a stable anatomical skeleton.

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