I like four here. A very good issue.
1. Another winner from Dranovsky! (Disclosure: we’re friends. Still.) Social isolation affects hippocampal stem cell accumulation.
Alex Dranovsky et al and Rene Hen (Omega) Experience Dictates Stem Cell Fate in the Adult Hippocampus. Neuron Volume 70, Issue 5, 9 June 2011, Pages 908-923
Summary: Adult hippocampal neurogenesis has been implicated in cognitive and emotional processes, as well as in response to antidepressant treatment. However, little is known about how the adult stem cell lineage contributes to hippocampal structure and function and how this process is modulated by the animal’s experience. Here we perform an indelible lineage analysis and report that neural stem cells can produce expanding and persisting populations of not only neurons, but also stem cells in the adult hippocampus. Furthermore, the ratio of stem cells to neurons depends on experiences of the animal or the location of the stem cell. Surprisingly, social isolation facilitated accumulation of stem cells, but not neurons. These results show that neural stem cells accumulate in the adult hippocampus and that the stem cell-lineage relationship is under control of anatomic and experiential niches. Our findings suggest that, in the hippocampus, fate specification may act as a form of cellular plasticity for adapting to environmental changes.
2. Dopamine: it’s not just for reward any longer. This forces a revision of the mantra “VTA DA to NAc equals RPE.” (Only slightly more difficult than om mani padme hum, and no (retro)beads to twirl simultaneously! Call it a wash.) Important for fans of the habenula, VTA, dopamine, incentive salience or reward prediction error. Is this a win for Berridge? PS I almost said reward prediction area. See? That’s out the window now.
Stephan Lammel,Daniela I. Ion, Jochen Roepe and Robert C. Malenka. Projection-Specific Modulation of Dopamine Neuron Synapses by Aversive and Rewarding Stimuli. Neuron Volume 70, Issue 5, 9 June 2011, Pages 855-862
Summary: Midbrain dopamine (DA) neurons are not homogeneous but differ in their molecular properties and responses to external stimuli. We examined whether the modulation of excitatory synapses on DA neurons by rewarding or aversive stimuli depends on the brain area to which these DA neurons project. We identified DA neuron subpopulations in slices after injection of “Retrobeads” into single target areas of adult mice and found differences in basal synaptic properties. Administration of cocaine selectively modified excitatory synapses on DA cells projecting to nucleus accumbens (NAc) medial shell while an aversive stimulus selectively modified synapses on DA cells projecting to medial prefrontal cortex. In contrast, synapses on DA neurons projecting to NAc lateral shell were modified by both rewarding and aversive stimuli, which presumably reflects saliency. These results suggest that the mesocorticolimbic DA system may be comprised of three anatomically distinct circuits, each modified by distinct aspects of motivationally relevant stimuli.
3. Wonderfully clinical – a glimpse of the future of psychiatry. Uses neuroscience to guide clinical interventions in disorders of fear (eg, PTSD). A huge winner.
Stephen Maren. Seeking a Spotless Mind: Extinction, Deconsolidation, and Erasure of Fear Memory (Review). Neuron, Volume 70, Issue 5, 9 June 2011, Pages 830-845
Summary: Learning to contend with threats in the environment is essential to survival, but dysregulation of memories for traumatic events can lead to disabling psychopathology. Recent years have witnessed an impressive growth in our understanding of the neural systems and synaptic mechanisms underlying emotional memory formation. As a consequence, interest has emerged in developing strategies for suppressing, if not eliminating, fear memories. Here, I review recent work employing sophisticated behavioral, pharmacological, and molecular tools to target fear memories, placing these memories firmly behind the crosshairs of neurobiologically informed interventions.
4. This one grows on you (ba-dum!). It gets better and better as it goes along. They work with an analogy between memory and cellular development that helps synthesize the material. They conclude with a fascinating speculation about why neurons don’t divide. An excellent choice for a journal club focused on periodically updating foundational concepts.
Jeremy J. Day and J. David Sweatt. Epigenetic Mechanisms in Cognition (Review). Neuron. Volume 70, Issue 5, 9 June 2011, Pages 813-829
Summary: Although the critical role for epigenetic mechanisms in development and cell differentiation has long been appreciated, recent evidence reveals that these mechanisms are also employed in postmitotic neurons as a means of consolidating and stabilizing cognitive-behavioral memories. In this review, we discuss evidence for an “epigenetic code” in the central nervous system that mediates synaptic plasticity, learning, and memory. We consider how specific epigenetic changes are regulated and may interact with each other during memory formation and how these changes manifest functionally at the cellular and circuit levels. We also describe a central role for mitogen-activated protein kinases in controlling chromatin signaling in plasticity and memory. Finally, we consider how aberrant epigenetic modifications may lead to cognitive disorders that affect learning and memory, and we review the therapeutic potential of epigenetic treatments for the amelioration of these conditions.Follow @peterfreed