59 results match your criteria: "Center for Neuroscience at the University of Pittsburgh[Affiliation]"

Neuroscience in recession?

Nat Rev Neurosci

May 2011

Department of Neurobiology, University of Pittsburgh School of Medicine, and the Center for Neuroscience at the University of Pittsburgh, Biomedical Science Tower 3, 6th Floor, Room 6057, 3501 Fifth Avenue, Pittsburgh, Pennsylvania 15260, USA.

As the global financial downturn continues, its impact on neuroscientists - both on an individual level and at the level of their research institute - becomes increasingly apparent. How is the economic crisis affecting neuroscience funding, career prospects, international collaborations and scientists' morale in different parts of the world? Nature Reviews Neuroscience gauged the opinions of a number of leading neuroscientists: the President of the Society for Neuroscience, the President Elect of the British Neuroscience Association, the former President of the Japan Neuroscience Society, the President of the Federation of European Neuroscience Societies and the Director of the US National Institute of Mental Health. Their responses provide interesting and important insights into the regional impact of the global financial downturn, with some causes for optimism for the future of neuroscience research.

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Trafficking of transcription factors between the cytoplasm and the nucleus is an essential aspect of signal transduction, which is particularly challenging in neurons due to their highly polarized structure. Disruption in the subcellular localization of many proteins, including transcription factors, is observed in affected neurons of human neurodegenerative diseases. In these diseases, there is also growing evidence supporting alterations in nuclear transport as potential mechanisms underlying the observed mislocalization of proteins.

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Cocaine users display a wide range of cognitive impairments. Because treatment outcome is dependent on baseline cognitive ability, it is clinically important to understand the underlying neurobiology of these deficits. Therefore, it is crucial to determine whether cocaine exposure by itself is an etiological factor and, if so, to determine the overall nature of cognitive deficits associated with cocaine use.

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Objective: We examined the distribution of artemin and its receptor, glial cell line-derived neurotrophic factor family receptor alpha3 (GFRalpha3), in the dura mater of rats.

Background: Artemin, a member of the glial cell line-derived neurotrophic factor family, is a vasculature-derived growth factor shown to regulate migration of sympathetic neuroblasts and targeting of sympathetic innervation. The artemin receptor, GFRalpha3, is present in both sympathetic efferents and a subpopulation of nociceptive afferents.

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Inactivation and adaptation of number neurons.

Behav Brain Sci

August 2009

Department of Neuroscience, Center for the Neural Basis of Cognition, Center for Neuroscience at the University of Pittsburgh, Pittsburgh, PA 15260, USA.

Single-neuron recordings may help resolve the issue of abstract number representation in the parietal lobes. Two manipulations in particular - reversible inactivation and adaptation of apparent numerosity - could provide important insights into the causal influence of "numeron" activity. Taken together, these tests can significantly advance our understanding of number processing in the brain.

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Intrathalamic mechanisms of visual attention.

J Neurophysiol

March 2009

Department of Neuroscience, Center for Neuroscience at the University of Pittsburgh, Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

The classical model of visual processing emphasizes the lateral geniculate nucleus (LGN) as the major intermediary between the retina and visual cortex. Yet, anatomical findings inspired Francis Crick to suggest an alternative model in which the thalamic reticular nucleus, which envelops the LGN, acts as the "guardian" of visual cortex by modulating LGN activity. Recent work by McAlonan and colleagues supports Crick's hypothesis, thereby enhancing our understanding of the early stages of visual processing.

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Corollary discharge circuits in the primate brain.

Curr Opin Neurobiol

December 2008

Department of Neuroscience, A210 Langley Hall, Center for the Neural Basis of Cognition, and Center for Neuroscience at the University of Pittsburgh, University of Pittsburgh, Pittsburgh, PA 15260, USA.

Movements are necessary to engage the world, but every movement results in sensorimotor ambiguity. Self-movements cause changes to sensory inflow as well as changes in the positions of objects relative to motor effectors (eyes and limbs). Hence the brain needs to monitor self-movements, and one way this is accomplished is by routing copies of movement commands to appropriate structures.

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Influence of the thalamus on spatial visual processing in frontal cortex.

Nature

November 2006

Department of Neuroscience, the Center for the Neural Basis of Cognition, and the Center for Neuroscience at the University of Pittsburgh, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA.

Each of our movements activates our own sensory receptors, and therefore keeping track of self-movement is a necessary part of analysing sensory input. One way in which the brain keeps track of self-movement is by monitoring an internal copy, or corollary discharge, of motor commands. This concept could explain why we perceive a stable visual world despite our frequent quick, or saccadic, eye movements: corollary discharge about each saccade would permit the visual system to ignore saccade-induced visual changes.

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