Place : Gonda 2303 (2nd Floor Conference Room)
 
Place : Gonda 2303 (2nd Floor Conference Room)
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Title: Attention enhances synaptic efficacy and the signal-to-noise ratio in neural circuits.
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Title: '''Attention enhances synaptic efficacy and the signal-to-noise ratio in neural circuits.'''
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Speaker: Michael Einstein (Golshani Lab)
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Speaker: '''Michael Einstein''' (Golshani Lab)
    
Attention enhances the processing of salient visual stimuli. Despite thirty years of research on the correlates of attention in the visual cortex, the mechanism by which attention boosts the signal of a salient visual stimulus is still of great debate. One argument is that attention depolarizes visual cortical cells, which could increase neuronal gain by raising the probability for inputs to trigger spiking. Others say that attention synchronizes specific neural populations in such a way that their impact on downstream neurons is increased. Briggs et al. (2013) adds a new piece to the puzzle by testing how attention alters synaptic weights between the LGN and primary visual cortex in monkeys. This research suggests that attention primarily synchronizes specific neural populations as a means to increase the signal to noise ratio of attended stimuli. To conclude, I will reflect on the impact of this paper and suggest future directions for the field.
 
Attention enhances the processing of salient visual stimuli. Despite thirty years of research on the correlates of attention in the visual cortex, the mechanism by which attention boosts the signal of a salient visual stimulus is still of great debate. One argument is that attention depolarizes visual cortical cells, which could increase neuronal gain by raising the probability for inputs to trigger spiking. Others say that attention synchronizes specific neural populations in such a way that their impact on downstream neurons is increased. Briggs et al. (2013) adds a new piece to the puzzle by testing how attention alters synaptic weights between the LGN and primary visual cortex in monkeys. This research suggests that attention primarily synchronizes specific neural populations as a means to increase the signal to noise ratio of attended stimuli. To conclude, I will reflect on the impact of this paper and suggest future directions for the field.
 
Place : Gonda 2303 (2nd Floor Conference Room)
 
Place : Gonda 2303 (2nd Floor Conference Room)
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Title: Selection of distinct populations of dentate granule cells in response to inputs as a mechanism for pattern separation in mice.
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Title: '''Selection of distinct populations of dentate granule cells in response to inputs as a mechanism for pattern separation in mice.'''
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Speaker: Denise Cai (Silva Lab)
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Speaker: '''Denise Cai''' (Silva Lab)
       
Place : Gonda 2303 (2nd Floor Conference Room)
 
Place : Gonda 2303 (2nd Floor Conference Room)
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Title: Maturation of silent synapses in amygdala-accumbens projection contributes to incubation of cocaine craving
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Title: '''Maturation of silent synapses in amygdala-accumbens projection contributes to incubation of cocaine craving'''
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Speaker: Paul Mathews (Otis Lab)
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Speaker: '''Paul Mathews''' (Otis Lab)
    
This week I have chosen to present a paper entitled "Maturation of silent synapses in amygdala-accumbens projections contributes to incubation of cocaine craving," by Lee at al. Previous research has shown that after repeated cocaine exposure there is a rapid "silencing" of dendritic synapses in medium spiny neurons of the nucleus accumbens. These silenced synapses become rapidly (over days) un-silenced through the incorporation of Ca2+ permeable, rather than Ca2+ impermeable AMPA receptors, which normally predominate the synapse. The authors of this paper present experiments that suggest that these newly un-silenced synapses composed of Ca2+ permeable AMPA receptors underlie the cellular basis for incubated cocaine craving. Given the wide range of experimentation, from behavior to cellular physiology I think this paper should have plenty to interest most ICLM journal club participants.
 
This week I have chosen to present a paper entitled "Maturation of silent synapses in amygdala-accumbens projections contributes to incubation of cocaine craving," by Lee at al. Previous research has shown that after repeated cocaine exposure there is a rapid "silencing" of dendritic synapses in medium spiny neurons of the nucleus accumbens. These silenced synapses become rapidly (over days) un-silenced through the incorporation of Ca2+ permeable, rather than Ca2+ impermeable AMPA receptors, which normally predominate the synapse. The authors of this paper present experiments that suggest that these newly un-silenced synapses composed of Ca2+ permeable AMPA receptors underlie the cellular basis for incubated cocaine craving. Given the wide range of experimentation, from behavior to cellular physiology I think this paper should have plenty to interest most ICLM journal club participants.
 
Place : Gonda 2303 (2nd Floor Conference Room)
 
Place : Gonda 2303 (2nd Floor Conference Room)
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<h4> Title : Metabotropic NMDA Receptor Function </h4>
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Title : '''Metabotropic NMDA Receptor Function'''