Difference between revisions of "ICLM Journal Club"

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=<font color="blue">'''This Week - 29 January 2021 (9:30 a.m., via Zoom)'''</font>=
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=<font color="blue">'''This Week - 05 February 2021 (9:30 a.m., via Zoom)'''</font>=
  
<u>Speaker:</u> ''' Jackie Giovanniello'''
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<u>Speaker:</u> ''' Peyman Golshani'''
  
<u>Title:</u> “Amygdala inhibitory neurons as loci for translation in emotional memories”
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<u>Title:</u> “ Perirhinal input to neocortical layer 1 controls learning.”
  
<u>Abstract:</u> To survive in a dynamic environment, animals need to identify and appropriately respond to stimuli that signal danger1. Survival also depends on suppressing the threat-response during a stimulus that predicts the absence of threat (safety). An understanding of the biological substrates of emotional memories during a task in which animals learn to flexibly execute defensive responses to a threat-predictive cue and a safety cue is critical for developing treatments for memory disorders such as post-traumatic stress disorder5. The centrolateral amygdala is an important node in the neuronal circuit that mediates defensive responses and a key brain area for processing and storing threat memories. Here we applied intersectional chemogenetic strategies to inhibitory neurons in the centrolateral amygdala of mice to block cell-type-specific translation programs that are sensitive to depletion of eukaryotic initiation factor 4E (eIF4E) and phosphorylation of eukaryotic initiation factor 2α (p-eIF2α). We show that de novo translation in somatostatin-expressing inhibitory neurons in the centrolateral amygdala is necessary for the long-term storage of conditioned-threat responses, whereas de novo translation in protein kinase Cδ-expressing inhibitory neurons in the centrolateral amygdala is necessary for the inhibition of a conditioned response to a safety cue. Our results provide insight into the role of de novo protein synthesis in distinct inhibitory neuron populations in the centrolateral amygdala during the consolidation of long-term memories.
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<u>Abstract:</u> Hippocampal output influences memory formation in the neocortex, but this process is poorly understood because the precise anatomical location and the underlying cellular mechanisms remain elusive. Here, we show that perirhinal input, predominantly to sensory cortical layer 1 (L1), controls hippocampal-dependent associative learning in rodents. This process was marked by the emergence of distinct firing responses in defined subpopulations of layer 5 (L5) pyramidal neurons whose tuft dendrites receive perirhinal inputs in L1. Learning correlated with burst firing and the enhancement of dendritic excitability, and it was suppressed by disruption of dendritic activity. Furthermore, bursts, but not regular spike trains, were sufficient to retrieve learned behavior. We conclude that hippocampal information arriving at L5 tuft dendrites in neocortical L1 mediates memory formation in the neocortex.
  
<u>Relevant Paper(s):</u>  https://www.nature.com/articles/s41586-020-2793-8
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<u>Relevant Paper(s):</u>  https://science.sciencemag.org/content/370/6523/eaaz3136
  
 
='''About Us'''=
 
='''About Us'''=

Revision as of 01:23, 3 February 2021

This Week - 05 February 2021 (9:30 a.m., via Zoom)

Speaker: Peyman Golshani

Title: “ Perirhinal input to neocortical layer 1 controls learning.”

Abstract: Hippocampal output influences memory formation in the neocortex, but this process is poorly understood because the precise anatomical location and the underlying cellular mechanisms remain elusive. Here, we show that perirhinal input, predominantly to sensory cortical layer 1 (L1), controls hippocampal-dependent associative learning in rodents. This process was marked by the emergence of distinct firing responses in defined subpopulations of layer 5 (L5) pyramidal neurons whose tuft dendrites receive perirhinal inputs in L1. Learning correlated with burst firing and the enhancement of dendritic excitability, and it was suppressed by disruption of dendritic activity. Furthermore, bursts, but not regular spike trains, were sufficient to retrieve learned behavior. We conclude that hippocampal information arriving at L5 tuft dendrites in neocortical L1 mediates memory formation in the neocortex.

Relevant Paper(s): https://science.sciencemag.org/content/370/6523/eaaz3136

About Us

Introduction

The Integrative Center for Learning and Memory (ICLM) is a multidisciplinary center of UCLA labs devoted to understanding the neural basis of learning and memory and its disorders. This will require a unified approach across different levels of analysis, including;

1. Elucidating the molecular cellular and systems mechanisms that allow neurons and synapses to undergo the long-term changes that ultimately correspond to 'neural memories'.

2. Understanding how functional dynamics and computations emerge from complex circuits of neurons, and how plasticity governs these processes.

3. Describing the neural systems in which different forms of learning and memory take place, and how these systems interact to ultimately generate behavior and cognition.

History of ICLM

The Integrative Center for Learning and Memory formally LMP started in its current form in 1998, and has served as a platform for many interactions and collaborations within UCLA. A key event organized by the group is the weekly ICLM Journal Club. For more than 10 years, graduate students, postdocs, principal investigators, and invited speakers have presented on topics ranging from the molecular mechanisms of synaptic plasticity, through computational models of learning, to behavior and cognition. Dean Buonomano oversees the ICLM journal club with help of student/post doctoral organizers. For other events organized by ICLM go to http://www.iclm.ucla.edu/Events.html.

Current Organizers:

Megha Sehgal (Silva Lab) & Giselle Fernandes (Silva Lab)

Current Faculty Advisor:

Dean Buonomano


Past Organizers:

i) Anna Matynia(Aug 2004 - Jun 2008) (Silva Lab)

ii) Robert Brown (Aug 2008 - Jun 2009) (Balleine Lab)

iii) Balaji Jayaprakash (Aug 2008 - Nov 2011) (Silva Lab)

iv) Justin Shobe & Thomas Rogerson (Dec 2011 - June 2013) (Silva Lab)

v) Walt Babiec (O'Dell Lab) (2013-2014)

vi) Walt Babiec (O'Dell Lab) & Helen Motanis (Buonomano Lab) (2014-2017)

vii) Helen Motanis (Buonomano Lab) & Shonali Dhingra (Mehta Lab) (2017-2018)

viii) Shonali Dhingra (Mehta Lab) (2018-2020)

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