6 results on '"De-Lin Pu"'
Search Results
2. A thalamocortical top-down circuit for associative memory
- Author
-
Henning Sprekeler, Teresa Spanò, Johannes J. Letzkus, M. Belén Pardi, Friedrich Kretschmer, De-Lin Pu, Laura Bella Naumann, Johanna Vogenstahl, and Tamas Dalmay
- Subjects
Patch-Clamp Techniques ,Computer science ,Thalamus ,Neocortex ,Sensory system ,Optogenetics ,Auditory cortex ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Calcium imaging ,Memory ,Neural Pathways ,medicine ,Animals ,030304 developmental biology ,Auditory Cortex ,0303 health sciences ,Multidisciplinary ,Association Learning ,Content-addressable memory ,Associative learning ,Mice, Inbred C57BL ,medicine.anatomical_structure ,Synapses ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Higher-order thalamus input to the cortex Sensory information can only be used meaningfully in the brain when integrated with and compared with internally generated top-down signals. However, we know little about the brainwide afferents that convey such top-down signals, their information content, and learning-related plasticity. Pardi et al. identified the higher-order thalamus as a major source of top-down input to mouse auditory cortex and investigated a circuit in cortical layer 1 that facilitates plastic changes and flexible responses. These results demonstrate how top-down feedback information can reach cortical areas through a noncortical structure that has received little attention despite its widespread connections with the cortex. Science , this issue p. 844
- Published
- 2020
3. The interhemispheric CA1 circuit governs rapid generalisation but not fear memory
- Author
-
Jing-Fei Huang, Xiaobing He, Gui-Jing Xiong, Lingjiang Li, Ning-Ning Song, Heng Zhou, Gal Richter-Levin, Qi-Xin Zhou, Liang Jing, Xun Tang, Lin Xu, Fuqiang Xu, Rong-Rong Mao, Yu-Qiang Ding, and De-Lin Pu
- Subjects
Male ,0301 basic medicine ,Fear memory ,Computer science ,Generalization ,Science ,Long-Term Potentiation ,General Physics and Astronomy ,Optogenetics ,Article ,Generalization, Psychological ,General Biochemistry, Genetics and Molecular Biology ,Encoding specificity principle ,Rats, Sprague-Dawley ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Memory ,Encoding (memory) ,Conditioning, Psychological ,Neural Pathways ,Animals ,lcsh:Science ,CA1 Region, Hippocampal ,Multidisciplinary ,Recall ,Synaptic efficacy ,Long-term potentiation ,Fear ,General Chemistry ,Rats ,Mice, Inbred C57BL ,030104 developmental biology ,Mental Recall ,Models, Animal ,Synapses ,lcsh:Q ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Encoding specificity theory predicts most effective recall by the original conditions at encoding, while generalization endows recall flexibly under circumstances which deviate from the originals. The CA1 regions have been implicated in memory and generalization but whether and which locally separated mechanisms are involved is not clear. We report here that fear memory is quickly formed, but generalization develops gradually over 24 h. Generalization but not fear memory is impaired by inhibiting ipsilateral (ips) or contralateral (con) CA1, and by optogenetic silencing of the ipsCA1 projections onto conCA1. By contrast, in vivo fEPSP recordings reveal that ipsCA1–conCA1 synaptic efficacy is increased with delay over 24 h when generalization is formed but it is unchanged if generalization is disrupted. Direct excitation of ipsCA1–conCA1 synapses using chemogenetic hM3Dq facilitates generalization formation. Thus, rapid generalization is an active process dependent on bilateral CA1 regions, and encoded by gradual synaptic learning in ipsCA1–conCA1 circuit., Previous work has documented a slow form of memory generalization although a rapid one is demanded. Here the authors elucidate the role of the interhemispheric CA1-CA1 projection in a form of rapid generalization of contextual fear memory via gradual potentiation of these synapses over 24 h.
- Published
- 2017
4. A Critical Role for Neocortical Processing of Threat Memory
- Author
-
Johannes J. Letzkus, Tamas Dalmay, Julijana Gjorgjieva, Philip Tovote, Jan Hartung, Jérémy Signoret-Genest, Sebastian Onasch, De-Lin Pu, Yave R. Lozano, Elisabeth Abs, and Rogier B. Poorthuis
- Subjects
0301 basic medicine ,Male ,Population ,Sensory system ,Neocortex ,Biology ,Optogenetics ,Auditory cortex ,Amygdala ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Calcium imaging ,Memory ,Cortex (anatomy) ,medicine ,Animals ,Learning ,education ,education.field_of_study ,Behavior, Animal ,General Neuroscience ,Fear ,Associative learning ,Mice, Inbred C57BL ,030104 developmental biology ,medicine.anatomical_structure ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Summary Memory of cues associated with threat is critical for survival and a leading model for elucidating how sensory information is linked to adaptive behavior by learning. Although the brain-wide circuits mediating auditory threat memory have been intensely investigated, it remains unclear whether the auditory cortex is critically involved. Here we use optogenetic activity manipulations in defined cortical areas and output pathways, viral tracing, pathway-specific in vivo 2-photon calcium imaging, and computational analyses of population plasticity to reveal that the auditory cortex is selectively required for conditioning to complex stimuli, whereas the adjacent temporal association cortex controls all forms of auditory threat memory. More temporal areas have a stronger effect on memory and more neurons projecting to the lateral amygdala, which control memory to complex stimuli through a balanced form of population plasticity that selectively supports discrimination of significant sensory stimuli. Thus, neocortical processing plays a critical role in cued threat memory.
- Published
- 2019
5. Learning-Related Plasticity in Dendrite-Targeting Layer 1 Interneurons
- Author
-
Karl-Klaus Conzelmann, Dahlia Kushinsky, Rogier B. Poorthuis, De Lin Pu, Daniella Apelblat, M. Belén Pardi, Karzan Muhammad, Elisabeth Abs, Leona Enke, Johannes J. Letzkus, Max Ferdinand Eizinger, and Ivo Spiegel
- Subjects
Male ,0301 basic medicine ,Mice, 129 Strain ,Conditioning, Classical ,Mice, Transgenic ,Dendrite ,Sensory system ,Optogenetics ,Biology ,Article ,03 medical and health sciences ,Mice ,Organ Culture Techniques ,0302 clinical medicine ,Calcium imaging ,Neurotrophic factors ,Memory ,medicine ,top-down processing ,Learning ,Animals ,ddc:610 ,somatostatin interneurons ,NDNF interneurons ,Neuronal Plasticity ,Neocortex ,fear learning ,interneurons ,General Neuroscience ,layer 1 ,Dendrites ,Fear ,Mice, Inbred C57BL ,GABAergic interneurons ,Electrophysiology ,030104 developmental biology ,medicine.anatomical_structure ,dendritic inhibition ,neocortical circuits ,Disinhibition ,connectivity ,genetic markers ,medicine.symptom ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Summary A wealth of data has elucidated the mechanisms by which sensory inputs are encoded in the neocortex, but how these processes are regulated by the behavioral relevance of sensory information is less understood. Here, we focus on neocortical layer 1 (L1), a key location for processing of such top-down information. Using Neuron-Derived Neurotrophic Factor (NDNF) as a selective marker of L1 interneurons (INs) and in vivo 2-photon calcium imaging, electrophysiology, viral tracing, optogenetics, and associative memory, we find that L1 NDNF-INs mediate a prolonged form of inhibition in distal pyramidal neuron dendrites that correlates with the strength of the memory trace. Conversely, inhibition from Martinotti cells remains unchanged after conditioning but in turn tightly controls sensory responses in NDNF-INs. These results define a genetically addressable form of dendritic inhibition that is highly experience dependent and indicate that in addition to disinhibition, salient stimuli are encoded at elevated levels of distal dendritic inhibition. Video Abstract, Highlights • NDNF is a selective marker for neocortical layer 1 interneurons • NDNF interneurons mediate prolonged inhibition of distal pyramidal neuron dendrites • Inhibition from Martinotti cells tightly controls NDNF interneuron responses • Dendritic inhibition by NDNF interneurons is highly experience dependent, Using a selective marker for neocortical layer 1 interneurons, Abs, Poorthuis, et al. identify these little-understood cells as a powerful, highly experience-dependent source of inhibition in pyramidal neuron dendrites that is in turn controlled by activity in the local circuit.
- Published
- 2018
6. The interhemispheric CA1 circuit governs rapid generalisation but not fear memory.
- Author
-
Gui-Jing Xiong, De-Lin Pu, Rong-Rong Mao, Qi-Xin Zhou, Heng Zhou, Lin Xu, Liang Jing, Xun Tang, Richter-Levin, Gal, Ning-Ning Song, Yu-Qiang Ding, Xiao-Bing He, Fu-Qiang Xu, Jing-Fei Huang, and Ling-Jiang Li
- Subjects
CORPUS callosum ,MEMORY ,NEURON development ,FEAR ,GENERALIZATION - Abstract
Encoding specificity theory predicts most effective recall by the original conditions at encoding, while generalization endows recall flexibly under circumstances which deviate from the originals. The CA1 regions have been implicated in memory and generalization but whether and which locally separated mechanisms are involved is not clear. We report here that fear memory is quickly formed, but generalization develops gradually over 24 h. Generalization but not fear memory is impaired by inhibiting ipsilateral (ips) or contralateral (con) CA1, and by optogenetic silencing of the ipsCA1 projections onto conCA1. By contrast, in vivo fEPSP recordings reveal that ipsCA1-conCA1 synaptic efficacy is increased with delay over 24 h when generalization is formed but it is unchanged if generalization is disrupted. Direct excitation of ipsCA1-conCA1 synapses using chemogenetic hM3Dq facilitates generalization formation. Thus, rapid generalization is an active process dependent on bilateral CA1 regions, and encoded by gradual synaptic learning in ipsCA1-conCA1 circuit. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.