24 research outputs found

    Learning in deep neural networks and brains with similarity-weighted interleaved learning

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    Understanding how the brain learns throughout a lifetime remains a long-standing challenge. In artificial neural networks (ANNs), incorporating novel information too rapidly results in catastrophic interference, i.e., abrupt loss of previously acquired knowledge. Complementary Learning Systems Theory (CLST) suggests that new memories can be gradually integrated into the neocortex by interleaving new memories with existing knowledge. This approach, however, has been assumed to require interleaving all existing knowledge every time something new is learned, which is implausible because it is time-consuming and requires a large amount of data. We show that deep, nonlinear ANNs can learn new information by interleaving only a subset of old items that share substantial representational similarity with the new information. By using such similarity-weighted interleaved learning (SWIL), ANNs can learn new information rapidly with a similar accuracy level and minimal interference, while using a much smaller number of old items presented per epoch (fast and data-efficient). SWIL is shown to work with various standard classification datasets (Fashion-MNIST, CIFAR10, and CIFAR100), deep neural network architectures, and in sequential learning frameworks. We show that data efficiency and speedup in learning new items are increased roughly proportionally to the number of nonoverlapping classes stored in the network, which implies an enormous possible speedup in human brains, which encode a high number of separate categories. Finally, we propose a theoretical model of how SWIL might be implemented in the brain

    Transforming growth factor β recruits persistent MAPK signaling to regulate long-term memory consolidation in Aplysia californica.

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    In this study, we explore the mechanistic relationship between growth factor signaling and kinase activity that supports the protein synthesis-dependent phase of long-term memory (LTM) consolidation for sensitization ofAplysia Specifically, we examine LTM for tail shock-induced sensitization of the tail-elicited siphon withdrawal (T-SW) reflex, a form of memory that requires both (i) extracellular signal-regulated kinase (ERK1/2; MAPK) activity within identified sensory neurons (SNs) that mediate the T-SW and (ii) the activation of transforming growth factor β (TGFβ) signaling. We now report that repeated tail shocks that induce intermediate-term (ITM) and LTM for sensitization, also induce a sustained post-training phase of MAPK activity in SNs (lasting at least 1 h). We identified two mechanistically distinct phases of post-training MAPK: (i) an immediate phase that does not require ongoing protein synthesis or TGFβ signaling, and (ii) a sustained phase that requires both protein synthesis and extracellular TGFβ signaling. We find that LTM consolidation requires sustained MAPK, and is disrupted by inhibitors of protein synthesis and TGFβ signaling during the consolidation window. These results provide strong evidence that TGFβ signaling sustains MAPK activity as an essential mechanistic step for LTM consolidation

    Early impairment of thalamocortical circuit activity and coherence in a mouse model of Huntington's disease

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    Huntington's disease (HD) is a progressive, fatal neurodegenerative disorder characterized by motor, cognitive, and psychiatric disturbances. There is no known cure for HD, but its progressive nature allows for early therapeutic intervention. Currently, much of the research has focused on the striatum, however, there is evidence suggesting that disruption of thalamocortical circuits could underlie some of the early symptoms of HD. Loss of both cortical pyramidal neurons (CPNs) and thalamic neurons occurs in HD patients, and cognitive, somatosensory, and attention deficits precede motor abnormalities. However, the role of thalamocortical pathways in HD progression has been understudied. Here, we measured single unit activity and local field potentials (LFPs) from electrode arrays implanted in the thalamus and primary motor cortex of 4–5 month-old male and female Q175 mice. We assessed neuronal activity under baseline conditions as well as during presentation of rewards delivered via actuation of an audible solenoid valve. HD mice showed a significantly delayed licking response to the reward stimulus. At the same time, neuronal activation to the reward was delayed in thalamic neurons, CPNs and fast-spiking cortical interneurons (FSIs) of HD mice. In addition, thalamocortical coherence increased at lower frequencies in HD relative to wildtype mice. Together, these data provide evidence that impaired cortical and thalamic responses to reward stimuli, and impaired thalamocortical coherence, may play an important early role in motor, cognitive, and learning deficits in HD patients. ⓒ 2021 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).1
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