How do the hippocampus and amygdala interact with thalamocortical systems to regulate cognitive and cognitive-emotional learning? Why do lesions of thalamus, amygdala, hippocampus, and cortex have differential effects depending on the phase of learning when they occur? In particular, why is the hippocampus typically needed for trace conditioning, but not delay conditioning, and what do the exceptions reveal? Why do amygdala lesions made before or immediately after training decelerate conditioning while those made later do not? Why do thalamic or sensory cortical lesions degrade trace conditioning more than delay conditioning? Why do hippocampal lesions during trace conditioning experiments degrade recent but not temporally remote learning? Why do orbitofrontal cortical lesions degrade temporally remote but not recent or post-lesion learning? How is temporally graded amnesia caused by ablation of prefrontal cortex after memory consolidation? How are attention and consciousness linked during conditioning? How do neurotrophins, notably brain-derived neurotrophic factor (BDNF), influence memory formation and consolidation? Is there a common output path for learned performance? A neural model proposes a unified answer to these questions that overcome problems of alternative memory models.
How do the hippocampus and amygdala interact with thalamocortical systems to regulate cognitive and cognitive-emotional learning? Why do lesions of thalamus, amygdala, hippocampus, and cortex have differential effects depending on the phase of learning when they occur? In particular, why is the hippocampus typically needed for trace conditioning, but not delay conditioning, and what do the exceptions reveal? Why do amygdala lesions made before or immediately after training decelerate conditioning while those made later do not? Why do thalamic or sensory cortical lesions degrade trace conditioning more than delay conditioning? Why do hippocampal lesions during trace conditioning experiments degrade recent but not temporally remote learning? Why do orbitofrontal cortical lesions degrade temporally remote but not recent or post-lesion learning? How is temporally graded amnesia caused by ablation of prefrontal cortex after memory consolidation? How are attention and consciousness linked during conditioning? How do neurotrophins, notably brain-derived neurotrophic factor (BDNF), influence memory formation and consolidation? Is there a common output path for learned performance? A neural model proposes a unified answer to these questions that overcome problems of alternative memory models.
“…We also would like to highlight the differences between our contribution and those presented in SOVEREIGN [1]. The authors of that study modeled a neural network that was based on characteristics of the animals' visual apparatus.…”
Section: Controller and Behaviormentioning
confidence: 96%
“…Traditionally, the problem of synthetic vision of autonomous agents (robots and virtual characters) has been approached with attempts to build models capable of preprocessing the sensor signals and drive the motor actions of the agents [1,2]. Another line of investigation tries to work with internal mental maps that represent the character's environment, where calculations can be made so that the agent can guide itself through the world.…”
“…Embodied agents need to be able to autonomously and adaptively interact with their environment. Grossberg presents a large-scale visuomotor architecture: the Self-Organizing, Vision, Expectation, Recognition, Emotion, Intelligent, Goal-oriented Navigation model (SOVEREIGN; Gnadt and Grossberg, 2008). This architecture consists of several sensory, motor and memory components and is able to perform motor sequences under different motivational states as well as to learn more efficient sequences in response to rewards.…”
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