From Conditioning to Emotion: Translating Animal Models of Learning to Human Psychopathology.
Aaron S HellerPublished in: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry (2019)
Emotional responses are not static but change as a consequence of learning. Organisms adapt to emotional events and these adaptations influence the way we think, behave, and feel when we encounter similar situations in the future. Integrating recent work from rodent models and research on human psychopathology, this article lays out a model describing how affective events cause learning and can lead to anxiety and depression: affective events are linked to conditioned stimuli and contexts. Affective experiences entrain oscillatory synchrony across distributed neural circuits, including the prefrontal cortex, hippocampus, amygdala, and nucleus accumbens, which form associations that constitute the basis of emotional memories. Consolidation of these experiences appears to be supported by replay in the hippocampus-a process by which hippocampal firing patterns recreate the firing pattern that occurred previously. Generalization of learning occurs to never before experienced contexts when associations form across distinct but related conditioned stimuli. The process of generalization, which requires cortical structures, can cause memories to become abstracted. During abstraction, the latent, overlapping features of the learned associations remain and result in the formation of schemas. Schemas are adaptive because they facilitate the rapid processing of conditioned stimuli and prime behavioral, cognitive, and affective responses that are the manifestations of the accumulation of an individual's conditioned experiences. However, schemas can be maladaptive when the generalization of aversive emotional responses are applied to stimuli and contexts in which affective reactions are unnecessary. I describe how this process can lead to not only mood and anxiety disorders but also psychotherapeutic treatment.
Keyphrases
- prefrontal cortex
- bipolar disorder
- endothelial cells
- mental health
- induced pluripotent stem cells
- cerebral ischemia
- autism spectrum disorder
- depressive symptoms
- pluripotent stem cells
- cognitive impairment
- physical activity
- mass spectrometry
- brain injury
- gram negative
- multidrug resistant
- blood brain barrier
- resting state