The Emergence of Emotions

Emotion is conscious experience. It is the affective aspect of consciousness. Emotion arises from sensory stimulation and is typically accompanied by physiological and behavioral changes in the body. Hence an emotion is a complex reaction pattern consisting of three components: a physiological component, a behavioral component, and an experiential (conscious) component. The reactions making up an emotion determine what the emotion will be recognized as. Three processes are involved in generating an emotion: (1) identification of the emotional significance of a sensory stimulus, (2) production of an affective state (emotion), and (3) regulation of the affective state. Two opposing systems in the brain (the reward and punishment systems) establish an affective value or valence (stimulus-reinforcement association) for sensory stimulation. This is process (1), the first step in the generation of an emotion. Development of stimulus-reinforcement associations (affective valence) serves as the basis for emotion expression (process 2), conditioned emotion learning acquisition and expression, memory consolidation, reinforcement-expectations, decision-making, coping responses, and social behavior. The amygdala is critical for the representation of stimulus-reinforcement associations (both reward and punishment-based) for these functions. Three distinct and separate architectural and functional areas of the prefrontal cortex (dorsolateral prefrontal cortex, orbitofrontal cortex, anterior cingulate cortex) are involved in the regulation of emotion (process 3). The regulation of emotion by the prefrontal cortex consists of a positive feedback interaction between the prefrontal cortex and the inferior parietal cortex resulting in the nonlinear emergence of emotion. This positive feedback and nonlinear emergence represents a type of working memory (focal attention) by which perception is reorganized and rerepresented, becoming explicit, functional, and conscious. The explicit emotion states arising may be involved in the production of voluntary new or novel intentional (adaptive) behavior, especially social behavior

The neuroanatomical basis of slow saccades in spinocerebellar ataxia type 2 (Wadia-subtype)

In a case of spinocerebellar ataxia type 2, Wadia-subtype (SCA2), with slow horizontal saccades, we used parvalbumin immunohistochemistry to identify the omnipause (OPNs) excitatory (EBNs), and inhibitory burst neurons (IBNs) of the saccade generator. Nissl sections was used to measure neuronal diameters, and synaptophysin staining to estimate of synaptic density on the cell somata. Morphometric and synaptic density measurements of the abducens motoneurons were identical in SCA2 and the control. A significant cell loss and reduced synaptic density on somata was found only in the EBN area. We conclude that degeneration of the EBNs is the most likely cause for the slowing of horizontal saccades