Ll changes brain arousal. Plasticity also occurs in the central nucleus of the amygdala (84?6) and in CS sensory processing areas (87). At the cellular and molecular levels, fear conditioning occurs when LA neurons that process the CS are weakly activated at the same time that the US strongly depolarizes the neurons (5, 53, 80, 81, 88, 89). This results in an increase in the strength of the synapses that process the CS, allowing it to more effectively activate amygdala circuits. Molecular mechanisms engaged result in gene expression and protein synthesis, stabilizing temporary changes in synaptic strength and creating longterm memories. Many of the molecular findings were pursued following leads from invertebrate work (14, 77, 90). Fear conditioning thus became a process that is carried out by cells, synapses, and molecules in specific circuits of the nervous system. As such, fear conditioning is explainable solely in terms of associations created and stored via cellular, synaptic, and molecular plasticity mechanisms in amygdala circuits. When the CS later occurs, it activates the association and leads to the expression of species-typical defensive responses that prepare the organism to cope with the danger signaled by the CS. There is no need for conscious feelings of fear to intervene. The circuit function is the intervening variable. Yet, I and others muddied the waters by continuing to call the circuits involved in detecting and responding to threats the fear system (4, 19, 54). Nonconscious Lumicitabine site Conditioned Fear in Humans Embedded in the intervening variable approach was the assumption that the relevant factors (the observable facts) in the brain could in principle be accounted for in introspecting and nonintrospecting organisms. And the neuroscience perspective described above provided a biological account that made it unnecessary to call upon conscious fear to account for the data. However, findings from studies of fear conditioning in humans made it unnecessary to further tiptoe around consciousness, because the relation between conscious and nonconscious processing can be directly evaluated in our species. Research on patients with brain damage revealed that fear conditioning creates implicit (nonconscious) memories that are distinct from explicit/declarative (conscious) memory (4, 5, 91, 92). Thus, damage to the hippocampus in humans disrupts explicit conscious memory of having been conditioned but has no effect on fear conditioning itself, whereas damage to the amygdala disrupts fear conditioning but not the conscious memory of having been conditioned (93, 94). Furthermore, behavioral studies in healthy humans have found that conditioned or unconditioned threats presented subliminally elicit physiological responses NS-018 web without the person being aware of the stimulus (95?LeDoux99) and without reporting any particular feeling, even when instructed to try to introspect about feelings (98). The conditioning process can also be carried out nonconsciously (99?01) and without awareness of the CS S contingency (102). Acquisition effects are sometimes weaker (101), but this is likely attributable to the degraded input required to prevent awareness than to the limits of nonconscious processing per se because complex cognitive and social processes that control human behavior are often carried out without conscious awareness of their occurrence in daily life (103?05). Also, functional imaging studies have shown that the amygdala is activated when.Ll changes brain arousal. Plasticity also occurs in the central nucleus of the amygdala (84?6) and in CS sensory processing areas (87). At the cellular and molecular levels, fear conditioning occurs when LA neurons that process the CS are weakly activated at the same time that the US strongly depolarizes the neurons (5, 53, 80, 81, 88, 89). This results in an increase in the strength of the synapses that process the CS, allowing it to more effectively activate amygdala circuits. Molecular mechanisms engaged result in gene expression and protein synthesis, stabilizing temporary changes in synaptic strength and creating longterm memories. Many of the molecular findings were pursued following leads from invertebrate work (14, 77, 90). Fear conditioning thus became a process that is carried out by cells, synapses, and molecules in specific circuits of the nervous system. As such, fear conditioning is explainable solely in terms of associations created and stored via cellular, synaptic, and molecular plasticity mechanisms in amygdala circuits. When the CS later occurs, it activates the association and leads to the expression of species-typical defensive responses that prepare the organism to cope with the danger signaled by the CS. There is no need for conscious feelings of fear to intervene. The circuit function is the intervening variable. Yet, I and others muddied the waters by continuing to call the circuits involved in detecting and responding to threats the fear system (4, 19, 54). Nonconscious Conditioned Fear in Humans Embedded in the intervening variable approach was the assumption that the relevant factors (the observable facts) in the brain could in principle be accounted for in introspecting and nonintrospecting organisms. And the neuroscience perspective described above provided a biological account that made it unnecessary to call upon conscious fear to account for the data. However, findings from studies of fear conditioning in humans made it unnecessary to further tiptoe around consciousness, because the relation between conscious and nonconscious processing can be directly evaluated in our species. Research on patients with brain damage revealed that fear conditioning creates implicit (nonconscious) memories that are distinct from explicit/declarative (conscious) memory (4, 5, 91, 92). Thus, damage to the hippocampus in humans disrupts explicit conscious memory of having been conditioned but has no effect on fear conditioning itself, whereas damage to the amygdala disrupts fear conditioning but not the conscious memory of having been conditioned (93, 94). Furthermore, behavioral studies in healthy humans have found that conditioned or unconditioned threats presented subliminally elicit physiological responses without the person being aware of the stimulus (95?LeDoux99) and without reporting any particular feeling, even when instructed to try to introspect about feelings (98). The conditioning process can also be carried out nonconsciously (99?01) and without awareness of the CS S contingency (102). Acquisition effects are sometimes weaker (101), but this is likely attributable to the degraded input required to prevent awareness than to the limits of nonconscious processing per se because complex cognitive and social processes that control human behavior are often carried out without conscious awareness of their occurrence in daily life (103?05). Also, functional imaging studies have shown that the amygdala is activated when.