Learned Fears

Fear learning allows organisms to channel their behavioral resources so they can evaluate potential threats and seek safety effectively. While the FEAR system has various intrinsic sensitivities (e.g., being aroused by painful and predatory stimuli), it also has the ability to become fearfully responsive to new inputs that inform the organisms about environmental events that may predict dangers. Organisms are prepared to make fearful associations to certain stimuli but not others (Ohman and Mineka, 2001). Autonomic fear responses classically condition more rapidly when electric shock is paired with angry faces than when paired with smiling ones (Ohman et al., 1989). Thus, it seems likely that the neural systems that decode angry emotional expressions have evolution-arily privileged and/or environmentally "sensitized" inputs to FEAR circuitry (Adolphs et al., 1994).

There is bound to be enormous variety in such sensory-perceptual channels to the FEAR system among different species. While humans are prepared to develop fears to dark and high places, approaching mean-faced strangers, as well as spiders and snakes, rats are more prone to fear well-illuminated, open spaces, the smell of cats, and other predators. But neutral stimuli, as well as fantasies in humans, may also probably come to conditionally access the FEAR system. During the past decade, several investigators have unraveled how environmental conditioning proceeds in the amygdala as a function of specific learning mechanisms.

Neutral lights and tones paired with painful shock can access the headwater of FEAR circuitry fairly directly through low-road thalamic sensory analyzers as well as the more complex high-road perceptual analyzers of the neocortex. With regard to the low road, there are direct anatomical connections from the medial geniculate of the thalamus to the central nucleus of amygdala, and with regard to the high road less direct neocortical ones (Davis et al., 1995; LeDoux et al., 1990). If one combines both affective and cognitive measures in an animal fear-learning paradigm, one can demonstrate that manipulations that reduce the unconditional emotional indicators (e.g., freezing) can be dissociated from the cognitive choices animals make to avoid fear stimuli (Killcross et al., 1997; Nader and LeDoux, 1997). This issue is especially important at a human level, where one can obviously have a cognitive appreciation of what is dangerous without feeling much trepidation, and vice versa.

The intraamygdaloid synaptic mechanisms by which fear learning transpires is being detailed (LeDoux, 2000). Fear associations are heavily influenced by gluta-matergic synapses (Schafe et al., 2001) as well as 6-adrenergic ones concentrated in the amygdala (Cahill et al., 1994). However, the FEAR system has multiple perceptual inputs. For instance, while the amygdalae primarily harvest information from discreet environmental cues, more complex spatial information is linked to contextual fear conditioning via the hippocampus (Fanselow et al., 1994; Phillips and Le Doux, 1992). Also, it remains likely that some conditioning can be elaborated at hypothala-mic and mesencephalic levels of the FEAR circuit, but that work is in the preliminary stages (e.g., De Oca et al., 1998).

As investigators work out the details of the associative mechanisms, new ideas should emerge about how one might de-condition learned fears with the assistance of neurochemical interventions (Muller et al., 1997). For instance, the consolidation of fearful memories is controlled by a glutamate-dependent synaptic facilitation process, as are all memories (Schafe et al., 2001). Thus, it comes as no surprise that the extinction of conditioned fears, which is an active learning process, is also mediated by the same chemistries (Falls et al., 1992). This suggests that existing fears will need to be de-conditioned by an active form of new learning mediated by the same synaptic chemistries (glutamate) as the original learning, making global neurochemical interventions in glutamatergic systems unlikely interventions for helping erase fearful memories. Many of the neuropeptides discussed above are concentrated in these circuits, but little is presently known about how they participate in the elaboration of learning. The possibility that other manipulations of these associative networks, for instance, by the menagerie of anxiolytic neuropeptides such as opioids and neu-ropeptide Y (Chapter 21), might be able to specifically facilitate the diminution of fearful, but not other types of memories, continues to intrigue scientists who study fear learning.

Getting to Know Anxiety

Getting to Know Anxiety

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