With this updated model, early stress in the form of CA induces neu-rodevelopmental modifications that are triggered by the nature of the experiences during critical, sensitive stages. These changes are, in effect, an adaptive response that is intended to allow individuals who are exposed to such stress to become accustomed to elevated levels of stress or deprivation throughout life. Assuming that the development of memory hinges on certain brain regions and systems (e.g., hippocampus), memory processes are thus predicted to be negatively impacted when CA occurs during those time frames of sensitivity for those very regions and systems. In other words, depending in part on the chronological or developmental age when CA happens, disparate memorial outcomes will arise. If an individual is born into a harsh, cruel, and stress-ridden environment, the sequelae of CA on later development may serve as an adaptation whereby the individual can call upon memory processes and skills to guide behavior for survival. In contrast, these modifications are less optimal for thriving in more benevolent circumstances in which memory is needed to succeed in prosocial endeavors.
The consequences of corticosteroids are also hypothesized to be a primary mechanism for this altered trajectory of neurodevelopment. Not surprisingly, the hippocampus possesses a high density of glucocorticoid receptors (Patel et al., 2000) and plays, in concert, a major role in memory processing, specifically the encoding and retrieval of episodic information ( Desgranges, Baron, & Eustache, 1998; Squire & Zola-Morgan, 1991). This brain region has been shown to be particularly vulnerable to prolonged exposure to stress hormones (Sapolsky, Krey, & McEwen, 1985). Pyramidal cell morphology alterations, pyramidal cell death, and suppression of new granule cell production can all be effected by exposure to stress or corticosteroids (Gould & Tanapat, 1999; Sapolsky, Uno, Rebert, & Finch, 1990). Conversely, evolution may have played a role in keeping the maturing hippocampus intact. Known as the "stress hyporesponsive" period in rodents (Oliver, Boudouresque, Lacroix, Anglade, & Grino, 1994), this early, postnatal developmental window prohibits a sizeable glucocor-ticoid response to a large number of stressors, which in turn protects the hippocampus from overexposure to glucocorticoids. Thus, memory processes that rely on hippocampal function may be safeguarded develop-mentally from the effects of CA—evidence to date supports this premise (see further on)—although deficits in memory may become unmasked at a later point in time.
Lastly, we postulate that CA influences neurodevelopment specific to the sensory modalities to which the abuse is delivered and received. That is, neural systems unique to auditory (including verbal), visual, tactile, olfactory, and kinesthetic stimulation are hypothesized to be negatively impacted depending on which stimuli are encoded. In a coming section, we provide preliminary evidence that the effects of exposure to CA preferentially rely on different sensory modalities for encoding experiences and environments.
Specifically, the left primary and secondary visual cortices seem especially sensitive to the consequences of childhood sexual abuse, which apparently is associated with a decrement in visual recognition memory.
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