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  • It is becoming clear that many of the functional asymmetries discussed in levitra sold online this chapter are in functions for which nonhuman primates are well adapted. ACKNOWLEDGMENTS We gratefully acknowledge support from the McDonnell-Pew Foundation in Cognitive Neuroscience , the International Human Frontier Science Program , and the National Institutes of Health (Grant Nos. Now, with the identification of a first set of asymmetry genes, we have ability to study carefully their conservation in nonhuman primates and understand the evolution of asymmetry. The only functional asymmetry for which a corresponding structural asymmetry has been supported by a body of converging evidence is that of language and Broca’s area, in spite of the large number of frontal lobe functions that appear lateralized. A detailed study of the degree of lateralization in these nonlanguage functions and their anatomical correlates in primates levitra sold online should provide important insights into the evolutionary origins of frontal lobe asymmetries, thus.

    Our emerging notions of the mirror neuron system provides one salient example of how such work can be accomplished. How functional asymmetries in sensorimotor integration in humans correspond to language lateralization in individual subjects should be of great interest, in the same vein. We anticipate that as physiological and anatomical studies in primates, and functional imaging studies in humans, continue to aid in the segregation of functional units within the frontal lobe, the morphological, physiological, and molecular asymmetries that contribute to these functional asymmetries will be elucidated.

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    Lu et al., levitra sold online 1999, 2002). Noradrenergic functional antagonists also blocked footshock-induced reinstatement (Erb et al., 1997. Reversible activation of both the central nucleus of the amygdala and the BNST with tetrodotoxin blocked the footshock-induced reinstatement of heroin responding , however.

    This effect appeared to levitra sold online be mediated by CRF1 receptors (Shaham et al., 1995. Suggesting that an important origin of the CRF terminals in the BNST for cocaine-induced reinstatement was the central nucleus of the amygdala , an asymmetric lesion procedure to functionally disconnect the CRF-containing pathway from the central nucleus of the amygdala to the BNST significantly reduced footshock-induced reinstatement. The brain site responsible for the actions of CRF antagonists on cocaine reinstatement appeared to be the ventral BNST since infusions of CRF into this area reinstate responding, and local administration of CRF antagonists into the ventral BNST blocked footshock-induced reinstatement, though administration into the central nucleus of the amygdala was without effect (Erb and Stewart, 1999).

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