These data identify an extended developmental period during which neurogenesis might be modulated to significantly impact the structure and function of the dentate gyrus in adulthood. “
“In human and nonhuman primates parietal cortex is formed by a multiplicity of areas. For those of the superior parietal lobule (SPL) there exists a certain homology between man and macaques. As a consequence, optic ataxia, a disturbed visual control of hand reaching, has similar features Cyclopamine cost in man and monkeys. Establishing such correspondence has
proven difficult for the areas of the inferior parietal lobule (IPL). This difficulty depends on many factors. First, no physiological information is available in man on the dynamic properties of cells in the IPL. Second, the number of IPL areas identified in the monkey is paradoxically higher
than that so far described in man, although this issue will probably be reconsidered in future years, thanks to comparative imaging studies. Third, the consequences of parietal lesions in monkeys do not always match those observed in humans. This is another paradox if one considers that, in certain cases, the functional properties of neurons in the monkey’s IPL would predict the presence of behavioral skills, such as construction capacity, that however do not seem this website to emerge in the wild. Therefore, constructional apraxia, which is well characterized in man, has never been described
in monkeys and apes. Finally, only certain aspects, i.e. hand directional hypokinesia and gaze apraxia (Balint’s psychic paralysis of gaze), of the multifaceted syndrome hemispatial neglect have been described in monkeys. These similarities, differences and paradoxes, among many others, make the study of the evolution and function of parietal cortex a challenging case. Lesions of posterior parietal cortex (PPC) in humans result in a constellation of symptoms often referred to as the ‘parietal syndrome’ (Balint, 1909; for an historical perspective see Husain & Stein, 1988; Harvey & Milner, 1995). Since its original description the core of the parietal syndrome consisted of optic ataxia, psychic paralysis Y-27632 2HCl of gaze and impaired spatial attention, now referred to as hemispatial neglect. In subsequent years, a number of action disorders such as constructional apraxia (Kleist, 1934; Benton, 1967; De Renzi et al., 1982) have also been described after parietal damage, calling for an interpretation of the consequences of parietal lesions in terms of a general impairment of spatial cognition. A century of intensive neuropsychological study today offers a picture of the parietal syndrome (see Husain & Stein, 1988; Harvey & Milner, 1995) which is more refined than that provided by earlier studies, in at least three main respects, i.e.