Hippocampus
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Neuronal mechanisms of episodic memory, the conscious recollection of autobiographical events, are largely unknown because electrophysiological studies in humans are conducted only in exceptional circumstances. Unit recording studies in animals are thus crucial for understanding the neurophysiological substrate that enables people to remember their individual past. Two features of episodic memory--autonoetic consciousness, the self-aware ability to "travel through time", and one-trial learning, the acquisition of information in one occurrence of the event--raise important questions about the validity of animal models and the ability of unit recording studies to capture essential aspects of memory for episodes. ⋯ We propose that the most powerful strategy for investigating neurophysiological mechanisms of episodic memory entails recording unit activity in brain areas homologous to those required for episodic memory in humans (e.g., hippocampus and prefrontal cortex) as animals perform tasks with explicitly defined episodic-like aspects. Within this framework, empirical data suggest that the basic structure of episodic memory is a temporally extended representation that distinguishes the beginning from the end of an event. Future research is needed to fully understand how neural encodings of context, sequences of items/events, and goals are integrated within mnemonic representations of autobiographical events.
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Infants passively exposed to morphine or heroin through their addicted mothers usually develop characteristic withdrawal syndrome of morphine after birth. In such early life, the central nervous system exhibits significant plasticity and can be altered by various prenatal influences, including prenatal morphine exposure. Here we studied the effects of prenatal morphine exposure on postsynaptic density protein 95 (PSD-95), an important cytoskeletal specialization involved in the anchoring of the NMDAR and neuronal nitric oxide synthase (nNOS), of the hippocampal CA1 subregion from young offspring at postnatal day 14 (P14). ⋯ Collectively, the study demonstrates that maternal exposure to morphine decreases the magnitude of PSD-95, nNOS, the phosphorylation of CREB(Serine-133), and LTD expression in hippocampal CA1 subregion of young offspring (e.g., P14). Such alterations within the developing brain may play a role for subsequent neurological impairments (e.g., impaired performance of long-term learning and memory). The results raise a possibility that postsynaptic density proteins could serve an important role, at least in part, for the neurobiological pathogenesis in offspring from the morphine-addicted mother and provide tentative therapeutic strategy.
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Neural activity often becomes rhythmic during mental processing. But there has been no direct proof that rhythmicity, per se, is important for mental function. We assessed this issue in relation to the contribution of hippocampal theta-frequency rhythmicity to learning in the Morris water maze by blocking theta (and other septal inputs to the hippocampus) and then using electrical stimulation to restore rhythmicity. ⋯ The results suggest that the precise frequency of rhythmicity may be important for hippocampal function. Functional rhythmicity needs, therefore, to be included in neural models of cognitive processing. The success of our procedure also suggests that simple alterations of rhythmicity could be used to ameliorate deficits in learning and memory. (c) 2006 Wiley-Liss, Inc.
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Gelsolin is an actin-binding protein that regulates actin filament-severing and capping activity in the various processes of cell motilities. Here, we report the expression of gelsolin mRNA and protein in the hippocampus following transections of the entorhinal afferents. ⋯ Double labeling of either gelsolin mRNA or protein with markers of glial cells (Griffonia simplicifolia IB4 and CD11b for microglial cells, GFAP for astroglial cells) revealed that gelsolin was highly expressed by both activated microglia and astrocytes. The results suggest that the spatiotemporal upregulation of gelsolin in the hippocampus is induced by entorhinal deafferentation, and that gelsolin would participate in the activation processes of both microglial and astroglial cells and thereby, indirectly play important roles in the subsequent lesion-induced neural reorganization in the hippocampus following entorhinal deafferentation.