Hippocampus
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Neuropsychologists have clearly implicated the hippocampus in the consolidation of memory, particularly episodic memory, the mental replay of past experiences. When recorded from behaving animals, by far the most obvious firing pattern of the primary neurons of the hippocampus is the place field: a cell tends to fire only when the animal's head is in a particular part of its environment. ⋯ However, we are currently still at a loss to explain how the firing of hippocampal neurons contributes to hippocampal function. This review seeks to examine the commonalities between place cells and episodic memory, and posits that an analogy can be made between the stabilization of place fields and the consolidation of memory.
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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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Traumatic brain injury (TBI) is a significant health issue that often causes enduring cognitive deficits, in particular memory dysfunction. The hippocampus, a structure crucial in learning and memory, is frequently damaged during TBI. Since long-term potentiation (LTP) is the leading cellular model underlying learning and memory, this study was undertaken to examine how injury affects area CA1 LTP in mice using lateral fluid percussion injury (FPI). ⋯ This study demonstrates that injury leads to significantly smaller N-methyl-D-aspartate potentials and glutamate-induced excitatory currents, increased dendritic spine size, and decreased expression of alpha-calcium calmodulin kinase II. These findings may underlie the injury-induced lack of LTP and thus, contribute to cognitive impairments often associated with TBI. Furthermore, these results provide attractive sites for potential therapeutic intervention directed toward alleviating the devastating consequences of human TBI.
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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.