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Neuroanatomy of basic cognitive function
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Mark J. Ashley, Jessica G. Ashley, Matthew J. Ashley
Memory consolidation implies a progression of staging of memory with variations in strength and reliability of memories across time. Consolidation occurs at the synaptic level and the systemic level. Much has been done recently to investigate the biological mechanisms of memory consolidation. Synaptic tagging was identified as a factor in the synaptic consolidation process whereby requisite proteins for protein synthesis necessary for LTP accumulate in confined regions within the dendrite until LTP is instituted.132,133 Genetic networks have been identified that, through upregulation or downregulation, are active in memory consolidation and memory retrieval and are necessary constituents in both.134 Memory is most recently viewed as a complex biological process whereby networks of neurons and genes function as the neurophysiological basis for memory.134 Genetic alteration in response to memory formation may be considered at both the synaptic and systemic levels of consolidation. At the systemic level of consolidation, information is stored in places other than the originally implicated synapses. Information is also altered once stored in systemic consolidation, seemingly comprised of a more synapse-efficient process.
Noradrenergic gating of long-lasting synaptic potentiation in the hippocampus: from neurobiology to translational biomedicine
Published in Journal of Neurogenetics, 2018
Peter V. Nguyen, Jennifer N. Gelinas
Impaired noradrenergic innervation of the hippocampus resulting from neurodegeneration of the LC occurs in the late stages of several dementias, including Alzheimer’s disease (AD; for review, see Weinshenker, 2018). Animal models of AD often express impaired hippocampal LTP and defective hippocampus-dependent memory (for instance, Li et al., 2017; Liu et al., 2008), and some evidence suggests that noradrenergic supplementation can improve memory in such models (Rorabaugh et al., 2017). Because AD pathology in the hippocampus blocks generation of adenylyl-cyclase mediated LTP (Bisel, Henkins, & Parfitt, 2007) and impairs expression of synaptic tagging/capture (Li et al., 2017), it is possible that disruption in β-AR modulation of synaptic state could decrease the likelihood of robust long-term memory in this disorder. Significant LC neural loss also occurs in Parkinson’s disease (PD), but the contribution of noradrenergic hippocampal synaptic plasticity to PD’s cognitive and mood symptoms remains to be fully explored (Weinshenker, 2018). Indeed, the ability of β-AR activation to facilitate LTP in the dentate gyrus decreases with rat age, in keeping with a change in neuromodulator-dependent learning that may be exacerbated by disease states (Twarkowski & Manahan-Vaughan, 2016).