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Extensive long-term verbal memory training is associated with brain plasticity.

ABSTRACT: The human brain has a remarkable capacity to store a lifetime of information through visual or auditory routes. It excels and exceeds any artificial memory system in mixing and integrating multiple pieces of information encoded. In this study, a group of verbal memory experts was evaluated by multiple structural brain analysis methods to record the changes in the brain structure. The participants were professional Hindu pandits (priests/scholars) trained in reciting Vedas and other forms of Hindu scriptures. These professional Vedic priests are experts in memorization and recitation of oral texts with precise diction. Vedas are a collection of hymns. It is estimated that there are more than 20,000 mantras and shlokas in the four Vedas. The analysis included the measurement of the grey and white matter density, gyrification, and cortical thickness in a group of Vedic pandits and comparing these measures with a matched control group. The results revealed an increased grey matter (GM) and white matter (WM) in the midbrain, pons, thalamus, parahippocampus, and orbitofrontal regions in pandits. The whole-brain corelation analysis using length of post-training teaching duration showed significant correlation with the left angular gyrus. We also found increased gyrification in the insula, supplementary motor area, medial frontal areas, and increased cortical thickness (CT) in the right temporal pole and caudate regions of the brain. These findings, collectively, provide unique information regarding the association between crucial memory regions in the brain and long-term practice of oral recitation of scriptures from memory with the proper diction that also involved controlled breathing.

SUBMITTER: Kumar U

PROVIDER: S-EPMC8102627 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:UnlabelledAlterations in cAMP signaling are thought to contribute to neurocognitive and neuropsychiatric disorders. Members of the cAMP-specific phosphodiesterase 4 (PDE4) family, which contains >25 different isoforms, play a key role in determining spatial cAMP degradation so as to orchestrate compartmentalized cAMP signaling in cells. Each isoform binds to a different set of protein complexes through its unique N-terminal domain, thereby leading to targeted degradation of cAMP in specific intracellular compartments. However, the functional role of specific compartmentalized PDE4 isoforms has not been examined in vivo Here, we show that increasing protein levels of the PDE4A5 isoform in mouse hippocampal excitatory neurons impairs a long-lasting form of hippocampal synaptic plasticity and attenuates hippocampus-dependent long-term memories without affecting anxiety. In contrast, viral expression of a truncated version of PDE4A5, which lacks the unique N-terminal targeting domain, does not affect long-term memory. Further, overexpression of the PDE4A1 isoform, which targets a different subset of signalosomes, leaves memory undisturbed. Fluorescence resonance energy transfer sensor-based cAMP measurements reveal that the full-length PDE4A5, in contrast to the truncated form, hampers forskolin-mediated increases in neuronal cAMP levels. Our study indicates that the unique N-terminal localization domain of PDE4A5 is essential for the targeting of specific cAMP-dependent signaling underlying synaptic plasticity and memory. The development of compounds to disrupt the compartmentalization of individual PDE4 isoforms by targeting their unique N-terminal domains may provide a fruitful approach to prevent cognitive deficits in neuropsychiatric and neurocognitive disorders that are associated with alterations in cAMP signaling.Significance statementNeurons exhibit localized signaling processes that enable biochemical cascades to be activated selectively in specific subcellular compartments. The phosphodiesterase 4 (PDE4) family coordinates the degradation of cAMP, leading to the local attenuation of cAMP-dependent signaling pathways. Sleep deprivation leads to increased hippocampal expression of the PDE4A5 isoform. Here, we explored whether PDE4A5 overexpression mimics behavioral and synaptic plasticity phenotypes associated with sleep deprivation. Viral expression of PDE4A5 in hippocampal neurons impairs long-term potentiation and attenuates the formation of hippocampus-dependent long-term memories. Our findings suggest that PDE4A5 is a molecular constraint on cognitive processes and may contribute to the development of novel therapeutic approaches to prevent cognitive deficits in neuropsychiatric and neurocognitive disorders that are associated with alterations in cAMP signaling.

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Extensive long-term verbal memory training is associated with brain plasticity.

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