Neurobiology of learning and memory
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Neurobiol Learn Mem · Sep 2020
Electrophysiological correlates of interference control at retrieval predict performance on a subsequent analogical reasoning task.
Previous research has shown that variations in the accessibility of relevant information that stem from retrieval practice may impair analogical reasoning. In the present study, we sought to examine the neural signatures of inhibitory control during selective retrieval and its effects on a subsequent analogical reasoning task by employing electrophysiological measures. At a behavioral level, we found that selective retrieval of a subset of potential solutions led to impaired performance on the analogy test. ⋯ During the analogy test, the production of control solutions (non-affected by prior retrieval practice) was characterized by more positive modulations of anterior frontal and parietal ERPs than the production of unstudied solutions, whereas inhibited solutions elicited similar amplitudes to unstudied solutions. This effect was restricted to the retrieval phase of the analogy where the actual solutions had to be retrieved, but it did not affect the mapping phase where the accessibility status of the possible solutions failed to reveal significant amplitude differences. These findings suggest that control during selective retrieval may lead to the downregulation of competing memory representations and advance our understanding of the neural correlates of analogical thinking.
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Neurobiol Learn Mem · Nov 2019
Pathobiology of Christianson syndrome: Linking disrupted endosomal-lysosomal function with intellectual disability and sensory impairments.
Christianson syndrome (CS) is a recently described rare neurogenetic disorder presenting early in life with a broad range of neurological symptoms, including severe intellectual disability with nonverbal status, hyperactivity, epilepsy, and progressive ataxia due to cerebellar atrophy. CS is due to loss-of-function mutations in SLC9A6, encoding NHE6, a sodium-hydrogen exchanger involved in the regulation of early endosomal pH. Here we review what is currently known about the neuropathogenesis of CS, based on insights from experimental models, which to date have focused on mechanisms that affect the CNS, specifically the brain. ⋯ In addition, the sensory issues exhibited by Slc9a6 KO mice, in combination with our neuropathological findings, are consistent with NHE6 loss of function impacting the entire nervous system. Sensory dysfunction in intellectually disabled individuals is challenging to assess and may impair patient safety and quality of life. Further mechanistic studies of the neurological impairments underlying CS and other genetic intellectual disability disorders must also take into account mechanisms affecting broader nervous system function in order to understand the full range of associated disabilities.
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Neurobiol Learn Mem · Jul 2019
Nitric oxide blockade in mediodorsal thalamus impaired nicotine/ethanol-induced memory retrieval in rats via inhibition of prefrontal cortical pCREB/CREB signaling pathway.
Reciprocal connections between the mediodorsal thalamic nucleus (MD) and the prefrontal cortex (PFC) are important for memory processes. Since the co-abuse of nicotine and ethanol affects memory formation, this study investigated the effect of nitric oxide inhibition in the MD on memory retrieval induced by co-administration of nicotine and ethanol. Subsequently, western blot analysis was used to evaluate how this change would alter the PFC pCREB/CREB signaling pathway. ⋯ Interestingly, the inhibitory effect of L-NAME and the potentiating effect of l-arginine on nicotine response were associated with the decrease and increase of the PFC p-CREB/CREB ratio respectively. It can be concluded that MD-PFC connections are involved in the combined effects of nicotine and ethanol on memory retrieval. The mediodorsal thalamic NO system possibly mediated this interaction via the pCREB/CREB signaling pathways in the PFC.
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Neurobiol Learn Mem · Jan 2019
High fat diet increases cognitive decline and neuroinflammation in a model of orexin loss.
Midlife obesity is a risk factor for cognitive decline and is associated with the earlier onset of Alzheimer's disease (AD). Diets high in saturated fat potentiate the onset of obesity, microglial activation, and neuroinflammation. Signaling deficiencies in the hypothalamic peptide orexin and/or orexin fiber loss are linked to neurodegeneration, cognitive impairment, and neuroinflammation. ⋯ Additionally, O/A3 mice had increased gene expression of the microglial activation marker Iba-1 (measured via qRT-PCR, p < 0.001). Further characterization of the microglial immune response genes in hippocampal tissue revealed a significant increase in CX3 chemokine receptor 1 (CX3CR1), tumor necrosis factor-alpha (TNF-α) and the mitochondria-associated enzyme immune responsive gene-1 (Irg1). Collectively, our results indicate that orexin loss impairs memory, and that HFD accelerates hippocampus-dependent learning deficits and the onset of neuroinflammation.
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Neurobiol Learn Mem · Oct 2018
ReviewHippocampal network oscillations as mediators of behavioural metaplasticity: Insights from emotional learning.
Behavioural metaplasticity is evident in experience-dependent changes of network activity patterns in neuronal circuits that connect the hippocampus, amygdala and medial prefrontal cortex. These limbic regions are key structures of a brain-wide neural network that translates emotionally salient events into persistent and vivid memories. Communication in this network by-and-large depends on behavioural state-dependent rhythmic network activity patterns that are typically generated and/or relayed via the hippocampus. ⋯ The hippocampal circuits that contribute to these network activities, at the same time, are subject to both Hebbian and non-Hebbian forms of plasticity during memory formation. Further, it has become evident that adaptive changes in the hippocampus-dependent network activity patterns provide an important means of adjusting synaptic plasticity. We here summarise our current knowledge on how these processes in the hippocampus in interaction with amygdala and medial prefrontal cortex mediate the formation and persistence of emotional memories.