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Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Figure 6.17 illustrates a model for the sequence of events leading to structural changes following the triggering of LTP. AMPA receptors are phosphorylated and inserted into the postsynaptic membrane causing an increase, in about 10 minutes after LTP induction, of the postsynaptic density (PSD) or active area of the postsynaptic membrane with attendant expansion of the presynaptic terminal. This is diagrammatically indicated in the change from Figure 6.17a to Figure 6.17b. About 30 minutes after LTP induction, the postsynaptic area splits into smaller areas in what are termed perforated synapses (Figure 6.17c). This is followed one to two hours after LTP induction by the formation of multiple spine boutons (MSBs) sharing the same presynaptic terminal (Figure 6.17d). Eventually, this leads to presynaptic remodeling and new synapses, with each of the newly formed spines having its own presynaptic terminal. It is believed that with disuse the reverse process of reduction in the number of synapses takes place.
Protein Kinase C Signal Transmission During Aging
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
Fiorenzo Battaini, Stefano Govoni, Marco Trabucchi
Data in monkeys have demonstrated that in areas important for visual processing, PKC γ follows an increased gradient (up to 10 times in expression of the immunoreactive protein) in parallel with the elaboration of visual input. Such a gradient, on the other hand, is not evident with the α and β isoforms that are expressed constantly throughout visual processing in cortical pathways.93 These data point to the importance of PKC γ in visual information memory. Accordingly, evidence in rodents exists correlating different kinds of learning with specific translocation of the PKC γ isoform in various brain areas.94,95 A different approach was taken by Tonegawa’s group. They generated a mouse mutant lacking PKC γ and investigated the importance of this PKC isoform in synaptic plasticity and learning paradigms. Their results indicate that PKC γ is a regulatory component for long-term synaptic changes96 and that mild changes in learning are dependent on the expression of this isoform.97 In addition, data from the Routtenberg laboratory have pointed to the importance of PKC γ in the process of stabilization of synapses after LTP induction.98 Our data showing that PKC γ is increased in aged rats at a hippocampal level could be reconciled with the possibility that the increase in PKC γ in aged rats might be detrimental for physiologic enzyme translocation. Analysis of specific isoform translocation could clarify this point and is one focus of our current experiments.
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
Long-term potentiation (LTP) occurring in the hippocampus serves as a component of synaptic consolidation. LTP in the hippocampus is largely dependent upon dopaminergic availability.76 Some authors suggest dopamine receptor (D1/D5) activation serves to initiate intracellular second messenger accumulation, functioning more in a modulatory role.77 There actually may be a synergistic role between D1/D5 receptor activation and N-methyl-D-aspartate (NDMA) receptor activation for LTP induction.78
Differential inhibitory effects of resveratrol on excitotoxicity and synaptic plasticity: involvement of NMDA receptor subtypes
Published in Nutritional Neuroscience, 2021
Chung-Pin Hsieh, Wei-Tang Chang, Linyi Chen, Hwei-Hsien Chen, Ming-Huan Chan
The previous study has indicated that resveratrol at 22 μM did not affect HFS-induced LTP [59]. Consistently, our data further demonstrated that resveratrol at 100 μM could not alter hippocampal LTP elicited by HFS. It is noted that LTP induction depends on high amplitude of NMDAR activation. NR2A-containing NMDARs are required for HFS-induced LTP, but not LFS-evoked LTD in hippocampal slices, whereas induction of LTD but not LTP requires the activation of NR2B-containing NMDARs [7]. Thus, selective inhibition of NMDARs by NR2A antagonists abolished LTP but not LTD induction. In contrast, preferential blockade of NMDARs by NR2B antagonists prevented LTD induction without affecting LTP production [7]. However, NR2A and NR2B subtypes may both be involved in LTP induction, since NR2B antagonist partially inhibited LTP induction in developing hippocampus with a high ratio of NR2B/2A [60]. Importantly, hippocampal LTP induction may not be altered under partial inhibition of NMDAR activity (less than 40%) either by NR2A or NR2B antagonists or by both in mature animal [61]. Our data show that resveratrol is highly selective for NR2B subtype, but has a much lower inhibitory effect on NR2A subtype. According to the evidence, it suggests that the differential inhibitory efficacy of resveratrol on NMDAR subtypes might be not sufficient to suppress LTP-induced by HFS in the mature hippocampus.
Phytohormone abscisic acid ameliorates cognitive impairments in streptozotocin-induced rat model of Alzheimer's disease through PPARβ/δ and PKA signaling
Published in International Journal of Neuroscience, 2019
Ali Khorasani, Mehdi Abbasnejad, Saeed Esmaeili-Mahani
In addition, recent studies have shown that ABA also acts as an activator of the cAMP/PKA signaling pathway [18,32]. Molecular studies have shown the importance of the cAMP/PKA/CREB pathway for synaptic plasticity and learning and memory [65]. Additionally, animals with the impairments in either PKA or CREB show changes in synaptic plasticity and long-term potentiation [66,67]. PKA is a key molecule for the induction of LTP because of the PKA antagonist could reduce LTP induction [68]. Some animal models of AD showed that there is a significant correlation between reduced PKA‐CREB signaling and learning and memory impairment [69,70]. It also has been reported that PKA-dependent phosphorylation of the transcription factor CREB is attenuated by Aβ administration, and can be restored by pharmacological agents that upregulate cAMP/PKA signaling [71]. The activation of PKA induces protective effects against synaptic and behavioral deficiencies in AD through the inhibition of tau hyperphosphorylation [72]. Therefore, it seems that PKA-dependent signaling are generally involved in memory processes and especially in the ABA-promoting effects on learning and memory in STZ-treated rat.
DL-3-n-butylphthalide (NBP) ameliorates cognitive deficits and CaMKII-mediated long-term potentiation impairment in the hippocampus of diabetic db/db mice
Published in Neurological Research, 2019
Ming Gao, Suxiao Ji, Jie Li, Songyun Zhang
The impairment of cognition in diabetes includes reduced information processing speed and impaired memory, attention, and executive functioning [6,7]. Impaired memory and decreased studying ability are related to long-term potentiation (LTP) in neurons. LTP induction in hippocampal area CA1 occurs during learning and can last for a long period [8], making it likely to be a mechanism involved in memory. The process of LTP at hippocampal CA1 synapses is initiated by brief periods of high-frequency presynaptic stimulation. Then, glutamate, the neurotransmitter that is released at these synapses, activates postsynaptic NMDA-type glutamate receptors (NMDARs) and AMPA-type glutamate receptors (AMPARs) [9]. The opening of NMDARs during the induction of LTP leads to calcium entry, which activates calcium/calmodulin-dependent protein kinase II (CaMKII). CaMKII subsequently translocates to the postsynaptic membrane and produces potentiation by phosphorylating subunits of AMPARs and increasing the number of AMPARs at the postsynaptic membrane [10]. NMDAR subtype 2B (NR2B) and AMPAR subtype 1 (GluR1) are pivotal subunits of NMDAR and AMPAR, respectively, in reinforcing LTP [10]. Therefore, we imply that cognitive deficits in T2DM may be caused by deterioration of CaMKII-mediated LTP in the hippocampal CA1 area.