Long‐term plasticity in the hippocampus: maintaining within and ‘tagging’ between synapses

Abstract

Synapses between neurons are malleable biochemical structures, strengthening and diminishing over time dependent on the type of information they receive. This phenomenon known as synaptic plasticity underlies learning and memory, and its different forms, Long-Term Potentiation (LTP) and Long-Term Depression (LTD) perform varied cognitive roles in reinforcement, relearning and associating memories. Moreover, both LTP and LTD can exist in an early transient form (early-LTP/LTD) or a late persistent form (late-LTP/LTD), which are triggered by different induction protocols, and also differ in their dependence on protein synthesis and the involvement of key molecular players. Beyond homosynaptic modifications, synapses can also interact with one another. This is encapsulated in the Synaptic Tagging and Capture hypothesis (STC), where synapses expressing early-LTP/LTD present a 'tag' that can capture the protein synthesis products generated during a temporally proximal late-LTP/LTD induction. This 'tagging' phenomenon forms the framework of synaptic interactions in various conditions, and accounts for the cellular basis of the time-dependent associativity of short-lasting and long-lasting memories. All these synaptic modifications take place under controlled neuronal conditions, regulated by subcellular elements such as epigenetic regulation, proteasomal degradation and neuromodulatory signals. Here, we review current understanding of the different forms of synaptic plasticity and its regulatory mechanisms in the hippocampus, a brain region critical for memory formation. We also discuss expression of plasticity in hippocampal CA2 area, a long-overlooked narrow hippocampal subfield, and the behavioural correlate of STC. Lastly, we put forth perspectives for an integrated view of memory representation in synapses.

Fisetin ameliorates cognitive impairment by activating mitophagy and suppressing neuroinflammation in rats with sepsis‐associated encephalopathy

“… 22 Based on recent studies, many brain areas, including the cortex, thalamus, hippocampus, striatum, basal ganglia, and corpus callosum could be affected by CLP. 23 , 24 , 25 Of note, the hippocampus region has a close association with cognitive impairment, 26 so the hippocampus tissue was selected for our research. As demonstrated in this study, septic rats showed significant cognitive deficits, including prolonged escape latency, increased escape passage, reduced frequency of cross to the platform, and enlarged neuronal apoptosis.…”

Donor Engineering Tuning the Analog Switching Range and Operational Stability of Organic Synaptic Transistors for Neuromorphic Systems

“…In contrast to STP, long‐term plasticity (LTP) plays an important role in memory and learning through altering the synaptic weight more persistently. [ 44 ] The STP can be transformed into LTP after continuous neuronal stimulation or repeated training. To simulate the transition process from STP to LTP, a series of presynaptic voltages with fixed pulse amplitude (−1.5 V) and duration (20 ms) were applied to the TOSTs.…”

Neuroimmune Mechanisms Underlying Neuropathic Pain: The Potential Role of TNF-α-Necroptosis Pathway

“…Clinical studies have shown that chronic pain accompanied by a reduction in the hippocampal volume can significantly reduce the learning ability of the body [221,222], resulting in short-and long-term memory defects [223]. At present, the widely accepted theory for the mechanism of pain-impaired memory is the alteration of hippocampal synaptic plasticity (long-term potentiation [LTP]), which is considered the molecular mechanism underlying learning and memory [224,225] or that underlying the effects of pain on memory [117,219]. In addition, morphological and biochemical changes in the hippocampal region underlie cognitive impairment in neuropathic pain [226].…”