Coexistence of Multiple Types of Synaptic Plasticity in Individual Hippocampal CA1 Pyramidal Neurons

Abstract

Understanding learning and memory mechanisms is an important goal in neuroscience. To gain insights into the underlying cellular mechanisms for memory formation, synaptic plasticity processes are studied with various techniques in different brain regions. A valid model to scrutinize different ways to enhance or decrease synaptic transmission is recording of long-term potentiation (LTP) or long-term depression (LTD). At the single cell level, spike timing-dependent plasticity (STDP) protocols have emerged as a powerful tool to investigate synaptic plasticity with stimulation paradigms that also likely occur during memory formation in vivo. Such kind of plasticity can be induced by different STDP paradigms with multiple repeat numbers and stimulation patterns. They subsequently recruit or activate different molecular pathways and neuromodulators for induction and expression of STDP. Dopamine (DA) and brain-derived neurotrophic factor (BDNF) have been recently shown to be important modulators for hippocampal STDP at Schaffer collateral (SC)-CA1 synapses and are activated exclusively by distinguishable STDP paradigms. Distinct types of parallel synaptic plasticity in a given neuron depend on specific subcellular molecular prerequisites. Since the basal and apical dendrites of CA1 pyramidal neurons are known to be heterogeneous, and distance-dependent dendritic gradients for specific receptors and ion channels are described, the dendrites might provide domain specific locations for multiple types of synaptic plasticity in the same neuron. In addition to the distinct signaling and expression mechanisms of various types of LTP and LTD, activation of these different types of plasticity might depend on background brain activity states. In this article, we will discuss some ideas why multiple forms of synaptic plasticity can simultaneously and independently coexist and can contribute so effectively to increasing the efficacy of memory storage and processing capacity of the brain. We hypothesize that resolving the subcellular location of t-LTP and t-LTD mechanisms that are regulated by distinct neuromodulator systems will be essential to reach a more cohesive understanding of synaptic plasticity in memory formation.

Microarray Analysis of microRNAs Expression Profiles in Adult and Aged Mice Hippocampus

“…Experimental data confirm this assumption, because the expression of synaptic plasticity, including LTP and LTD of synaptic transmission, is altered in the brain of memory deficient aged animals [42] [43]. Through bioinformation analysis, here from 10 months old to 20 months old ageing process, miR-15b, miR-195 may bind with Grin1 mRNA; miR-30c, miR-125a-5p, miR-125b-5p may bind with Grin2a mRNA; miR-125a-5p, miR-125b-5p, miR-9 may bind with Rhoq mRNA; miR-101b may bind with Grm1 mRNA; and miR-23a, miR-23b, miR-30c may bind with Grm5 mRNA, and these miRNAs may be involved in the regulation of LTP related signal pathways (Table 3, Figure 5(B)).…”

Synergistic Gating of Electro‐Iono‐Photoactive 2D Chalcogenide Neuristors: Coexistence of Hebbian and Homeostatic Synaptic Metaplasticity

“…These distinct types of parallel synaptic plasticity also reflect specific subcellular molecular prerequisites and depend on background brain activity states. For example, dopamine and brain‐derived neurotrophic factor modulates unique hippocampal STDP at Schaffer collateral‐CA1 synapses . To the best of our knowledge, this is the first demonstration of interplay between multimodal synaptic signatures achieved in a single neural element.…”

Remembering rewarding futures: A simulation‐selection model of the hippocampus

“…Then, after sufficient exploration, the synapses between those CA3 and CA1 neurons with overlapping place fields near a reward (or non‐reward) location should be strongly (or weakly) potentiated via activity‐dependent synaptic plasticity. Even though precise rules and factors governing CA3–CA1 STDP are not fully understood (Edelmann, Cepeda‐Prado, & Lessmann, ; Kwag & Paulsen, ; Nishiyama, Togashi, Aihara, & Hong, ; Sugisaki, Fukushima, Tsukada, & Aihara, ; Tsukada, Aihara, Kobayashi, & Shimazaki, ; Wittenberg & Wang, ), CA3/CA1 place cell spike patterns recorded in freely moving rats induced long‐term potentiation at CA3–CA1 synapses, demonstrating naturally occurring spike patterns during navigation can potentiate CA3–CA1 synapses (Isaac, Buchanan, Muller, & Mellor, ). Such activity‐dependent synaptic weight changes may lead to the preferential replaying of rewarding sequences, both experienced and unexperienced, in CA1 during subsequent offline SWR episodes (Figure b–d).…”

“…An alternative possibility is that the CA3 projections to CA1 mediate both its value‐related activity and subsequent role in filtering. For example, dopamine may control synaptic transmission (Rosen, Cheung, & Siegelbaum, ) and/or plasticity (Edelmann et al, ; Frey & Morris, ; Frey, Schroeder, & Matthies, ; Li, Cullen, Anwyl, & Rowan, ; Navakkode, Sajikumar, & Frey, ; O'Carroll & Morris, ; Otmakhova & Lisman, ) in CA3–CA1 connections in a value‐dependent manner (Figure ). The putative dopamine concentration gradient during exploration (Howe et al, ) may control the transmission/plasticity of CA3–CA1 connections during exploration such that CA1 neurons show value‐dependent neural activity during exploration and also mediate preferential replays of high‐value sequences during an offline state (Figure ).…”