Two different forms of long-term potentiation at CA1 subiculum 2025

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A variety of electrical stimulation protocols including the HFS, TBS and PBs stimulation are used to induce LTP in the hippocampus area CA1. Among them, the PBs is based on two prominent physiological features of the hippocampus, the complex spike discharge and the theta rhythm.
The subiculum can be distinguished from the proximally situated CA1 and the distally situated presubiculum by a principle cell layer that is more loosely packed. The border with CA1 is further demarcated by the widening of the middle layer of the subiculum. The principle cell layer contains large pyramidal cells.
Long-term depression (LTD) is the opposite of LTP, and is characterized by a decrease in postsynaptic strength. This happens by dephosphorylation of AMPA receptors and the facilitation of their movement away from the synaptic junction.
Pathway Summary A majority of synapses that experience LTP (e.g. in the hippocampus) involve a postsynaptic increase in calcium which is mediated through activation of the ionotropic glutamate receptor N-methyl-D-aspartic acid (NMDA) receptor.
1 Long-term potentiation. LTP, which is defined as a persistent increase in synaptic strength, can be either NMDA receptor-dependent or NMDA receptor-independent. LTP can also be divided into three sequential phases: short term potentiation, early LTP (E-LTP), and late LTP (L-LTP).
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LTP can be initiated by depolarizing postsynaptic neurons, activating NMDA receptor channels, and allowing the influx of Ca2+ into the postsynaptic neuron. Different protocols, such as high-frequency or theta burst stimulation, can be used to induce LTP.
Two distinct forms of long-term depression (LTD), one dependent on the activation of NMDA receptors (NMDARs) and the other dependent on the activation of metabotropic glutamate receptors (mGluRs), are shown to coexist in CA1 hippocampal pyramidal cells of juvenile (1135 day-old) rats.
It is generally accepted that at CA1 hippocampal synapses, NMDA receptors provide the foremost source of Ca2+ for LTP induction following stimulation frequencies near the threshold for synaptic modification (Johnston et al., 1992; Cavus and Teyler, 1996).

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