Developmental onset of enduring long‐term potentiation in mouse hippocampus

Abstract

Analysis of long-term potentiation (LTP) provides a powerful window into cellular mechanisms of learning and memory. Prior work shows late LTP (L-LTP), lasting >3 hr, occurs abruptly at postnatal day 12 (P12) in the stratum radiatum of rat hippocampal area CA1. The goal here was to determine the developmental profile of synaptic plasticity leading to L-LTP in the mouse hippocampus. Two mouse strains and two mutations known to affect synaptic plasticity were chosen: C57BL/6J and Fmr1 −/y on the C57BL/6J background, and 129SVE and Hevin −/− (Sparcl1 −/−) on the 129SVE background. Like rats, hippocampal slices from all of the mice showed test pulse-induced depression early during development that was gradually resolved with maturation by 5 weeks. All the mouse strains showed a gradual progression between P10-P35 in the expression of short-term potentiation (STP), lasting ≤1 hr. In the 129SVE mice, L-LTP onset (>25% of slices) occurred by 3 weeks, reliable L-LTP

Gut dysbiosis impairs hippocampal plasticity and behaviors by remodeling serum metabolome

“…Subsequently, we evaluated whether disruption of gut microbiota exerted any effect on long-term potentiation (LTP) of synaptic transmission, the main form of synaptic plasticity, as a cellular substrate of learning and memory. 31 The field excitatory postsynaptic potentials (fEPSPs) were recorded. Application of a brief high-frequency stimulation (tetanus) induced LTP of fEPSP in vehicle-treated group, whereas only transient increase of fEPSP was observed in antibiotic-treated mice Figure 4c , indicating an impaired LTP.…”

Disturbed Balance of Inhibitory Signaling Links Hearing Loss and Cognition

“…The increased hemodynamic BOLD fMRI response during this critical time period is linked with pronounced neurovascular and systemic changes, including increases in vascular density, synaptogenesis, energy metabolism, and sensitivity of the cerebral microcirculation to vasoactive stimuli (Nehlig et al, 1989;Colonnese et al, 2008;Goyal et al, 2014;Engl et al, 2017;Iadecola, 2017). The time of increased hemodynamic BOLD fMRI responses is also the time when in rodents, long-term potentiation in the hippocampus gradually matures (Ostrovskaya et al, 2020). (A) Independent of aging or differences in hearing thresholds, cochlear synaptopathy can differ, depending on whether de-afferentation due to low-SR auditory nerve fiber loss dominates (A, low-SR in light green) or high-SR auditory nerve fiber loss dominates (B, high-SR in orange).…”

“…The increased hemodynamic BOLD fMRI response during this critical time period is linked with pronounced neurovascular and systemic changes, including increases in vascular density, synaptogenesis, energy metabolism, and sensitivity of the cerebral microcirculation to vasoactive stimuli ( Nehlig et al, 1989 ; Colonnese et al, 2008 ; Goyal et al, 2014 ; Engl et al, 2017 ; Iadecola, 2017 ). The time of increased hemodynamic BOLD fMRI responses is also the time when in rodents, long-term potentiation in the hippocampus gradually matures ( Ostrovskaya et al, 2020 ).…”

Maternal gastrointestinal nematode infection alters hippocampal neuroimmunity, promotes synaptic plasticity, and improves resistance to direct infection in offspring.

“…Calcium in ux triggers post-synaptic biochemical cascades, through activation of calcium/calmodulin-dependent protein kinase II (CaMKII), protein kinase C (PKC), and mitogen-activated protein kinases (MAPK), that results in the phosphorylation and insertion of additional AMPARs into the post-synaptic membrane, thus strengthening the synaptic response to future glutamate release [19][20][21] . LTP in the mouse hippocampal slice preparation is found in the second postnatal week [22] ; however depending on strain, this can be delayed until 4-to 5-weeks [23] . Neuroin ammation inhibits LTP, whereas several immunoregulatory factors can promote LTP [24] ; as H. bakeri induces an immunoregulatory response, we hypothesized that maternal H. bakeri infection will induce an immunoregulatory response in the offspring hippocampus, promoting hippocampal LTP to explain the earlier development of spatial memory in the offspring of infected dams [10] .…”