Altered Plasticity in Hippocampal CA1, But Not Dentate Gyrus, Following Long-Term Environmental Enrichment

2010 ◽  
Vol 103 (6) ◽  
pp. 3320-3329 ◽  
Author(s):  
Michael J. Eckert ◽  
David K. Bilkey ◽  
Wickliffe C. Abraham

Exposure to an enriched environment can improve cognitive functioning in normal animals as well as in animal models of neurological disease and impairment. However, the physiological processes that mediate these changes are poorly understood. Previously we and others have found changes in hippocampal synaptic transmission and plasticity after 2–4 wk of enrichment although others have not observed effects. To determine whether long-term enrichment produces more robust changes, we housed rats continuously in an enriched environment for a minimum of 3 mo and then tested for effects on hippocampal physiology in vitro and in vivo. Enriched housing improved spatial learning compared with social and isolated housing, but surprisingly this was not accompanied by changes in basal synaptic transmission in either CA1 or the dentate gyrus as measured either in vitro or in vivo. This lack of change may reflect the operation of homeostatic mechanisms that keep global synaptic weights within a narrow range. In tests of synaptic plasticity, the induction of long-term potentiation was not changed in either CA1 or the dentate gyrus. However, in CA1 of enriched rats, there was less long-term depression in stratum radiatum, less depotentiation in stratum oriens, and altered paired-pulse inhibition of population spikes evoked in stratum oriens. These effects suggest that there are altered synaptic and network dynamics in hippocampal CA1 that contribute to the enrichment-related cognitive improvement.

Author(s):  
Julia Muellerleile ◽  
Matej Vnencak ◽  
Angelo Ippolito ◽  
Dilja Krueger-Burg ◽  
Tassilo Jungenitz ◽  
...  

Abstract Neuroligin-3 (Nlgn3), a neuronal adhesion protein implicated in autism spectrum disorder (ASD), is expressed at excitatory and inhibitory postsynapses and hence may regulate neuronal excitation/inhibition balance. To test this hypothesis, we recorded field excitatory postsynaptic potentials (fEPSPs) in the dentate gyrus of Nlgn3 knockout (KO) and wild-type mice. Synaptic transmission evoked by perforant path stimulation was reduced in KO mice, but coupling of the fEPSP to the population spike was increased, suggesting a compensatory change in granule cell excitability. These findings closely resemble those in neuroligin-1 (Nlgn1) KO mice and could be partially explained by the reduction in Nlgn1 levels we observed in hippocampal synaptosomes from Nlgn3 KO mice. However, unlike Nlgn1, Nlgn3 is not necessary for long-term potentiation. We conclude that while Nlgn1 and Nlgn3 have distinct functions, both are required for intact synaptic transmission in the mouse dentate gyrus. Our results indicate that interactions between neuroligins may play an important role in regulating synaptic transmission and that ASD-related neuroligin mutations may also affect the synaptic availability of other neuroligins.


2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
James E. Orfila ◽  
Nicole McKinnon ◽  
Myriam Moreno ◽  
Guiying Deng ◽  
Nicholas Chalmers ◽  
...  

Ischemic long-term potentiation (iLTP) is a form of synaptic plasticity that occurs in acute brain slices following oxygen-glucose deprivation. In vitro, iLTP can occlude physiological LTP (pLTP) through saturation of plasticity mechanisms. We used our murine cardiac arrest and cardiopulmonary resuscitation (CA/CPR) model to produce global brain ischemia and assess whether iLTP is induced in vivo, contributing to the functionally relevant impairment of pLTP. Adult male mice were subjected to CA/CPR, and slice electrophysiology was performed in the hippocampal CA1 region 7 or 30 days later. We observed increased miniature excitatory postsynaptic current amplitudes, suggesting a potentiation of postsynaptic AMPA receptor function after CA/CPR. We also observed increased phosphorylated GluR1 in the postsynaptic density of hippocampi after CA/CPR. These data support the in vivo induction of ischemia-induced plasticity. Application of a low-frequency stimulus (LFS) to CA1 inputs reduced excitatory postsynaptic potentials in slices from mice subjected to CA/CPR, while having no effects in sham controls. These results are consistent with a reversal, or depotentiation, of iLTP. Further, depotentiation with LFS partially restored induction of pLTP with theta burst stimulation. These data provide evidence for iLTP following in vivo ischemia, which occludes pLTP and likely contributes to network disruptions that underlie memory impairments.


2015 ◽  
Vol 210 (5) ◽  
pp. 771-783 ◽  
Author(s):  
Norbert Bencsik ◽  
Zsófia Szíber ◽  
Hanna Liliom ◽  
Krisztián Tárnok ◽  
Sándor Borbély ◽  
...  

Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is dependent on PKD activity. Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation. We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.


2004 ◽  
Vol 370 (2-3) ◽  
pp. 155-159 ◽  
Author(s):  
Tatsuhiro Akaishi ◽  
Ken Nakazawa ◽  
Kaoru Sato ◽  
Yasuo Ohno ◽  
Yoshihisa Ito

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