scholarly journals Cellular and molecular mechanisms involved in LTP induced by mild theta-burst stimulation in hippocampal slices from young male rats: from weaning to adulthood

2021 ◽  
Author(s):  
NC Rodrigues ◽  
A Silva-Cruz ◽  
A Caulino-Rocha ◽  
A Bento-Oliveira ◽  
JA Ribeiro ◽  
...  
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Male Rats ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Cellular Models ◽  
Erk Mapk ◽  
Ca1 Area ◽  
Theta Burst

AbstractLong-term potentiation (LTP) is a highly studied phenomenon yet the essential vs. modulatory transduction and GABAergic pathways involved in LTP elicited by theta-burst stimulation (TBS) in the CA1 area of the hippocampus are still unclear, due to the use of different TBS intensities and patterns or of different rodent/cellular models. We now characterized the essential transduction and GABAergic pathways in mild TBS-induced LTP in the CA1 area of the rat hippocampus. LTP induced by TBS (5×4) (5 bursts of 4 pulses delivered at 100Hz) lasted for up to 3h and was increasingly greater from weaning to adulthood. Stronger TBS patterns - TBS (15×4) or three TBS (15×4) separated by 6 min induced nearly maximal LTP not being the best choice to study the value of LTP-enhancing drugs. LTP induced by TBS (5×4) was fully dependent on NMDA receptor and CaMKII activity but independent on PKA or PKC activity. In addition, it was partially dependent on GABAB receptor activation and was potentiated by GABAA receptor blockade and less by GAT-1 transporter blockade. AMPA GluA1 phosphorylation on Ser831 (CaMKII target) but not GluA1 Ser845 (PKA target) was essential for LTP expression. The phosphorylation of the Kv4.2 channel was observed at Ser438 (targeted by CaMKII) but not at Thr602 or Thr607 (ERK/MAPK pathway). This suggests that cellular kinases like PKA, PKC or kinases of the ERK/MAPK family although important modulators of TBS (5×4)-induced LTP are not essential for its expression in the CA1 area of the hippocampus.

scholarly journals Augmenting saturated LTP by broadly spaced episodes of theta-burst stimulation in hippocampal area CA1 of adult rats and mice

2014 ◽  
Vol 112 (8) ◽  
pp. 1916-1924 ◽  
Author(s):  
Guan Cao ◽  
Kristen M. Harris
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Sprague Dawley ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Cellular Mechanisms ◽  
Adult Rats ◽  
Area Ca1 ◽  
Hippocampal Area ◽  
Theta Burst

Hippocampal long-term potentiation (LTP) is a model system for studying cellular mechanisms of learning and memory. Recent interest in mechanisms underlying the advantage of spaced over massed learning has prompted investigation into the effects of distributed episodes of LTP induction. The amount of LTP induced in hippocampal area CA1 by one train (1T) of theta-burst stimulation (TBS) in young Sprague-Dawley rats was further enhanced by additional bouts of 1T given at 1-h intervals. However, in young Long-Evans (LE) rats, 1T did not initially saturate LTP. Instead, a stronger LTP induction paradigm using eight trains of TBS (8T) induced saturated LTP in hippocampal slices from both young and adult LE rats as well as adult mice. The saturated LTP induced by 8T could be augmented by another episode of 8T following an interval of at least 90 min. The success rate across animals and slices in augmenting LTP by an additional episode of 8T increased significantly with longer intervals between the first and last episodes, ranging from 0% at 30- and 60-min intervals to 13–66% at 90- to 180-min intervals to 90–100% at 240-min intervals. Augmentation above initially saturated LTP was blocked by the N-methyl-d-aspartate (NMDA) glutamate receptor antagonist d-2-amino-5-phosphonovaleric acid (d-APV). These findings suggest that the strength of induction and interval between episodes of TBS, as well as the strain and age of the animal, are important components in the augmentation of LTP.

scholarly journals PKA drives an increase in AMPA receptor unitary conductance during LTP in the hippocampus

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Pojeong Park ◽  
John Georgiou ◽  
Thomas M. Sanderson ◽  
Kwang-Hee Ko ◽  
Heather Kang ◽  
...  
Keyword(s):  
Ampa Receptors ◽  
Single Channel ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Theta Burst Stimulation ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Necessary And Sufficient ◽  
Theta Burst

AbstractLong-term potentiation (LTP) at hippocampal CA1 synapses can be expressed by an increase either in the number (N) of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors or in their single channel conductance (γ). Here, we have established how these distinct synaptic processes contribute to the expression of LTP in hippocampal slices obtained from young adult rodents. LTP induced by compressed theta burst stimulation (TBS), with a 10 s inter-episode interval, involves purely an increase in N (LTPN). In contrast, either a spaced TBS, with a 10 min inter-episode interval, or a single TBS, delivered when PKA is activated, results in LTP that is associated with a transient increase in γ (LTPγ), caused by the insertion of calcium-permeable (CP)-AMPA receptors. Activation of CaMKII is necessary and sufficient for LTPN whilst PKA is additionally required for LTPγ. Thus, two mechanistically distinct forms of LTP co-exist at these synapses.

Theta-burst stimulation of primary afferents drives long-term potentiation in the spinal cord and persistent pain via α2δ-1–bound NMDA receptors

2021 ◽  
pp. JN-RM-1968-21
Author(s):  
Yuying Huang (黄玉莹) ◽  
Shao-Rui Chen (陈少瑞) ◽  
Hong Chen (陈红) ◽  
Jing-Jing Zhou (周京京) ◽  
Daozhong Jin (金道忠) ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Nmda Receptors ◽  
Long Term Potentiation ◽  
Primary Afferents ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Term Potentiation ◽  
Theta Burst ◽  
Stimulation Of

scholarly journals Proteasome and Autophagy-Mediated Impairment of Late Long-Term Potentiation (l-LTP) after Traumatic Brain Injury in the Somatosensory Cortex of Mice

2019 ◽  
Vol 20 (12) ◽  
pp. 3048 ◽  
Author(s):  
Feldmann ◽  
Le Prieult ◽  
Felzen ◽  
Thal ◽  
Engelhard ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protein Degradation ◽  
Long Term Potentiation ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Ipsilateral Hemisphere ◽  
Term Potentiation ◽  
Theta Burst

Traumatic brain injury (TBI) can lead to impaired cognition and memory consolidation.The acute phase (24–48 h) after TBI is often characterized by neural dysfunction in the vicinity ofthe lesion, but also in remote areas like the contralateral hemisphere. Protein homeostasis is crucialfor synaptic long-term plasticity including the protein degradation systems, proteasome andautophagy. Still, little is known about the acute effects of TBI on synaptic long-term plasticity andprotein degradation. Thus, we investigated TBI in a controlled cortical impact (CCI) model in themotor and somatosensory cortex of mice ex vivo-in vitro. Late long-term potentiation (l-LTP) wasinduced by theta-burst stimulation in acute brain slices after survival times of 1–2 days. Proteinlevels for the plasticity related protein calcium/calmodulin-dependent protein kinase II (CaMKII)was quantified by Western blots, and the protein degradation activity by enzymatical assays. Weobserved missing maintenance of l-LTP in the ipsilateral hemisphere, however not in thecontralateral hemisphere after TBI. Protein levels of CaMKII were not changed but, interestingly,the protein degradation revealed bidirectional changes with a reduced proteasome activity and anincreased autophagic flux in the ipsilateral hemisphere. Finally, LTP recordings in the presence ofpharmacologically modified protein degradation systems also led to an impaired synaptic plasticity:bath-applied MG132, a proteasome inhibitor, or rapamycin, an activator of autophagy, bothadministered during theta burst stimulation, blocked the induction of LTP. These data indicate thatalterations in protein degradation pathways likely contribute to cognitive deficits in the acute phaseafter TBI, which could be interesting for future approaches towards neuroprotective treatmentsearly after traumatic brain injury.

Proteolysis of spectrin by calpain accompanies theta-burst stimulation in cultured hippocampal slices

1995 ◽  
Vol 32 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Peter Vanderklish ◽  
Takaomi C. Saido ◽  
Christine Gal ◽  
Amy Arai ◽  
Gary Lynch
Keyword(s):  
Hippocampal Slices ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Theta Burst

scholarly journals Exposure to Forced Swim Stress Alters Local Circuit Activity and Plasticity in the Dentate Gyrus of the Hippocampus

2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Orli Yarom ◽  
Mouna Maroun ◽  
Gal Richter-Levin
Keyword(s):  
Dentate Gyrus ◽  
Neural Plasticity ◽  
Acute Stress ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Local Circuit ◽  
Forced Swim ◽  
Theta Burst

Studies have shown that, depending on its severity and context, stress can affect neural plasticity. Most related studies focused on synaptic plasticity and long-term potentiation (LTP) of principle cells. However, evidence suggests that following high-frequency stimulation, which induces LTP in principal cells, modifications also take place at the level of complex interactions with interneurons within the dentate gyrus, that is, at the local circuit level. So far, the possible effects of stress on local circuit activity and plasticity were not studied. Therefore, we set out to examine the possible alterations in local circuit activity and plasticity following exposure to stress. Local circuit activity and plasticity were measured by using frequency dependant inhibition (FDI) and commissural modulation protocols following exposure to a 15 minute-forced swim trial. Exposure to stress did not alter FDI. The application of theta-burst stimulation (TBS) reduced FDI in both control and stressed rats, but this type of plasticity was greater in stressed rats. Commissural-induced inhibition was significantly higher in stressed rats both before and after applying theta-burst stimulation. These findings indicate that the exposure to acute stress affects aspects of local circuit activity and plasticity in the dentate gyrus. It is possible that these alterations underlie some of the behavioral consequences of the stress experience.

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