scholarly journals Long-Term Potentiation by Theta-Burst Stimulation Using Extracellular Field Potential Recordings in Acute Hippocampal Slices

2016 ◽  
Vol 2016 (6) ◽  
pp. pdb.prot091298 ◽  
Author(s):  
Therese Abrahamsson ◽  
Txomin Lalanne ◽  
Alanna J. Watt ◽  
P. Jesper Sjöström
Keyword(s):  
Hippocampal Slices ◽  
Field Potential ◽  
Long Term Potentiation ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Term Potentiation ◽  
Acute Hippocampal Slices ◽  
Theta Burst

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.

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

2020 ◽  
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, involved 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 was activated, resulted in LTP that was associated with a transient increase in γ (LTPγ). This γ increase was due to the insertion of calcium-permeable (CP)-AMPA receptors. Activation of CaMKII was necessary and sufficient for LTPN whilst PKA was additionally required for LTPγ. Thus, two mechanistically distinct forms of LTP co-exist at these synapses.

scholarly journals Subsequent Acupuncture Reverses the Aftereffects of Intermittent Theta-Burst Stimulation

2021 ◽  
Vol 15 ◽  
Author(s):  
Xiao-Kuo He ◽  
Hui-Hua Liu ◽  
Shan-Jia Chen ◽  
Qian-Qian Sun ◽  
Guo Yu ◽  
...  
Keyword(s):  
Motor Evoked Potential ◽  
Long Term Potentiation ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Learning Skill ◽  
Term Potentiation ◽  
Acupuncture Intervention ◽  
High Level ◽  
Theta Burst

ObjectiveThis study explored whether acupuncture affects the maintenance of long-term potentiation (LTP)-like plasticity induced by transcranial magnetic stimulation (TMS) and the acquisition of motor skills following repetitive sequential visual isometric pinch task (SVIPT) training.MethodsThirty-six participants were recruited. The changes in the aftereffects induced by intermittent theta-burst stimulation (iTBS) and followed acupuncture were tested by the amplitude motor evoked potential (MEP) at pre-and-post-iTBS for 30 min and at acupuncture-in and -off for 30 min. Secondly, the effects of acupuncture on SVIPT movement in inducing error rate and learning skill index were tested.ResultsFollowing one session of iTBS, the MEP amplitude was increased and maintained at a high level for 30 min. The facilitation of MEP was gradually decreased to the baseline level during acupuncture-in and did not return to a high level after needle extraction. The SVIPT-acupuncture group had a lower learning skill index than those in the SVIPT group, indicating that acupuncture intervention after SVIPT training may restrain the acquisition ability of one’s learning skills.ConclusionAcupuncture could reverse the LTP-like plasticity of the contralateral motor cortex induced by iTBS. Subsequent acupuncture may negatively affect the efficacy of the acquisition of learned skills in repetitive exercise training.

scholarly journals Complexity of dendritic SER increases at enlarging synapses during LTP

2015 ◽  
Author(s):  
Michael Chirillo ◽  
Jennifer Bourne ◽  
Laurence Lindsey ◽  
Kristen Harris
Keyword(s):  
Smooth Endoplasmic Reticulum ◽  
Structural Complexity ◽  
Long Term Potentiation ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Adult Rat ◽  
Term Potentiation ◽  
Functional Implications ◽  
Theta Burst

Smooth endoplasmic reticulum (SER) forms a membranous network that extends throughout neurons. SER regulates intracellular calcium and the posttranslational modification and trafficking of membrane and proteins. As the structure of dendritic SER shifts from a tubular to a more complex, branched form, the movement of membrane cargo slows and delivery to nearby spines increases. Here we discovered changes in the structural complexity of SER that have important functional implications during long-term potentiation (LTP) in adult rat hippocampus. By 2 hours after the induction of LTP with theta-burst stimulation, synapse enlargement was greatest on spines that contained SER. More spines had an elaborate spine apparatus than a simple tubule of SER. The SER in dendritic shafts became more complex beneath spines with both polyribosomes and SER, and less complex along aspiny dendritic regions. The findings suggest that local changes in dendritic SER support enhanced growth of specific synapses during LTP.

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