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.

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.

Long-Term Potentiation in the Hippocampal CA1 Region Does Not Require Insertion and Activation of GluR2-Lacking AMPA Receptors

2007 ◽  
Vol 98 (4) ◽  
pp. 2488-2492 ◽  
Author(s):  
Erin E. Gray ◽  
Ann E. Fink ◽  
Joshua Sariñana ◽  
Bryce Vissel ◽  
Thomas J. O'Dell
Keyword(s):  
Glutamate Receptor ◽  
Ampa Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Old Mice

Activity-dependent insertion of AMPA-type glutamate receptors is thought to underlie long-term potentiation (LTP) at Schaffer collateral fiber synapses on pyramidal cells in the hippocampal CA1 region. Although it is widely accepted that the AMPA receptors at these synapses contain glutamate receptor type 2 (GluR2) subunits, recent findings suggest that LTP in hippocampal slices obtained from 2- to 3-wk-old rodents is dependent on the transient postsynaptic insertion and activation of Ca2+-permeable, GluR2-lacking AMPA receptors. Here we examined whether LTP in slices prepared from adult animals exhibits similar properties. In contrast to previously reported findings, pausing synaptic stimulation for as long as 30 min post LTP induction had no effect on LTP maintenance in slices from 2- to 3-mo-old mice. LTP was also not disrupted by postinduction application of a selective blocker of GluR2-lacking AMPA receptors or the broad-spectrum glutamate receptor antagonist kynurenate. Although these results suggest that the role of GluR2-lacking AMPA receptors in LTP might be regulated during postnatal development, LTP in slices obtained from 15- to 21-day-old mice also did not require postinduction synaptic stimulation or activation of GluR2-lacking AMPA receptors. Thus the insertion and activation of GluR2-lacking AMPA receptors do not appear to be fundamental processes involved in LTP at excitatory synapses in the hippocampal CA1 region.

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.

Quantifying the Magnitude of Changes in Synaptic Level Parameters With Long-Term Potentiation

2006 ◽  
Vol 96 (3) ◽  
pp. 1478-1491 ◽  
Author(s):  
William R. Holmes ◽  
Lawrence M. Grover
Keyword(s):  
Ampa Receptors ◽  
Single Channel ◽  
Long Term Potentiation ◽  
Channel Conductance ◽  
Single Channel Conductance ◽  
Vesicle Release ◽  
Silent Synapses ◽  
Term Potentiation ◽  
Synaptic Level

Experimental evidence supports a number of mechanisms for the synaptic change that occurs with long-term potentiation (LTP) including insertion of AMPA receptors, an increase in AMPA receptor single channel conductance, unmasking silent synapses, and increases in vesicle release probability. Here we combine experimental and modeling studies to quantify the magnitude of the change needed at the synaptic level to explain LTP with these proposed mechanisms. Whole cell patch recordings were used to measure excitatory postsynaptic potential (EPSP) amplitude in response to near minimal afferent stimulation before and after LTP induction in CA1 pyramidal cells. Detailed neuron and synapse level models were constructed to estimate quantitatively the changes needed to explain the experimental results. For cells in normal artificial cerebrospinal fluid (ACSF), we found a 60% average increase in EPSP amplitude with LTP. This was explained in the models by a 63% increase in the number of activated synapses, a 64% increase in the AMPA receptor single channel conductance, or a 73% increase in the number of AMPA receptors per potentiated synapse. When the percentage LTP was above the average, the required increases through the proposed mechanisms became nonlinear, particularly for increases in the number of receptors. Given constraints from other experimental studies, our quantification suggests that neither unmasking silent synapses nor increasing the numbers of AMPA receptors at synapses is sufficient to explain the magnitude of LTP we observed, but increasing AMPA single channel conductance or vesicle release probability can be sufficient. Our results are most compatible with a combination of mechanisms producing LTP.

Prenatal Dietary Choline Supplementation Decreases the Threshold for Induction of Long-Term Potentiation in Young Adult Rats

1998 ◽  
Vol 79 (4) ◽  
pp. 1790-1796 ◽  
Author(s):  
Gowri K. Pyapali ◽  
Dennis A. Turner ◽  
Christina L. Williams ◽  
Warren H. Meck ◽  
H. Scott Swartzwelder
Keyword(s):  
Young Adult ◽  
Hippocampal Slices ◽  
Threshold Level ◽  
Long Term Potentiation ◽  
Adult Rats ◽  
Hippocampal Synaptic Plasticity ◽  
Term Potentiation ◽  
Dietary Choline ◽  
Theta Burst

Pyapali, Gowri K., Dennis A. Turner, Christina L. Williams, Warren H. Meck, and H. Scott Swartzwelder. Prenatal dietary choline supplementation decreases the threshold for induction of long-term potentiation in young adult rats. J. Neurophysiol. 79: 1790–1796, 1998. Choline supplementation during gestation in rats leads to augmentation of spatial memory in adulthood. We hypothesized that prenatal (E12–E17) choline supplementation in the rat would lead to an enhancement of hippocampal synaptic plasticity as assessed by long-term potentiation (LTP) at 3–4 mo of age. LTP was assessed blindly in area CA1 of hippocampal slices with first suprathreshold (above threshold for LTP generation in control slices) theta-burst stimulus trains. The magnitude of potentiation after these stimuli was not different between slices from control and prenatally choline supplemented animals. Next, threshold (reliably leading to LTP generation in control slices) or subthreshold theta-burst stimulus trains were applied to slices from control, prenatally choline-supplemented, and prenatally choline-deprived rats. Threshold level stimulus trains induced LTP in slices from both the control and choline-supplemented rats but not in those from the choline-deficient rats. Subthreshold stimulus trains led to LTP induction in slices from prenatally choline-supplemented rats only. These observations indicate that prenatal dietary manipulation of the amino acid, choline, leads to subsequent significant alterations of LTP induction threshold in adult animals.

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