Facilitation of hippocampal long-term potentiation and reactivation of latent HIV-1 via AMPK activation: Common mechanism of action linking learning, memory, and the potential eradication of HIV-1

2018 ◽  
Vol 116 ◽  
pp. 61-73 ◽  
Author(s):  
Jahahreeh Finley
Keyword(s):  
Mechanism Of Action ◽  
Long Term Potentiation ◽  
Common Mechanism ◽  
Ampk Activation ◽  
Term Potentiation ◽  
Latent Hiv ◽  
Hiv 1

scholarly journals LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Daniela Puzzo ◽  
Roberto Piacentini ◽  
Mauro Fá ◽  
Walter Gulisano ◽  
Domenica D Li Puma ◽  
...  
Keyword(s):  
Associative Memory ◽  
Memory Impairment ◽  
Long Term Potentiation ◽  
Neuronal Uptake ◽  
Common Mechanism ◽  
Tau Oligomers ◽  
Term Potentiation ◽  
Induced Defects ◽  
Oligomeric Forms

The concurrent application of subtoxic doses of soluble oligomeric forms of human amyloid-beta (oAβ) and Tau (oTau) proteins impairs memory and its electrophysiological surrogate long-term potentiation (LTP), effects that may be mediated by intra-neuronal oligomers uptake. Intrigued by these findings, we investigated whether oAβ and oTau share a common mechanism when they impair memory and LTP in mice. We found that as already shown for oAβ, also oTau can bind to amyloid precursor protein (APP). Moreover, efficient intra-neuronal uptake of oAβ and oTau requires expression of APP. Finally, the toxic effect of both extracellular oAβ and oTau on memory and LTP is dependent upon APP since APP-KO mice were resistant to oAβ- and oTau-induced defects in spatial/associative memory and LTP. Thus, APP might serve as a common therapeutic target against Alzheimer's Disease (AD) and a host of other neurodegenerative diseases characterized by abnormal levels of Aβ and/or Tau.

A novel cholinergic induction of long-term potentiation in rat hippocampus

1994 ◽  
Vol 72 (4) ◽  
pp. 2034-2040 ◽  
Author(s):  
J. M. Auerbach ◽  
M. Segal
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Extracellular Recording ◽  
Long Term Potentiation ◽  
Common Mechanism ◽  
Excitatory Postsynaptic Potential ◽  
Tetanic Stimulation ◽  
Term Potentiation ◽  
Bath Application

1. We studied long-term cholinergic effects on synaptic transmission in submerged hippocampal slices using intra- and extracellular recording techniques. 2. Bath application of submicromolar concentrations of carbachol (CCh) produced a gradually developing, long-lasting increase in the CA1 excitatory postsynaptic potential and population spike. This potentiation was blocked by atropine and, hence, named muscarinic long-term potentiation (LTPm). Application of DL-2-amino-5-phosphonovaleric acid had no effect on LTPm, indicating that this phenomenon is N-methyl-D-aspartate receptor independent. 3. These effects of CCh were not likely to be due to the blockade of one of several K+ conductances by the drug; the time and concentration dependence of LTPm were different from those associated with cholinergic blockade of K+ conductances. 4. Removal of extracellular calcium (Cao2+) from the bath blocked synaptic transmission. CCh added in calcium-free medium induced LTPm, which was revealed upon removal of the drug by washing with normal calcium-containing medium. Neither cutting CA1-CA3 connections nor cessation of synaptic stimulation interfered with LTPm induction. 5. Application of thapsigargin or H-7 together with CCh blocked LTPm, suggesting the involvement of intracellular calcium (Cai2+) stores and protein kinases, respectively, in the LTPm mechanism. 6. Subthreshold cholinergic stimulation coupled with subthreshold tetanic stimulation caused LTP. CCh had no effect when administered after the LTP mechanism had been saturated by repeated suprathreshold tetani. Tetanic stimulation failed to cause LTP when applied after LTPm had been induced by CCh. These experiments indicate that tetanus-induced potentiation and LTPm share a common mechanism and provide a direct link between ACh and mechanisms of synaptic plasticity.

HIV-1 inhibits long-term potentiation and attenuates spatial learning

2004 ◽  
Vol 55 (3) ◽  
pp. 362-371 ◽  
Author(s):  
Sheng-Tian Li ◽  
Masayuki Matsushita ◽  
Akiyoshi Moriwaki ◽  
Yasunori Saheki ◽  
Yun-Fei Lu ◽  
...  
Keyword(s):  
Spatial Learning ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Hiv 1

scholarly journals Incorporation of inwardly rectifying AMPA receptors at silent synapses during hippocampal long-term potentiation

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130156 ◽  
Author(s):  
Daiju Morita ◽  
Jong Cheol Rah ◽  
John T. R. Isaac
Keyword(s):  
Ampa Receptors ◽  
Calcium Influx ◽  
Critical Role ◽  
Long Term Potentiation ◽  
Subunit Composition ◽  
Common Mechanism ◽  
Silent Synapses ◽  
Term Potentiation ◽  
Inwardly Rectifying

Despite decades of study, the mechanisms by which synapses express the increase in strength during long-term potentiation (LTP) remain an area of intense interest. Here, we have studied how AMPA receptor subunit composition changes during the early phases of hippocampal LTP in CA1 pyramidal neurons. We studied LTP at silent synapses that initially lack AMPA receptors, but contain NMDA receptors. We show that strongly inwardly rectifying AMPA receptors are initially incorporated at silent synapses during LTP and are then subsequently replaced by non-rectifying AMPA receptors. These findings suggest that silent synapses initially incorporate GluA2-lacking, calcium-permeable AMPA receptors during LTP that are then replaced by GluA2-containing calcium-impermeable receptors. We also show that LTP consolidation at CA1 synapses requires a rise in intracellular calcium concentration during the early phase of expression, indicating that calcium influx through the GluA2-lacking AMPA receptors drives their replacement by GluA2-containing receptors during LTP consolidation. Taken together with previous studies in hippocampus and in other brain regions, these findings suggest that a common mechanism for the expression of activity-dependent glutamatergic synaptic plasticity involves the regulation of GluA2-subunit composition and highlights a critical role for silent synapses in this process.

scholarly journals Transcranial direct current stimulation induces long-term potentiation-like plasticity in the human visual cortex

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lukas Frase ◽  
Lydia Mertens ◽  
Arno Krahl ◽  
Kriti Bhatia ◽  
Bernd Feige ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Mechanism Of Action ◽  
Direct Current ◽  
Transcranial Direct Current Stimulation ◽  
Long Term Potentiation ◽  
Constant Current ◽  
Direct Current Stimulation ◽  
Term Potentiation ◽  
Significant Difference

AbstractTranscranial direct current stimulation (tDCS) is increasingly used as a form of noninvasive brain stimulation to treat psychiatric disorders; however, its mechanism of action remains unclear. Prolonged visual stimulation (PVS) can enhance evoked EEG potentials (visually evoked potentials, VEPs) and has been proposed as a tool to examine long-term potentiation (LTP) in humans. The objective of the current study was to induce and analyze VEP plasticity and examine whether tDCS could either modulate or mimic plasticity changes induced by PVS. Thirty-eight healthy participants received tDCS, PVS, either treatment combined or neither treatment, with stimulation sessions being separated by one week. One session consisted of a baseline VEP measurement, one stimulation block, and six test VEP measurements. For PVS, a checkerboard reversal pattern was presented, and for tDCS, a constant current of 1 mA was applied via each bioccipital anodal target electrode for 10 min (Fig. S1). Both stimulation types decreased amplitudes of C1 compared to no stimulation (F = 10.1; p = 0.002) and led to a significantly smaller increase (PVS) or even decrease (tDCS) in N1 compared to no stimulation (F = 4.7; p = 0.034). While all stimulation types increased P1 amplitudes, the linear mixed effects model did not detect a significant difference between active stimulation and no stimulation. Combined stimulation induced sustained plastic modulation of C1 and N1 but with a smaller effect size than what would be expected for an additive effect. The results demonstrate that tDCS can directly induce LTP-like plasticity in the human cortex and suggest a mechanism of action of tDCS relying on the restoration of dysregulated synaptic plasticity in psychiatric disorders such as depression and schizophrenia.

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