Factors regulating the magnitude of long-term potentiation induced by theta pattern stimulation

Arai, Amy; Lynch, Gary

doi:10.1016/0006-8993(92)90181-8

Cited by 173 publications

(104 citation statements)

References 38 publications

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“…AMPA receptor modulators that alter receptor kinetics may influence long-term potentiation, long-term depression (22)(23)(24), and various forms of memory function in both animals (23,25,26) and humans (27,28). Mice with either a GRIA1 or GRIA3 gene deletion showed significant changes in hippocampal long-term potentiation (18,29).…”

Section: Discussionmentioning

confidence: 99%

Mutations in ionotropic AMPA receptor 3 alter channel properties and are associated with moderate cognitive impairment in humans

Arai

Rumbaugh

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

104

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Ionotropic ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (iGluRs) mediate the majority of excitatory synaptic transmission in the CNS and are essential for the induction and maintenance of long-term potentiation and long-term depression, two cellular models of learning and memory. We identified a genomic deletion (0.4 Mb) involving the entire GRIA3 (encoding iGluR3) by using an X-array comparative genomic hybridization (CGH) and four missense variants (G833R, M706T, R631S, and R450Q) in functional domains of iGluR3 by sequencing 400 males with X-linked mental retardation (XLMR). Three variants were found in males with moderate MR and were absent in 500 control males. Expression studies in HEK293 cells showed that G833R resulted in a 78% reduction of iGluR3 due to protein misfolding. Whole-cell recording studies of iGluR3 homomers in HEK293 cells revealed that neither iGluR3-M706T (S2 domain) nor iGluR3-R631S (near channel core) had substantial channel function, whereas R450Q (S1 domain) was associated with accelerated receptor desensitization. When forming heteromeric receptors with iGluR2 in HEK293 cells, all four iGluR3 variants had altered desensitization kinetics. Our study provides the genetic and functional evidence that mutant iGluR3 with altered kinetic properties is associated with moderate cognitive impairment in humans.glutamate receptor ͉ X-linked mental retardation

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Section: Discussionmentioning

confidence: 99%

Mutations in ionotropic AMPA receptor 3 alter channel properties and are associated with moderate cognitive impairment in humans

Arai

Rumbaugh

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

104

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“…At the concentration used here (10 M), Fsk alone did not cause lasting potentiation as compared with the baseline in either WT or STX1A Ϫ/Ϫ mice. In this study, we used 12 bursts of TBS, which is sufficient to induce near maximal LTP (Arai and Lynch, 1992). To confirm the possibility that the reduction in LTP in STX1A Ϫ/Ϫ mice was caused by a rise in the stimulus strength required for the induction of LTP, more robust stimulation was used to induce LTP.…”

Section: Synaptic Plasticity In Stx1amentioning

confidence: 99%

Impairment of Catecholamine Systems during Induction of Long-Term Potentiation at Hippocampal CA1 Synapses in HPC-1/Syntaxin 1A Knock-out Mice

Mishima

Fujiwara²,

Kofuji³

et al. 2012

J. Neurosci.

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The membrane protein HPC-1/syntaxin 1A is believed to play a key role in synaptic vesicle exocytosis, and it was recently suggested to be required for synaptic plasticity. Despite evidence for the function of HPC-1/syntaxin 1A in synaptic plasticity, the underlying cellular mechanism is unclear. We found that although fast synaptic transmission and long-term depression were unaffected, HPC-1/syntaxin 1A knock-out (STX1A Ϫ/Ϫ ) mice showed impaired long-term potentiation (LTP) in response to theta-burst stimulation in CA1 hippocampal slices. The impairment in LTP was rescued by the application of forskolin, an adenylyl cyclase activator, or more robust stimulation, suggesting that cAMP/protein kinase A signaling was suppressed in these mice. In addition, catecholamine release from the hippocampus was significantly reduced in STX1A Ϫ/Ϫ mice. Because HPC-1/syntaxin 1A regulates exocytosis of dense-core synaptic vesicles, which contain neuromodulatory transmitters such as noradrenaline, dopamine and 5-HT, we examined the effect of neuromodulatory transmitters on LTP induction. Noradrenaline and dopamine enhanced LTP induction in STX1A Ϫ/Ϫ mice, whereas catecholamine depletion reduced LTP induction in wild-type mice. Theses results suggest that HPC-1/syntaxin 1A regulates catecholaminergic systems via exocytosis of dense-core synaptic vesicles, and that deletion of HPC-1/syntaxin 1A causes impairment of LTP induction.

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“…The results also reinforce a previous conclusion that plasticity of the basal dendritic synapses is significantly different than that in their apical counterparts. Earlier studies had shown that LTP has a lower threshold (requires fewer theta bursts) and is greater in magnitude in the basal than in the apical dendrites in field CA1 (Arai et al, 1994;Roth and Leung, 1995;Leung and Shen, 1999), an effect that can probably be attributed to regional differences in the incidence of potassium channels that mediate the after-hyperpolarizing potentials (AHPs) initiated by individual theta bursts (Arai and Lynch, 1992;Arai et al, 1994;Sah and Bekkers, 1996;Stackman et al, 2002). LTP also differs between the two dendritic domains with regard to the degree to which it stabilizes.…”

Section: Loss Of Synaptic Plasticity In Early Middle Agementioning

confidence: 99%

Synaptic plasticity in early aging

Lynch

Rex

Gall

2006

Ageing Research Reviews

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Studies of how aging affects brain plasticity have largely focused on old animals. However, deterioration of memory begins well in advance of old age in animals, including humans; the present review is concerned with the possibility that changes in synaptic plasticity, as found in the long-term potentiation (LTP) effect, are responsible for this. Recent results indicate that impairments to LTP are in fact present by early middle age in rats but only in certain dendritic domains. The search for the origins of these early aging effects necessarily involves ongoing analyses of how LTP is induced, expressed, and stabilized. Such work points to the conclusion that cellular mechanisms responsible for LTP are redundant and modulated both positively and negatively by factors released during induction of potentiation. Tests for causes of the localized failure of LTP during early aging suggest that the problem lies in excessive activity of a negative modulator. The view of LTP as having redundant and modulated substrates also suggests a number of approaches for reversing age-related losses. Particular attention will be given to the idea that induction of brain-derived neurotrophic factor, an extremely potent positive modulator, can be used to provide long periods of normal plasticity with very brief pharmacological interventions. The review concludes with a consideration of how the selective, regional deficits in LTP found in early middle age might be related to the global phenomenon of brain aging. #

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Factors regulating the magnitude of long-term potentiation induced by theta pattern stimulation

Cited by 173 publications

References 38 publications

Mutations in ionotropic AMPA receptor 3 alter channel properties and are associated with moderate cognitive impairment in humans

Mutations in ionotropic AMPA receptor 3 alter channel properties and are associated with moderate cognitive impairment in humans

Impairment of Catecholamine Systems during Induction of Long-Term Potentiation at Hippocampal CA1 Synapses in HPC-1/Syntaxin 1A Knock-out Mice

Synaptic plasticity in early aging

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