Effect of d-2 amino-5-phosphonopentanoate and nifedipine on postsynaptic calcium changes associated with long-term potentiation in hippocampal CA1 area

Matias, Carlos M.; Dionisio, José; Arif, Mona; Quinta‐Ferreira, Mário

doi:10.1016/s0006-8993(03)02698-2

Cited by 11 publications

(5 citation statements)

References 46 publications

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“…These data correspond with data from coronal slices where thalamo-amygdala HFS-induced LTP was only dependent on NMDA receptors (Bauer et al 2002). In contrast, it is known that L-type calcium channels may be involved in the mediation of CA1-LTP in adult rats, in addition to NMDA receptors (Cavus and Teyler 1996;Matias et al 2003). These or other differences in signal cascades may be responsible for the different time courses of LTP curves in the amygdala and the hippocampus in kindled rats compared to controls.…”

Section: Effect Of Kindling Procedures On Ltp Magnitudesupporting

confidence: 82%

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Schubert¹,

Siegmund²,

Pape³

et al. 2005

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Temporal lobe epilepsy (TLE) is often accompanied by interictal behavioral abnormalities, such as fear and memory impairment. To identify possible underlying substrates, we analyzed long-term synaptic plasticity in two relevant brain regions, the lateral amygdala (LA) and the CA1 region of the hippocampus, in the kindling model of epilepsy. Wistar rats were kindled through daily administration of brief electrical stimulations to the left basolateral nucleus of the amygdala. Field potential recordings were performed in slices obtained from kindled rats 48 h after the last induced seizure, and in slices from sham-implanted and nonimplanted controls. Kindling resulted in a significant impairment of long-term potentiation (LTP) in both the LA and the CA1, the magnitude of which was dependent on the number of prior stage V seizures. Saturation of CA1-LTP, assessed through repeated spaced delivery of high-frequency stimulation, occurred at lower levels in kindled compared to sham-implanted animals, consistent with the hypothesis of reduced capacity of further synaptic strengthening. Furthermore, theta pulse stimulation elicited long-term depression in the amygdala in nonimplanted and sham-implanted controls, whereas the same stimulation protocol stimulation caused LTP in kindled rats. In conclusion, kindling differentially affects the magnitude, saturation, and polarity of LTP in the CA1 and LA, respectively, most likely indicating an activity-dependent mechanism in the context of synaptic metaplasticity.Convulsive diseases in humans such as temporal lobe epilepsy (TLE) are often accompanied by impairments of learning and memory. In addition, TLE patients typically display emotional disturbances, in particular negative emotions such as fear, anxiety, and depression (Kalynchuk 2000). A wealth of data has established that the amygdala plays a critical role in neuronal activity and synaptic plasticity related to both emotionally modulated signal processing and epilepsy (Gloor 1990;Maren 1999;LeDoux 2000). Synapses in the amygdala display long-term potentiation (LTP) (Chapman and Chattarji 2000; LeDoux 2000; Maren 2001), a long-lasting increase of synaptic strength that is widely believed to be a cellular basis of learning and memory (Bliss and Collingridge 1993). The amygdala possesses the lowest threshold for the induction of kindling (Löscher 1997), an established experimental model of TLE in which daily electrical stimulation results in a gradual progression and intensification of limbic motor seizures (Goddard et al. 1969). Although kindling has been extensively investigated in the context of its clinical relevance to epilepsy and seizure-induced synaptic potentiation, only a few studies that relate to plastic synaptic changes after kindling are available. Therefore, the present study was undertaken to systematically analyze the influence of kindling 48 h after the last seizure on long-term synaptic plasticity, LTP, and long-term depression (LTD) in the lateral nucleus of the amygdala (LA) in rats. The LA was chosen ...

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Section: Effect Of Kindling Procedures On Ltp Magnitudesupporting

confidence: 82%

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Schubert¹,

Siegmund²,

Pape³

et al. 2005

Learn. Mem.

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“…This is consistent with the study by Matias et al . () showing that intracellular calcium release is not involved in baseline synaptic transmission, but is essential for synaptic plasticity. As a final control, we used ryanodine at low concentrations, which has been shown to induce calcium release, as well as at high concentrations, which have been demonstrated to block calcium release from internal stores (Caillard et al .…”

Section: Resultsmentioning

confidence: 99%

Synaptopodin is regulated by aromatase activity

Fester¹,

Zhou²,

Ossig³

et al. 2016

Journal of Neurochemistry

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Locally synthesized estradiol plays an important role in synaptic plasticity in the hippocampus. We have previously shown that in hippocampal neurons, activity of the enzyme aromatase, which converts testosterone into estradiol, is reduced via Ca 2+-dependent phosphorylation. Synaptopodin is a highly estrogen responsive protein, and it has been shown that it is an important regulator of synaptic plasticity, mediated by its close association with internal calcium stores. In this study, we show that the expression of synaptopodin is stronger in the hippocampus of female animals than in that of male animals. Phosphorylation of aromatase, using letro-zole, however, down-regulates synaptopodin immunohisto-chemistry in the hippocampus of both male and females. Similarly, in aromatase knockout mice synaptopodin expression in the hippocampus is reduced sex independently. Using primary-dissociated hippocampal neurons, we found that evoked release of Ca 2+ from internal stores down-regulates aromatase activity, which is paralleled by reduced expression of synaptopodin. Opposite effects were achieved after inhibition of the release. Calcium-dependent regulation of synaptopodin expression was abolished when the control of aromatase activity by the Ca 2+ transients was disrupted. Our data suggest that the regulation of aromatase activity by Ca 2+ transients in neurons contributes to synaptic plasticity in the hippocampus of male and female animals as an on-site regulatory mechanism.

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“…A number of genes activated by neuronal electrical activity, among them c-fos and BDNF, have functional CRE sequences in their promoters (Sheng et al 1990;Tao et al 1998); in the last few years these findings have prompted many studies on the cellular factors that regulate CREB activation. Participation of Ca 2C release from intracellular stores in LTP induction has been described (Auerbach & Segal 1994;Wang et al 1996;Reyes-Harde et al 1999;Lu & Hawkins 2002;Lauri et al 2003;Matias et al 2003;Lynch 2004). LTP induction in most hippocampal synapses requires a rise in intracellular postsynaptic [Ca 2C ] mediated by N-methyl-D-aspartate (NMDA) receptors, with contributions from L-type channel activation and intracellular Ca 2C stores (Matias et al 2003;Lynch 2004).…”

Section: Neuronsmentioning

confidence: 99%

“…Participation of Ca 2C release from intracellular stores in LTP induction has been described (Auerbach & Segal 1994;Wang et al 1996;Reyes-Harde et al 1999;Lu & Hawkins 2002;Lauri et al 2003;Matias et al 2003;Lynch 2004). LTP induction in most hippocampal synapses requires a rise in intracellular postsynaptic [Ca 2C ] mediated by N-methyl-D-aspartate (NMDA) receptors, with contributions from L-type channel activation and intracellular Ca 2C stores (Matias et al 2003;Lynch 2004). In the CA1 hippocampal region, RyR blockade significantly reduces tetanic-, NO-and cGMP-induced LTP, and decreases P-CREB immunofluorescence in postsynaptic neurons of hippocampal slices (Lu & Hawkins 2002).…”

Section: Neuronsmentioning

confidence: 99%

Cross talk between Ca²⁺and redox signalling cascades in muscle and neurons through the combined activation of ryanodine receptors/Ca²⁺release channels

Hidalgo

2005

Phil. Trans. R. Soc. B

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Calcium release mediated by the ryanodine receptors (RyR) Ca 2C release channels is required for muscle contraction and contributes to neuronal plasticity. In particular, Ca 2C activation of RyRmediated Ca 2C release can amplify and propagate Ca 2C signals initially generated by Ca 2C entry into cells. Redox modulation of RyR function by a variety of non-physiological or endogenous redox molecules has been reported. The effects of RyR redox modification on Ca 2C release in skeletal muscle as well as the activation of signalling cascades and transcription factors in neurons will be reviewed here. Specifically, the different effects of S-nitrosylation or S-glutathionylation of RyR cysteines by endogenous redox-active agents on the properties of skeletal muscle RyRs will be discussed. Results will be presented indicating that these cysteine modifications change the activity of skeletal muscle RyRs, modify their behaviour towards both activators and inhibitors and affect their interactions with FKBP12 and calmodulin. In the hippocampus, sequential activation of ERK1/2 and CREB is a requisite for Ca 2C -dependent gene expression associated with long-lasting synaptic plasticity. The effects of reactive oxygen/nitrogen species on RyR channels from neurons and RyR-mediated sequential activation of neuronal ERK1/2 and CREB produced by hydrogen peroxide and other stimuli will be discussed as well.

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Effect of d-2 amino-5-phosphonopentanoate and nifedipine on postsynaptic calcium changes associated with long-term potentiation in hippocampal CA1 area

Cited by 11 publications

References 46 publications

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Synaptopodin is regulated by aromatase activity

Cross talk between Ca²⁺and redox signalling cascades in muscle and neurons through the combined activation of ryanodine receptors/Ca²⁺release channels

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Effect of d-2 amino-5-phosphonopentanoate and nifedipine on postsynaptic calcium changes associated with long-term potentiation in hippocampal CA1 area

Cited by 11 publications

References 46 publications

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Synaptopodin is regulated by aromatase activity

Cross talk between Ca2+and redox signalling cascades in muscle and neurons through the combined activation of ryanodine receptors/Ca2+release channels

Contact Info

Product

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Cross talk between Ca²⁺and redox signalling cascades in muscle and neurons through the combined activation of ryanodine receptors/Ca²⁺release channels