Inhibition by [Arg8]-Vasopressin of Long Term Potentiation in Guinea Pig Hippocampal Slice

Sakurai, Einosuke; Maeda, Takehiko; Kaneko, Shuji; Akaike, Akinori; Satoh, Masamichi

doi:10.1254/jjp.77.103

Cited by 8 publications

(7 citation statements)

References 12 publications

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“…This might indicate a potential protective effect of prenatal sGC exposure on LTP during periods of acute stress in female offspring. However, glucocorticoids do not act independently, since other HPA axis markers, such as arginine vasopressin and catecholamines, correlate with learning and memory and, in turn, can modulate LTP (Izumi et al 1992; Sakurai et al 1998). Further, other structures, such as the amygdala, are key components in stress‐induced effects on LTP (Kim et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Effects of repeated prenatal glucocorticoid exposure on long‐term potentiation in the juvenile guinea‐pig hippocampus

Setiawan¹,

Jackson²,

MacDonald³

et al. 2007

The Journal of Physiology

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Synthetic glucocorticoids (sGCs) are routinely used to treat women at risk of preterm labour to promote fetal lung maturation. There is now strong evidence that exposure to excess glucocorticoid during periods of rapid brain development has permanent consequences for endocrine function and behaviour in the offspring. Prenatal exposure to sGC alters the expression of N -methyl-D-aspartate receptor (NMDA-R) subunits in the fetal and neonatal hippocampus. Given the integral role of the NMDA-R in synaptic plasticity, we hypothesized that prenatal sGC exposure will have effects on hippocampal long-term potentiation (LTP) after birth. Further, this may occur in either the presence or absence of elevated cortisol concentrations, in vitro. Pregnant guinea-pigs were injected with betamethasone (Beta, 1 mg kg −1 ) or vehicle on gestational days (gd) 40, 41, 50, 51, 60 and 61 (term ∼70 days), a regimen comparable to that given to pregnant women. On postnatal day 21, LTP was examined at Schaffer collateral synapses in the CA1 region of hippocampal slices prepared from juvenile animals exposed to betamethasone or vehicle, in utero. Subsequently, the acute glucocorticoid receptor (GR)-and mineralocorticoid receptor (MR)-dependent effects of cortisol (0.1-10 μM; bath applied 30 min before LTP induction) were examined. There was no effect of prenatal sGC treatment on LTP under basal conditions. The application of 10 μM cortisol depressed excitatory synaptic transmission in all treatment groups regardless of sex. Similarly, LTP was depressed by 10 μM cortisol in all groups, with the exception of Beta-exposed females, in which LTP was unaltered. Hippocampal MR and GR protein levels were increased in Beta-exposed females, but not in any other prenatal treatment group. This study reveals sex-specific effects of prenatal exposure to sGC on LTP in the presence of elevated cortisol, a situation that would occur in vivo during stress.

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Section: Discussionmentioning

confidence: 99%

Effects of repeated prenatal glucocorticoid exposure on long‐term potentiation in the juvenile guinea‐pig hippocampus

Setiawan¹,

Jackson²,

MacDonald³

et al. 2007

The Journal of Physiology

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“…Arg‐vasopressin was proposed as a physiological IRAP substrate [85] and facilitated LTP in the CA1 of rat hippocampal slices [139] and in the rat dentate gyrus (Dubrovsky et al, 2003) [140]. At higher concentrations, Arg‐vasopressin inhibited LTP in the CA1 of guinea pig hippocampal slices [141]. Oxytocin enhanced LTP in the CA1 of female mice hippocampal slices [142] and induced LTD in the male rat dentate gyrus [143].…”

Section: Effects Of Ang II and Ang Iv On Synaptic Transmission And Plmentioning

confidence: 99%

Ang II and Ang IV: Unraveling the Mechanism of Action on Synaptic Plasticity, Memory, and Epilepsy

Bundel¹,

Smolders²,

Vanderheyden³

et al. 2008

CNS Neuroscience & Therapeutics

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The central angiotensin system plays a crucial role in cardiovascular regulation. More recently, angiotensin peptides have been implicated in stress, anxiety, depression, cognition, and epilepsy. Angiotensin II (Ang II) exerts its actions through AT(1) and AT(2) receptors, while most actions of its metabolite Ang IV were believed to be independent of AT(1) or AT(2) receptor activation. A specific binding site with high affinity for Ang IV was discovered and denominated "AT(4) receptor". The beneficiary effects of AT(4) ligands in animal models for cognitive impairment and epileptic seizures initiated the search for their mechanism of action. This proved to be a challenging task, and after 20 years of research, the nature of the "AT(4) receptor" remains controversial. Insulin-regulated aminopeptidase (IRAP) was first identified as the high-affinity binding site for AT(4) ligands. Recently, the hepatocyte growth factor receptor c-MET was also proposed as a receptor for AT(4) ligands. The present review focuses on the effects of Ang II and Ang IV on synaptic transmission and plasticity, learning, memory, and epileptic seizure activity. Possible interactions of Ang IV with the classical AT(1) and AT(2) receptor subtypes are evaluated, and other potential mechanisms by which AT(4) ligands may exert their effects are discussed. Identification of these mechanisms may provide a valuable target in the development in novel drugs for the treatment of cognitive disorders and epilepsy.

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“…In the rat dentate gyrus in vitro , Chen et al [34] observed that nanomolar concentrations of AVP, via activation of a V1 receptor, induced a prolonged increase in slope and amplitude of the EPSP in the presence of 1.5 mM calcium and a prolonged depression in the presence of 2.5 mM calcium, but this was not reproduced in vivo [35]. In the guinea pig CA1 and CA3 hippocampal areas, AVP prevents LTP without affecting the basal EPSP [36]. By contrast, we observed an absence of AVP action on the mouse SC-CA1 neuron synapse.…”

Section: Discussionmentioning

confidence: 99%

Vasopressin Inhibits LTP in the CA2 Mouse Hippocampal Area

et al. 2012

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Growing evidence points to vasopressin (AVP) as a social behavior regulator modulating various memory processes and involved in pathologies such as mood disorders, anxiety and depression. Accordingly, AVP antagonists are actually envisaged as putative treatments. However, the underlying mechanisms are poorly characterized, in particular the influence of AVP on cellular or synaptic activities in limbic brain areas involved in social behavior. In the present study, we investigated AVP action on the synapse between the entorhinal cortex and CA2 hippocampal pyramidal neurons, by using both field potential and whole-cell recordings in mice brain acute slices. Short application (1 min) of AVP transiently reduced the synaptic response, only following induction of long-term potentiation (LTP) by high frequency stimulation (HFS) of afferent fibers. The basal synaptic response, measured in the absence of HFS, was not affected. The Schaffer collateral-CA1 synapse was not affected by AVP, even after LTP, while the Schaffer collateral-CA2 synapse was inhibited. Although investigated only recently, this CA2 hippocampal area appears to have a distinctive circuitry and a peculiar role in controlling episodic memory. Accordingly, AVP action on LTP-increased synaptic responses in this limbic structure may contribute to the role of this neuropeptide in controlling memory and social behavior.

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Inhibition by [Arg8]-Vasopressin of Long Term Potentiation in Guinea Pig Hippocampal Slice

Cited by 8 publications

References 12 publications

Effects of repeated prenatal glucocorticoid exposure on long‐term potentiation in the juvenile guinea‐pig hippocampus

Effects of repeated prenatal glucocorticoid exposure on long‐term potentiation in the juvenile guinea‐pig hippocampus

Ang II and Ang IV: Unraveling the Mechanism of Action on Synaptic Plasticity, Memory, and Epilepsy

Vasopressin Inhibits LTP in the CA2 Mouse Hippocampal Area

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