Short communicationRepeated ECS induces GluR1 mRNA but not NMDAR1A-G mRNA in the rat hippocampus
References (27)
- et al.
Electroconvulsive treatment reduces long-term potentiation in rat hippocampus
Brain Res.
(1987) - et al.
Long-term potentiation in the dentate gyrus: Induction and increased glutamate release are blocked by D-aminophosphonovalerate
Neuroscience
(1987) - et al.
In-situ hybridization histochemistry and the study of gene expression in the human brain
Prog. Neurobiol.
(1990) - et al.
Changes in glutamate receptor and proenkephalin gene expression after kindled seizures
Mol. Brain Res.
(1994) - et al.
Proactive and retroactive effects of repeated electroconvulsive shock on passive avoidance retention in rats
Physiol. Behav.
(1986) - et al.
Electroconvulsive stimulation and synaptic plasticity in the rat
Brain Res.
(1993) - et al.
Ketamine prevents ECS-induced synaptic enhancement in rat hippocampus
Neurosci. Lett.
(1994) - et al.
Elimination of long-term potentiation in the hippocampus by phencyclidine and ketamine
Brain Res.
(1983) - et al.
Structures and properties of seven isoforms of the NMDA receptor generated by alternative splicing
Biochem. Biophys. Res. Commun.
(1992) - et al.
Long-term potentiation is associated with increased [3H]AMPA binding in rat hippocampus
Brain Res.
(1992)
Differential effects of kindled and electrically induced seizures on a glutamate receptor (GluR1) gene expression
Epilepsy Res.
The relative contribution of NMDA receptor channels in the expression of long-term potentiation in the CA1 region
Eur. J. Neurosci.
Long-tern potentiation of NMDA receptor-mediated synaptic transmission in the hippocampus
Nature
Cited by (47)
Fast-acting antidepressant activity of ketamine: highlights on brain serotonin, glutamate, and GABA neurotransmission in preclinical studies
2019, Pharmacology and TherapeuticsCitation Excerpt :AMPA-R is strongly involved in synaptic plasticity, in particular those containing GluA1-subunit. Using in situ hybridization studies (Naylor, Stewart, Wright, Pearson, & Reid, 1996; Wong et al., 1993), it was shown that repeated electroconvulsive shock (ECS) in rats increased GluA1 mRNA expression in hippocampus areas that are connected to the LTP and consequently increased synaptic efficacy. Compelling evidence suggests that classical antidepressant drugs up-regulate AMPA-R function, which in turn may lead to changes in synaptic strength and plasticity.
An excitatory synapse hypothesis of depression
2015, Trends in NeurosciencesCitation Excerpt :Similar to conventional LTP, this ECT-induced potentiation is inhibited by an NMDAR antagonist [131] and is accompanied by an increase in phosphorylation of ser831 of GluA1 and S1301 of GluN2B. Changes in overall receptor expression were observed in some studies [132], but not others [133]. Interestingly, ECT also promoted an NMDAR-dependent increase in BDNF expression in animal models [134,135].
The role of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in depression: Central mediators of pathophysiology and antidepressant activity?
2015, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Importantly, GluA1 levels are not only affected by classical antidepressants; antidepressant doses of ketamine also elevate GluA1 levels in the rat medial PFC (Li et al., 2010). Moreover, repeated electroconvulsive shock treatment increased Gria1 mRNA in hippocampus of rats (Naylor et al., 1996). Taken together, data from animal studies suggest that AMPA receptor expression is altered by antidepressant treatment.
Roles of glutamate signaling in preclinical and/or mechanistic models of depression
2012, Pharmacology Biochemistry and BehaviorCitation Excerpt :In this section, studies on the effects of chronic ECS treatment on the glutamatergic system in normal animals are reviewed (Table 5). Using in situ hybridization techniques, repeated ECS was found to markedly increase the mRNA expression for the GluR1 subunit of AMPA receptors, but not the NMDAR1A-G subtypes of NMDA receptors, relative to control treatments (Naylor et al., 1996). The mGluR1a and mGluR5a immunoreactivities were also significantly increased in the rat hippocampus after chronic ECS treatment (Śmiałowska et al., 2002).
Synaptic Adaptations of CA1 Pyramidal Neurons Induced by a Highly Effective Combinational Antidepressant Therapy
2010, Biological PsychiatryCitation Excerpt :These neuronal alterations parallel the significant therapeutic action of the combinational treatment and could therefore represent a necessary condition for their beneficial action. The increase in BDNF levels and in postsynaptic glutamatergic transmission induced by scRI treatment is in line with previous biochemical and in situ hybridization data demonstrating an increase in the expression of various AMPAR subunits after chronic AD administration (24–27). Also, exogenous BDNF application increases synaptic delivery of AMPARs in cultured hippocampal neurons and organotypic slices (49), and long-term treatment of hippocampal cultures with BDNF enhances the amplitude of AMPAR-mediated mEPSCs (50).
Involvement of AMPA receptors in the antidepressant-like effects of lithium in the mouse tail suspension test and forced swim test
2008, NeuropharmacologyCitation Excerpt :Similar to our findings with lithium, it has been reported that monamine-acting antidepressants increase membrane levels of AMPA receptors (Martinez-Turrillas et al., 2002, 2005). Electroconvulsive shock, an animal model of electroconvulsive therapy, was shown to increase the levels of GluR1 mRNA in the rat hippocampus (Naylor et al., 1996). It is unclear what the mechanism is by which modulation of AMPA receptors may be involved in the mechanism of antidepressant action, or to what extent AMPA activation is required for therapeutic action in humans (Bleakman et al., 2007).