The effects of serotonin depletion and raphe grafts on hippocampal electrophysiology and behavior

Richter‐Levin, Gal; Segal, Menahem

doi:10.1523/jneurosci.11-06-01585.1991

Cited by 81 publications

(29 citation statements)

References 48 publications

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“…It is well recognized that synaptic plasticity, which can be assessed by altered LTP and/or morphology of synapses, is a prerequisite of learning and memory. By measuring the alterations of the amplitude of PS and the slope of EPSP, the accepted parameters for the in vivo measurement of LTP (Richter-Levin and Segal, 1991), and manipulating the activity of GSK-3 both pharmacologically and genetically, we demonstrated in the present study that overactivation of GSK-3 inhibited the induction of LTP in rat hippocampus. With activation of GSK-3, both presynaptic release of glutamate and postsynaptic expression of PSD93 and NR2A/B proteins decreased prominently, and the LTP-associated synapse impairments were also observed morphologically.…”

Section: Discussionsupporting

confidence: 52%

Activation of Glycogen Synthase Kinase-3 Inhibits Long-Term Potentiation with Synapse-Associated Impairments

Zhu

Wang²,

Liú³

et al. 2007

J. Neurosci.

214

165

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Activation of glycogen synthase kinase-3 (GSK-3) can cause memory deficits as seen in Alzheimer's disease, the most common ageassociated dementia, but the mechanism is not understood. Here, we found that activation of GSK-3 by wortmannin or transient overexpression of wild-type GSK-3␤ could suppress the induction of long-term potentiation (LTP) in rat hippocampus, whereas simultaneous inhibition of GSK-3 by lithium or SB216763 or transient expression of a dominant-negative GSK-3␤ mutant (dnGSK-3␤) preserved the LTP. After high-frequency stimulation (HFS), the presynaptic release of glutamate and the expression/clustering of synapsin I, a synaptic vesicle protein playing an important role in neurotransmitter release, decreased markedly after upregulation of GSK-3. In vitro studies further demonstrated that GSK-3 inhibited the expression of SynI independent of HFS. In postsynaptic level, the expression of PSD93 and NR2A/B proteins decreased significantly when GSK-3 was activated. The LTP-associated synapse impairments including less presynaptic active zone, thinner postsynaptic density, and broader synaptic cleft were also prominent in the hippocampal slices after HFS with activation of GSK-3. These synaptic impairments were attenuated when GSK-3 was simultaneously inhibited by LiCl or SB216763 or transient expression of dnGSK-3. We conclude that upregulation of GSK-3 impairs the synaptic plasticity both functionally and structurally, which may underlie the GSK-3-involved memory deficits.

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Section: Discussionsupporting

confidence: 52%

Activation of Glycogen Synthase Kinase-3 Inhibits Long-Term Potentiation with Synapse-Associated Impairments

Zhu

Wang²,

Liú³

et al. 2007

J. Neurosci.

214

165

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“…For the spatial learning task a 12 ϫ 12 cm escape platform was hidden with the top surface 2-3 cm below the water level at one of four positions in the pool. The swim path of the rat was recorded manually, and the escape latency was measured using a stopwatch (Richter-Levin and Segal, 1991). Rats were given two blocks of three trials each per day for 5 d followed by a 1 min quadrant analysis test with no escape platform in the maze (Richter-Levin et al, 1994).…”

Section: Behaviormentioning

confidence: 99%

Biphasic Modulation of Hippocampal Plasticity by Behavioral Stress and Basolateral Amygdala Stimulation in the Rat

1999

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Explicit memory may depend on the hippocampus, whereas the amygdala may be part of an emotional memory system. Priming stimulation of the basolateral group of the amygdala (BLA) resulted in an enhanced long-term potentiation (LTP) in the dentate gyrus (DG) to perforant path (PP) stimulation 30, 90, 150, and 180 min after high-frequency stimulation (HFS). Exposure of rats to a behavioral stress is reported to inhibit DG LTP. Because the amygdala is thought to mediate emotional responses, we examined the apparent discrepancy between the effects of behavioral stress induced 1 hr before HFS to the PP and of amygdala priming on hippocampal plasticity by stimulating the BLA 1 hr before HFS to the PP. The two delayed protocols inhibited the expression of LTP to PP stimulation, whereas priming the BLA immediately before HFS to the PP enhanced DG LTP. Moreover, exposure to the behavioral stress blocked the enhancing effects of BLA priming on LTP. We propose that the activation of the BLA (either by behavioral stress or by direct electrical stimulation) has a biphasic effect on hippocampal plasticity: an immediate excitatory effect and a longer-lasting inhibitory effect.

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“…Rats were prepared for acute stimulation of the perforant path and for recording of field potentials in the dentate gyrus under chloral hydrate anesthesia using standard procedures (21). Briefly, a bipolar 125-,um stimulating electrode was implanted in the perforant pathway [AP -8, L 4.2 relative to Bregma according to Paxinos and Watson (22), depth adjusted to yield maximal response of the dentate gyrus].…”

mentioning

confidence: 99%

Long-term potentiation increases tyrosine phosphorylation of the N-methyl-D-aspartate receptor subunit 2B in rat dentate gyrus in vivo.

Rosenblum

Dudai

Richter‐Levin

1996

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

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165

112

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Long-term potentiation (LTP) is a form of synaptic memory that may subserve developmental and behavioral plasticity. An intensively investigated form of LTP is dependent upon N-methyl-D-aspartate (NMDA) receptors and can be elicited in the dentate gyrus and hippocampal CAI. Induction of this type of LTP is triggered by influx of Ca2+ through activated NMDA receptors, but the downstream mechanisms of induction, and even more so of LTP maintenance, remain controversial. It has been reported that the function of NMDA receptor channel can be regulated by protein tyrosine kinases and protein phosphatases and that inhibition of protein tyrosine kinases impairs induction of LTP. Herein we report that LTP in the dentate gyrus is specifically correlated with tyrosine phosphorylation of the NMDA receptor subunit 2B in an NMDA receptor-dependent manner. The effect is observed with a delay of several minutes after LTP induction and persists in vivo for several hours. The potential relevance of this post-translational modification to mechanisms of LTP and circuit plasticity' is discussed.Long-term potentiation (LTP) is regarded as a form of synaptic memory that may subserve experience-dependent plasticity at the circuit and behavioral level (1). Although the relevance of experimentally induced LTP to normal brain function remains uncertain (2, 3), there is widespread agreement that cellular cascades recruited in LTP play a role in brain development (4, 5) and in learning (6-8). An intensively studied form of LTP is dependent upon N-methyl-D-aspartate (NMDA) receptors and can be elicited in the dentate gyrus and hippocampal CAl. Induction of this type of LTP is triggered by influx of Ca2+ through activated NMDA receptors, but the downstream mechanisms of induction, and even more so of LTP maintenance, are controversial (1, 6). These mechanisms may involve modulation of protein kinases and phosphatases, long implicated in short-and intermediate-term neuronal plasticity (9-11). Major candidates are ubiquitous serine/threonine protein kinases (12). Activation of Ca2+/calmodulin-dependent protein kinase II (CAM kinase II) has been specifically implicated in induction, and CAM kinase II-upregulation of a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors in induction and possibly in maintenance of NMDA receptor-dependent LTP (6, 13). Protein tyrosine kinase have also been implicated in LTP; thus, it has been reported that inhibitors of tyrosine kinases impair LTP induction in the dentate gyrus and CAl (14,15) We have recently reported that sensory experience results in enhanced tyrosine phosphorylation of a set of synaptic proteins in the insular cortex of the behaving rat (17). One of these proteins, of 180 kDa, is concentrated in the post-synaptic density and displays properties of the NMDA receptor subunit 2B (NR2B) (18,19). This finding led us to test whether an experimentally controlled form of experience-dependent synaptic modification (i.e., LTP) also results in enhanced tyrosine phosphorylation of the...

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The effects of serotonin depletion and raphe grafts on hippocampal electrophysiology and behavior

Cited by 81 publications

References 48 publications

Activation of Glycogen Synthase Kinase-3 Inhibits Long-Term Potentiation with Synapse-Associated Impairments

Activation of Glycogen Synthase Kinase-3 Inhibits Long-Term Potentiation with Synapse-Associated Impairments

Biphasic Modulation of Hippocampal Plasticity by Behavioral Stress and Basolateral Amygdala Stimulation in the Rat

Long-term potentiation increases tyrosine phosphorylation of the N-methyl-D-aspartate receptor subunit 2B in rat dentate gyrus in vivo.

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