<i>N</i>‐Methyl‐D‐Aspartate Receptor Activation and Ca<sup>2+</sup> Account for Poor Pyramidal Cell Structure in Hippocampal Slices

Feig, Sherry L.; Lipton, Peter

doi:10.1111/j.1471-4159.1990.tb04160.x

Cited by 81 publications

(43 citation statements)

References 46 publications

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“…The brain was rapidly removed and cross-chopped cerebral cortex slices were prepared and incubated in batch as previously described (2). Nominally Ca 2ϩ -free Krebs-Henseleit bicarbonate saline (KHBS) was supplemented with 10 mM MgCl 2 for slicing and restorative incubations because this buffer has been shown to prevent damage that occurs when slices are incubated in normal physiological buffer immediately after slicing (10). After the first 45 min of incubation, MgCl 2 was returned to normal (1 mM).…”

Section: Methodsmentioning

confidence: 99%

The antibipolar drug valproate mimics lithium in stimulating glutamate release and inositol 1,4,5-trisphosphate accumulation in brain cortex slices but not accumulation of inositol monophosphates and bisphosphates

Dixon

Hokin

1997

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

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Valproic acid and lithium are effective antibipolar drugs. We recently showed that lithium stimulated the release of glutamate in monkey and mouse cerebral cortex slices, which, through activation of the N-methyl-D-aspartate receptor, increased accumulation of inositol 1,4,5-trisphosphate [Ins(1,4,5)P 3 ]. We show here that valproate behaves similarly to lithium in that at therapeutic concentrations it stimulates glutamate release and Ins(1,4,5)P 3 accumulation in mouse cerebral cortex slices. The fact that these two effects are a common denominator for two structurally unrelated antibipolar drugs suggests that these effects are important in their antibipolar action. The effects of maximal concentrations of lithium and valproate on glutamate release are additive, suggesting different mechanisms for release, which are discussed. The additivity of the two drugs on glutamate release is consistent with the clinical benefit of combining the two drugs in the treatment of subsets of bipolar patients, e.g., in rapid cycling manic-depression. Unlike lithium, valproate does not increase accumulation of inositol monophosphates, inositol bisphosphates, or inositol 1,3,4-trisphosphate. This is additional evidence against the ''inositol depletion'' hypothesis, which states that, by trapping inositol in the form of inositol monophosphates and certain inositol polyphosphates, lithium exerts its antimanic action by inhibiting resynthesis of phosphoinositides with resultant blunting of Ins(1,4,5)P 3 signaling.

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Section: Methodsmentioning

confidence: 99%

The antibipolar drug valproate mimics lithium in stimulating glutamate release and inositol 1,4,5-trisphosphate accumulation in brain cortex slices but not accumulation of inositol monophosphates and bisphosphates

Dixon

Hokin

1997

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

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“…To test whether the protein content of dead slice edges (typically 35-50 m) (Feig and Lipton, 1990;Sikló s et al, 1997;Frenguelli et al, 2003) results in an underestimate of ATP in the viable core of the slice, we prepared neocortical/hippocampal slices of different thickness, thereby changing the ratio of dead to viable tissue. Because there were no significant changes in the TAN levels between slice cutting and 5 h incubation (Fig.…”

Section: The Tissue Suffers From Physical Damage Causing Additional Lmentioning

confidence: 99%

Intracellular ATP Influences Synaptic Plasticity in Area CA1 of Rat Hippocampus via Metabolism to Adenosine and Activity-Dependent Activation of Adenosine A₁Receptors

Nedden¹,

Hawley²,

Pentland³

et al. 2011

J. Neurosci.

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The extent to which brain slices reflect the energetic status of the in vivo brain has been a subject of debate. We addressed this issue to investigate the recovery of energetic parameters and adenine nucleotides in rat hippocampal slices and the influence this has on synaptic transmission and plasticity. We show that, although adenine nucleotide levels recover appreciably within 10 min of incubation, it takes 3 h for a full recovery of the energy charge (to Ն0.93) and that incubation of brain slices at 34°C results in a significantly higher ATP/AMP ratio and a threefold lower activity of AMP-activated protein kinase compared with slices incubated at room temperature. Supplementation of artificial CSF with D-ribose and adenine (Rib/Ade) increased the total adenine nucleotide pool of brain slices, which, when corrected for the influence of the dead cut edges, closely approached in vivo values. Rib/Ade did not affect basal synaptic transmission or paired-pulse facilitation but did inhibit long-term potentiation (LTP) induced by tetanic or weak theta-burst stimulation. This decrease in LTP was reversed by strong theta-burst stimulation or antagonizing the inhibitory adenosine A 1 receptor suggesting that the elevated tissue ATP levels had resulted in greater activity-dependent adenosine release during LTP induction. This was confirmed by direct measurement of adenosine release with adenosine biosensors. These observations provide new insight into the recovery of adenine nucleotides after slice preparation, the sources of loss of such compounds in brain slices, the means by which to restore them, and the functional consequences of doing so.

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“…Slices were incubated on 0.4 m porous culture plate inserts (Millipore, Bedford, MA) for 60 min at room temperature in ACSF (in mM: 117 NaCl, 5.3 KCl, 26 NaHCO 3 , 1 NaH 2 PO 4 , 1.5 MgSO 4 , 2.5 CaCl 2 , and 10 glucose, pH 7.4, equilibrated with 95% O 2 /5% CO 2 ) with Ca 2ϩ removed to avoid excitotoxic damage (Feig and Lipton, 1990). Subsequently, incubation was continued at either 37 or 4°C for 9 hr in ACSF saturated with 95% O 2 /5% CO 2 after which slices were prepared for DiO labeling or electron microscopy by microwave-assisted fixation (Jensen and Harris, 1989).…”

Section: Methodsmentioning

confidence: 99%

Hypothermia-Associated Loss of Dendritic Spines

Roelandse¹,

Matus²

2004

J. Neurosci.

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Mechanisms of synaptic plasticity in CNS circuits are commonly investigated using in vitro preparations such as brain slices or slice culture. During their preparation, slices are exposed to low temperatures, and electrophysiological measurements are sometimes made below physiological temperature. Because dendritic spines, which occur at the majority of excitatory synapses, are morphologically plastic, we investigated the influence of reduced temperature on their morphology and plasticity using live cell imaging of hippocampal slices from transgenic mice expressing a green fluorescent protein-based neuronal surface marker and electron microscopy of adult brain slices. Our data show that dendritic spines are highly sensitive to reduced temperature with rapid loss of actin-based motility followed at longer times by reversible loss of the entire spine structure. Thus, reduced temperature significantly affects synaptic morphology, which is in turn known to influence several key aspects of synaptic transmission. Evidence that hypothermia potentiates anesthesia and is associated with spine loss in hibernating animals further suggests that spine morphology may have a widespread influence on brain function.

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N‐Methyl‐D‐Aspartate Receptor Activation and Ca²⁺ Account for Poor Pyramidal Cell Structure in Hippocampal Slices

Cited by 81 publications

References 46 publications

The antibipolar drug valproate mimics lithium in stimulating glutamate release and inositol 1,4,5-trisphosphate accumulation in brain cortex slices but not accumulation of inositol monophosphates and bisphosphates

The antibipolar drug valproate mimics lithium in stimulating glutamate release and inositol 1,4,5-trisphosphate accumulation in brain cortex slices but not accumulation of inositol monophosphates and bisphosphates

Intracellular ATP Influences Synaptic Plasticity in Area CA1 of Rat Hippocampus via Metabolism to Adenosine and Activity-Dependent Activation of Adenosine A₁Receptors

Hypothermia-Associated Loss of Dendritic Spines

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N‐Methyl‐D‐Aspartate Receptor Activation and Ca2+ Account for Poor Pyramidal Cell Structure in Hippocampal Slices

Cited by 81 publications

References 46 publications

The antibipolar drug valproate mimics lithium in stimulating glutamate release and inositol 1,4,5-trisphosphate accumulation in brain cortex slices but not accumulation of inositol monophosphates and bisphosphates

The antibipolar drug valproate mimics lithium in stimulating glutamate release and inositol 1,4,5-trisphosphate accumulation in brain cortex slices but not accumulation of inositol monophosphates and bisphosphates

Intracellular ATP Influences Synaptic Plasticity in Area CA1 of Rat Hippocampus via Metabolism to Adenosine and Activity-Dependent Activation of Adenosine A1Receptors

Hypothermia-Associated Loss of Dendritic Spines

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N‐Methyl‐D‐Aspartate Receptor Activation and Ca²⁺ Account for Poor Pyramidal Cell Structure in Hippocampal Slices

Intracellular ATP Influences Synaptic Plasticity in Area CA1 of Rat Hippocampus via Metabolism to Adenosine and Activity-Dependent Activation of Adenosine A₁Receptors