Early expression of glycine and GABAA receptors in developing spinal cord neurons. Effects on neurite outgrowth

Tapia, Juan Carlos; Mentis, George Z.; Olivares-Navarrete, René; Nualart, Francisco; Figueroa, Eric E.; Sánchez, Alexandra; Aguayo, Luis G.

doi:10.1016/s0306-4522(01)00348-7

Cited by 35 publications

(32 citation statements)

References 50 publications

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“…Hippocampal Cultures-Hippocampal neurons were obtained from 18-day-old mice embryos as described previously (16) in accordance with National Institutes of Health recommendations. The neuronal feeding medium consisted of 90% minimal essential medium (Invitrogen), 5% heat-inactivated horse serum, 5% fetal bovine serum, and a mixture of nutrient supplements.…”

Section: Methodsmentioning

confidence: 99%

β-Amyloid Causes Depletion of Synaptic Vesicles Leading to Neurotransmission Failure

Parodí

Sepúlveda

Roa

et al. 2010

Journal of Biological Chemistry

161

120

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Alzheimer disease is a progressive neurodegenerative brain disorder that leads to major debilitating cognitive deficits. It is believed that the alterations capable of causing brain circuitry dysfunctions have a slow onset and that the full blown disease may take several years to develop. Therefore, it is important to understand the early, asymptomatic, and possible reversible states of the disease with the aim of proposing preventive and disease-modifying therapeutic strategies. It is largely unknown how amyloid ␤-peptide (A␤), a principal agent in Alzheimer disease, affects synapses in brain neurons. In this study, we found that similar to other pore-forming neurotoxins, A␤ induced a rapid increase in intracellular calcium and miniature currents, indicating an enhancement in vesicular transmitter release. Significantly, blockade of these effects by low extracellular calcium and a peptide known to act as an inhibitor of the A␤-induced pore prevented the delayed failure, indicating that A␤ blocks neurotransmission by causing vesicular depletion. This new mechanism for A␤ synaptic toxicity should provide an alternative pathway to search for small molecules that can antagonize these effects of A␤.

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Section: Methodsmentioning

confidence: 99%

β-Amyloid Causes Depletion of Synaptic Vesicles Leading to Neurotransmission Failure

Parodí

Sepúlveda

Roa

et al. 2010

Journal of Biological Chemistry

161

120

View full text Add to dashboard Cite

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“…Primary neuronal cultures obtained from 18-to 19-day-old embryos were prepared according to previously published protocols (Tapia et al, 2001). All experiments were performed in cultures maintained for 10e12 days in vitro.…”

Section: Primary Hippocampal Culturesmentioning

confidence: 99%

Low concentrations of ethanol protect against synaptotoxicity induced by Aβ in hippocampal neurons

Muñoz

Urrutia

Burgos

et al. 2015

Neurobiology of Aging

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“…Some of the GABA effects on migration required membrane depolarization and Ca 2ϩ elevation (Behar et al, 1996(Behar et al, , 1998, consistent with the excitatory action of GABA in developing neurons. In addition to the effects on migration, neurite growth was influenced by GABA A receptor activation in various systems (Barbin et al, 1993;Marty et al, 1996;Maric et al, 2001;Tapia et al, 2001;Borodinsky et al, 2003), an effect that could be reproduced by agents that elevate GABA synthesis or activate L-type Ca 2ϩ channels Tapia et al, 2001;Borodinsky et al, 2003). Interestingly, neurite growth could also be antagonized by furosemide, which inhibits Cl Ϫ transporters , again suggesting the involvement of GABA A receptor activation and Ca 2ϩ elevation.…”

Section: Introductionmentioning

confidence: 96%

Excitatory GABA Action Is Essential for Morphological Maturation of Cortical NeuronsIn Vivo

Cancedda¹,

Fiumelli²,

Chen³

et al. 2007

J. Neurosci.

350

358

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GABA exerts excitatory actions on embryonic and neonatal cortical neurons, but the in vivo function of this GABA excitation is essentially unknown. Using in utero electroporation, we eliminated the excitatory action of GABA in a subpopulation of rat ventricular progenitors and cortical neurons derived from these progenitors by premature expression of the Cl Ϫ transporter KCC2, as confirmed by the changes in the reversal potential of GABA-induced currents and the resting membrane potential after GABA A receptor blockade. We found that radial migration to layer II/III of the somatosensory cortex of neurons derived from the transfected progenitors was not significantly affected, but their morphological maturation was markedly impaired. Furthermore, reducing neuronal excitability of cortical neurons in vivo by overexpressing an inward-rectifying K ϩ channel, which lowered the resting membrane potential, mimicked the effect of premature KCC2 expression. Thus, membrane depolarization caused by early GABA excitation is critical for morphological maturation of neonatal cortical neurons in vivo.

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Early expression of glycine and GABAA receptors in developing spinal cord neurons. Effects on neurite outgrowth

Cited by 35 publications

References 50 publications

β-Amyloid Causes Depletion of Synaptic Vesicles Leading to Neurotransmission Failure

β-Amyloid Causes Depletion of Synaptic Vesicles Leading to Neurotransmission Failure

Low concentrations of ethanol protect against synaptotoxicity induced by Aβ in hippocampal neurons

Excitatory GABA Action Is Essential for Morphological Maturation of Cortical NeuronsIn Vivo

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