Restraint stress increases hemichannel activity in hippocampal glial cells and neurons

Juan A. Orellana, Rodrigo Moraga-Amaro, Raúl Díaz-Galarce, Sebastián Rojas, Carola J. Maturana, Jimmy Stehberg, Juan C. Sáez

Resultado de la investigación: Article

33 Citas (Scopus)

Resumen

Stress affects brain areas involved in learning and emotional responses, which may contribute in the development of cognitive deficits associated with major depression. These effects have been linked to glial cell activation, glutamate release and changes in neuronal plasticity and survival including atrophy of hippocampal apical dendrites, loss of synapses and neuronal death. Under neuro-inflammatory conditions, we recently unveiled a sequential activation of glial cells that release ATP and glutamate via hemichannels inducing neuronal death due to activation of neuronal NMDA/P2X7 receptors and pannexin1 hemichannels. In the present work, we studied if stressinduced glia activation is associated to changes in hemichannel activity. To this end, we compared hemichannel activity of brain cells after acute or chronic restraint stress in mice. Dye uptake experiments in hippocampal slices revealed that acute stress induces opening of both Cx43 and Panx1 hemichannels in astrocytes, which were further increased by chronic stress; whereas enhanced Panx1 hemichannel activity was detected in microglia and neurons after acute/chronic and chronic stress, respectively. Moreover, inhibition of NMDA/P2X7 receptors reduced the chronic stress-induced hemichannel opening, whereas blockade of Cx43 and Panx1 hemichannels fully reduced ATP and glutamate release in hippocampal slices from stressed mice. Thus, we propose that gliotransmitter release through hemichannels may participate in the pathogenesis of stress-associated psychiatric disorders and possibly depression.

Idioma originalEnglish
Páginas (desde-hasta)1-12
Número de páginas12
PublicaciónFrontiers in Cellular Neuroscience
Volumen9
N.ºAPR
DOI
EstadoPublished - 2 abr 2015

Huella dactilar

Purinergic P2X7 Receptors
Neuroglia
Glutamic Acid
Connexin 43
N-Methyl-D-Aspartate Receptors
Neurons
Adenosine Triphosphate
Depression
Neuronal Plasticity
Brain
Microglia
Dendrites
Astrocytes
Synapses
Atrophy
Psychiatry
Coloring Agents
Learning
Inhibition (Psychology)

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Citar esto

Orellana, J. A., Moraga-Amaro, R., Díaz-Galarce, R., Rojas, S., Maturana, C. J., Stehberg, J., & Sáez, J. C. (2015). Restraint stress increases hemichannel activity in hippocampal glial cells and neurons. Frontiers in Cellular Neuroscience, 9(APR), 1-12. https://doi.org/10.3389/fncel.2015.00102
Orellana, Juan A. ; Moraga-Amaro, Rodrigo ; Díaz-Galarce, Raúl ; Rojas, Sebastián ; Maturana, Carola J. ; Stehberg, Jimmy ; Sáez, Juan C. / Restraint stress increases hemichannel activity in hippocampal glial cells and neurons. En: Frontiers in Cellular Neuroscience. 2015 ; Vol. 9, N.º APR. pp. 1-12.
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Orellana, JA, Moraga-Amaro, R, Díaz-Galarce, R, Rojas, S, Maturana, CJ, Stehberg, J & Sáez, JC 2015, 'Restraint stress increases hemichannel activity in hippocampal glial cells and neurons', Frontiers in Cellular Neuroscience, vol. 9, n.º APR, pp. 1-12. https://doi.org/10.3389/fncel.2015.00102

Restraint stress increases hemichannel activity in hippocampal glial cells and neurons. / Orellana, Juan A.; Moraga-Amaro, Rodrigo; Díaz-Galarce, Raúl; Rojas, Sebastián; Maturana, Carola J.; Stehberg, Jimmy; Sáez, Juan C.

En: Frontiers in Cellular Neuroscience, Vol. 9, N.º APR, 02.04.2015, p. 1-12.

Resultado de la investigación: Article

TY - JOUR

T1 - Restraint stress increases hemichannel activity in hippocampal glial cells and neurons

AU - Orellana, Juan A.

AU - Moraga-Amaro, Rodrigo

AU - Díaz-Galarce, Raúl

AU - Rojas, Sebastián

AU - Maturana, Carola J.

AU - Stehberg, Jimmy

AU - Sáez, Juan C.

PY - 2015/4/2

Y1 - 2015/4/2

N2 - Stress affects brain areas involved in learning and emotional responses, which may contribute in the development of cognitive deficits associated with major depression. These effects have been linked to glial cell activation, glutamate release and changes in neuronal plasticity and survival including atrophy of hippocampal apical dendrites, loss of synapses and neuronal death. Under neuro-inflammatory conditions, we recently unveiled a sequential activation of glial cells that release ATP and glutamate via hemichannels inducing neuronal death due to activation of neuronal NMDA/P2X7 receptors and pannexin1 hemichannels. In the present work, we studied if stressinduced glia activation is associated to changes in hemichannel activity. To this end, we compared hemichannel activity of brain cells after acute or chronic restraint stress in mice. Dye uptake experiments in hippocampal slices revealed that acute stress induces opening of both Cx43 and Panx1 hemichannels in astrocytes, which were further increased by chronic stress; whereas enhanced Panx1 hemichannel activity was detected in microglia and neurons after acute/chronic and chronic stress, respectively. Moreover, inhibition of NMDA/P2X7 receptors reduced the chronic stress-induced hemichannel opening, whereas blockade of Cx43 and Panx1 hemichannels fully reduced ATP and glutamate release in hippocampal slices from stressed mice. Thus, we propose that gliotransmitter release through hemichannels may participate in the pathogenesis of stress-associated psychiatric disorders and possibly depression.

AB - Stress affects brain areas involved in learning and emotional responses, which may contribute in the development of cognitive deficits associated with major depression. These effects have been linked to glial cell activation, glutamate release and changes in neuronal plasticity and survival including atrophy of hippocampal apical dendrites, loss of synapses and neuronal death. Under neuro-inflammatory conditions, we recently unveiled a sequential activation of glial cells that release ATP and glutamate via hemichannels inducing neuronal death due to activation of neuronal NMDA/P2X7 receptors and pannexin1 hemichannels. In the present work, we studied if stressinduced glia activation is associated to changes in hemichannel activity. To this end, we compared hemichannel activity of brain cells after acute or chronic restraint stress in mice. Dye uptake experiments in hippocampal slices revealed that acute stress induces opening of both Cx43 and Panx1 hemichannels in astrocytes, which were further increased by chronic stress; whereas enhanced Panx1 hemichannel activity was detected in microglia and neurons after acute/chronic and chronic stress, respectively. Moreover, inhibition of NMDA/P2X7 receptors reduced the chronic stress-induced hemichannel opening, whereas blockade of Cx43 and Panx1 hemichannels fully reduced ATP and glutamate release in hippocampal slices from stressed mice. Thus, we propose that gliotransmitter release through hemichannels may participate in the pathogenesis of stress-associated psychiatric disorders and possibly depression.

KW - Connexins

KW - Glia

KW - Hemichannels

KW - Hippocampus

KW - Neuron

KW - Pannexins

KW - Stress

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U2 - 10.3389/fncel.2015.00102

DO - 10.3389/fncel.2015.00102

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SP - 1

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JO - Frontiers in Cellular Neuroscience

JF - Frontiers in Cellular Neuroscience

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