Depletion of ATP and release of presynaptic inhibition in the CA1 region of hippocampal slices during hypoglycemic hypoxia

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4 Citations (Scopus)

Abstract

Transient recovery (TR) of evoked synaptic potentials and ATP depletion during the late stage of hypoxic hypoglycemic insults were investigated in rat hippocampal slices. TR was observed not only in the late stage of insult, but also during recovery. The concentration of ATP corresponded to the appearance (27% of control) and disappearance (15% of control) of TR. Paired pulse studies showed the presynaptic nature of the release of inhibition of synaptic transmission during TR. Both N- and P/Q-type voltage-dependent calcium channels were involved in the appearance of TR. This evidence suggests that underlying mechanisms of TR appearance during hypoxic hypoglycemic insult might be related to ATP depletion and release of A1 adenosine receptor mediated inhibition of presynaptic voltage-dependent calcium channels.

Original languageEnglish
Pages (from-to)56-60
Number of pages5
JournalNeuroscience Letters
Volume411
Issue number1
DOIs
Publication statusPublished - 2007 Jan 3

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Hippocampal CA1 Region
Hypoglycemic Agents
Adenosine Triphosphate
Adenosine A1 Receptors
Synaptic Potentials
Calcium Channels
Evoked Potentials
Synaptic Transmission
Hypoxia

Keywords

  • A1 adenosine receptor
  • Hypoglycemic hypoxia
  • Synaptic depression
  • Transient recovery
  • Voltage-dependent calcium channels

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Depletion of ATP and release of presynaptic inhibition in the CA1 region of hippocampal slices during hypoglycemic hypoxia",
abstract = "Transient recovery (TR) of evoked synaptic potentials and ATP depletion during the late stage of hypoxic hypoglycemic insults were investigated in rat hippocampal slices. TR was observed not only in the late stage of insult, but also during recovery. The concentration of ATP corresponded to the appearance (27{\%} of control) and disappearance (15{\%} of control) of TR. Paired pulse studies showed the presynaptic nature of the release of inhibition of synaptic transmission during TR. Both N- and P/Q-type voltage-dependent calcium channels were involved in the appearance of TR. This evidence suggests that underlying mechanisms of TR appearance during hypoxic hypoglycemic insult might be related to ATP depletion and release of A1 adenosine receptor mediated inhibition of presynaptic voltage-dependent calcium channels.",
keywords = "A1 adenosine receptor, Hypoglycemic hypoxia, Synaptic depression, Transient recovery, Voltage-dependent calcium channels",
author = "Kim, {Jong Hyun} and Kim, {Jae Hak} and Joo-Han Kim and Kim, {Kyung Han} and Taek-Hyun Kwon and Youn-Kwan Park",
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T1 - Depletion of ATP and release of presynaptic inhibition in the CA1 region of hippocampal slices during hypoglycemic hypoxia

AU - Kim, Jong Hyun

AU - Kim, Jae Hak

AU - Kim, Joo-Han

AU - Kim, Kyung Han

AU - Kwon, Taek-Hyun

AU - Park, Youn-Kwan

PY - 2007/1/3

Y1 - 2007/1/3

N2 - Transient recovery (TR) of evoked synaptic potentials and ATP depletion during the late stage of hypoxic hypoglycemic insults were investigated in rat hippocampal slices. TR was observed not only in the late stage of insult, but also during recovery. The concentration of ATP corresponded to the appearance (27% of control) and disappearance (15% of control) of TR. Paired pulse studies showed the presynaptic nature of the release of inhibition of synaptic transmission during TR. Both N- and P/Q-type voltage-dependent calcium channels were involved in the appearance of TR. This evidence suggests that underlying mechanisms of TR appearance during hypoxic hypoglycemic insult might be related to ATP depletion and release of A1 adenosine receptor mediated inhibition of presynaptic voltage-dependent calcium channels.

AB - Transient recovery (TR) of evoked synaptic potentials and ATP depletion during the late stage of hypoxic hypoglycemic insults were investigated in rat hippocampal slices. TR was observed not only in the late stage of insult, but also during recovery. The concentration of ATP corresponded to the appearance (27% of control) and disappearance (15% of control) of TR. Paired pulse studies showed the presynaptic nature of the release of inhibition of synaptic transmission during TR. Both N- and P/Q-type voltage-dependent calcium channels were involved in the appearance of TR. This evidence suggests that underlying mechanisms of TR appearance during hypoxic hypoglycemic insult might be related to ATP depletion and release of A1 adenosine receptor mediated inhibition of presynaptic voltage-dependent calcium channels.

KW - A1 adenosine receptor

KW - Hypoglycemic hypoxia

KW - Synaptic depression

KW - Transient recovery

KW - Voltage-dependent calcium channels

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