Ammonia-induced upregulation of peripheral-type benzodiazepine receptors in cultured astrocytes labeled with [3H]PK 11195

Yossef Itzhak, Michael D Norenberg

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

Evidence suggests that peripheral-type benzodiazepine receptors (PBRs) may play a role in hepatic encephalopathy (HE), a condition associated with increased levels of ammonia in brain. In the present study, the regulation of [3H]PK 11195-binding to PBRs in cultured rat astrocytes that had been previously exposed to NH4Cl was investigated. 24 h treatment of 21-28-day-old cultures with 2, 5 or 10 mM NH4Cl resulted in 25 ± 3, 48 ± 3 and 42 ± 4% increase in the number of [3H]PK 11195-binding sites, respectively. No further change in [3H]PK 11195-binding was observed after exposure of astrocytes to 5 mM NH4Cl for 48 or 72 h. Ammonia treatment did not cause any significant alteration in the affinity of [3H]PK 11195 for PBRs. The present study demonstrates the susceptibility of the PK 11195-binding site of PBRs in cultured astrocytes to ammonia and suggests that increase in brain ammonia concentration causes a supersensitivity of PBRs.

Original languageEnglish
Pages (from-to)35-38
Number of pages4
JournalNeuroscience Letters
Volume177
Issue number1-2
DOIs
StatePublished - Aug 15 1994

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GABA-A Receptors
Ammonia
Astrocytes
Up-Regulation
Binding Sites
Hepatic Encephalopathy
Brain
PK 11195

Keywords

  • Ammonia
  • Astrocyte
  • Hepatic encephalopathy
  • Peripheral benzodiazepine receptor

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Ammonia-induced upregulation of peripheral-type benzodiazepine receptors in cultured astrocytes labeled with [3H]PK 11195. / Itzhak, Yossef; Norenberg, Michael D.

In: Neuroscience Letters, Vol. 177, No. 1-2, 15.08.1994, p. 35-38.

Research output: Contribution to journalArticle

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abstract = "Evidence suggests that peripheral-type benzodiazepine receptors (PBRs) may play a role in hepatic encephalopathy (HE), a condition associated with increased levels of ammonia in brain. In the present study, the regulation of [3H]PK 11195-binding to PBRs in cultured rat astrocytes that had been previously exposed to NH4Cl was investigated. 24 h treatment of 21-28-day-old cultures with 2, 5 or 10 mM NH4Cl resulted in 25 ± 3, 48 ± 3 and 42 ± 4{\%} increase in the number of [3H]PK 11195-binding sites, respectively. No further change in [3H]PK 11195-binding was observed after exposure of astrocytes to 5 mM NH4Cl for 48 or 72 h. Ammonia treatment did not cause any significant alteration in the affinity of [3H]PK 11195 for PBRs. The present study demonstrates the susceptibility of the PK 11195-binding site of PBRs in cultured astrocytes to ammonia and suggests that increase in brain ammonia concentration causes a supersensitivity of PBRs.",
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N2 - Evidence suggests that peripheral-type benzodiazepine receptors (PBRs) may play a role in hepatic encephalopathy (HE), a condition associated with increased levels of ammonia in brain. In the present study, the regulation of [3H]PK 11195-binding to PBRs in cultured rat astrocytes that had been previously exposed to NH4Cl was investigated. 24 h treatment of 21-28-day-old cultures with 2, 5 or 10 mM NH4Cl resulted in 25 ± 3, 48 ± 3 and 42 ± 4% increase in the number of [3H]PK 11195-binding sites, respectively. No further change in [3H]PK 11195-binding was observed after exposure of astrocytes to 5 mM NH4Cl for 48 or 72 h. Ammonia treatment did not cause any significant alteration in the affinity of [3H]PK 11195 for PBRs. The present study demonstrates the susceptibility of the PK 11195-binding site of PBRs in cultured astrocytes to ammonia and suggests that increase in brain ammonia concentration causes a supersensitivity of PBRs.

AB - Evidence suggests that peripheral-type benzodiazepine receptors (PBRs) may play a role in hepatic encephalopathy (HE), a condition associated with increased levels of ammonia in brain. In the present study, the regulation of [3H]PK 11195-binding to PBRs in cultured rat astrocytes that had been previously exposed to NH4Cl was investigated. 24 h treatment of 21-28-day-old cultures with 2, 5 or 10 mM NH4Cl resulted in 25 ± 3, 48 ± 3 and 42 ± 4% increase in the number of [3H]PK 11195-binding sites, respectively. No further change in [3H]PK 11195-binding was observed after exposure of astrocytes to 5 mM NH4Cl for 48 or 72 h. Ammonia treatment did not cause any significant alteration in the affinity of [3H]PK 11195 for PBRs. The present study demonstrates the susceptibility of the PK 11195-binding site of PBRs in cultured astrocytes to ammonia and suggests that increase in brain ammonia concentration causes a supersensitivity of PBRs.

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