Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 165-71 |
| Number of pages | 7 |
| Journal | Brain Research |
| Volume | 857 |
| Issue number | 1-2 |
| Publication status | Published - 28 Feb 2000 |
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Keywords
- Animals
- Benzopyrans
- Corpus Striatum
- Dizocilpine Maleate
- Excitatory Amino Acid Antagonists
- Gentisates
- Glutamic Acid
- Hydroxybenzoic Acids
- Hydroxyl Radical
- Male
- Microdialysis
- Piperazines
- Rats
- Rats, Wistar
- Receptors, N-Methyl-D-Aspartate
- excitotoxicity
- glutamate
- hydroxyl radical
- Ensaculin
- microdialysis
- neuroprotection
- D-ASPARTATE ANTAGONISTS
- ALZHEIMERS-DISEASE
- OXIDATIVE STRESS
- NMDA RECEPTOR
- PARKINSONS-DISEASE
- MPP+ NEUROTOXICITY
- TERT-BUTYLNITRONE
- SUBSTANTIA-NIGRA
- NITRIC-OXIDE
Cite this
Comparison of the novel drug Ensaculin with MK-801 on the reduction of hydroxyl radical production in rat striatum after local application of glutamate. / Teismann, Peter; Ferger, B.
In: Brain Research, Vol. 857, No. 1-2, 28.02.2000, p. 165-71.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Comparison of the novel drug Ensaculin with MK-801 on the reduction of hydroxyl radical production in rat striatum after local application of glutamate
AU - Teismann, Peter
AU - Ferger, B
PY - 2000/2/28
Y1 - 2000/2/28
N2 - Ensaculin interacts with various neurotransmitter systems (e.g., dopaminergic, serotoninergic, glutamatergic) and was originally designed for the treatment of dementia. In the present study Ensaculin was tested for its possible reduction of glutamate-induced hydroxyl free radical formation in vivo. The microdialysis experiment was carried out in non-anaesthetized Wistar rats, which were implanted with a microdialysis probe into the striatum. Salicylate (10 nmol/2 microl/min) was incorporated into the perfusion fluid to measure indirectly hydroxyl radicals indicated by 2,3-dihydroxybenzoic acid (DHBA) formation. After baseline recording, glutamate (100 or 500 nmol/2 microl/min) was perfused through the microdialysis probe (CMA 12, 4 mm, flow rate 2 microl/min). Ensaculin (0.1, 1 and 10 mg/kg), MK-801 (1 mg/kg) or saline was injected i.p. 20 min after the onset of glutamate perfusion (500 nmol/2 microl/min). Glutamate (100 nmol/2 microl/min) and (500 nmol/2 microl/min) perfusion produced a 2.6- and 17-fold increase of 2,3-DHBA, respectively. Treatment with Ensaculin (1 and 10 mg/kg i.p. ) significantly antagonized the formation of 2,3-DHBA, to values of 60.5% and 56.7% of control levels, respectively. In comparison, MK-801 attenuated 2,3-DHBA levels, to values of 65.8% compared to control values. Ensaculin may be useful in the treatment of neurodegenerative disorders associated with elevated hydroxyl free radicals and excitotoxicity.
AB - Ensaculin interacts with various neurotransmitter systems (e.g., dopaminergic, serotoninergic, glutamatergic) and was originally designed for the treatment of dementia. In the present study Ensaculin was tested for its possible reduction of glutamate-induced hydroxyl free radical formation in vivo. The microdialysis experiment was carried out in non-anaesthetized Wistar rats, which were implanted with a microdialysis probe into the striatum. Salicylate (10 nmol/2 microl/min) was incorporated into the perfusion fluid to measure indirectly hydroxyl radicals indicated by 2,3-dihydroxybenzoic acid (DHBA) formation. After baseline recording, glutamate (100 or 500 nmol/2 microl/min) was perfused through the microdialysis probe (CMA 12, 4 mm, flow rate 2 microl/min). Ensaculin (0.1, 1 and 10 mg/kg), MK-801 (1 mg/kg) or saline was injected i.p. 20 min after the onset of glutamate perfusion (500 nmol/2 microl/min). Glutamate (100 nmol/2 microl/min) and (500 nmol/2 microl/min) perfusion produced a 2.6- and 17-fold increase of 2,3-DHBA, respectively. Treatment with Ensaculin (1 and 10 mg/kg i.p. ) significantly antagonized the formation of 2,3-DHBA, to values of 60.5% and 56.7% of control levels, respectively. In comparison, MK-801 attenuated 2,3-DHBA levels, to values of 65.8% compared to control values. Ensaculin may be useful in the treatment of neurodegenerative disorders associated with elevated hydroxyl free radicals and excitotoxicity.
KW - Animals
KW - Benzopyrans
KW - Corpus Striatum
KW - Dizocilpine Maleate
KW - Excitatory Amino Acid Antagonists
KW - Gentisates
KW - Glutamic Acid
KW - Hydroxybenzoic Acids
KW - Hydroxyl Radical
KW - Male
KW - Microdialysis
KW - Piperazines
KW - Rats
KW - Rats, Wistar
KW - Receptors, N-Methyl-D-Aspartate
KW - excitotoxicity
KW - glutamate
KW - hydroxyl radical
KW - Ensaculin
KW - microdialysis
KW - neuroprotection
KW - D-ASPARTATE ANTAGONISTS
KW - ALZHEIMERS-DISEASE
KW - OXIDATIVE STRESS
KW - NMDA RECEPTOR
KW - PARKINSONS-DISEASE
KW - MPP+ NEUROTOXICITY
KW - TERT-BUTYLNITRONE
KW - SUBSTANTIA-NIGRA
KW - NITRIC-OXIDE
M3 - Article
C2 - 10700564
VL - 857
SP - 165
EP - 171
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -