TY - JOUR
T1 - Prejunctional α2-adrenoceptors and peroxide-induced potentiation of norepinephrine release from the bovine iris
AU - Opere, Catherine A.
AU - Ohia, Sunny E.
N1 - Funding Information:
The authors thank Greater Omaha Packing Company for their generous donation of cow eyeballs and Ms. Dawn Trojanowski for her excellent secretarial assistance. This study was supported in part by a grant from the National Institutes of Health (#EY11023).
PY - 1998
Y1 - 1998
N2 - Peroxides can enhance field-stimulated [3H]norepinephrine ([3H]NE) release in isolated irides from several mammalian species. In the present study, we investigated the role of prejunctional α2-adrenoceptors in peroxide-induced potentiation of sympathetic neurotransmission in bovine isolated irides. Isolated hemi-irides were incubated in a Krebs buffered- solution containing [3H]NE and prepared for studies of neurotransmitter release using the superfusion method. α2-Adrenoceptor agonists, oxymetazoline, UK-14304 and clonidine inhibited field-stimulated [3H]NE overflow without affecting basal tritium efflux. Pretreatment of tissues with H2O2 (300 μM) had no effect on inhibition of evoked [3H]NE release caused by the α2-adrenergic agonists. However, H2O2 (300 μM) caused significant (P <0.01) leftward shifts of excitatory concentration-response curves to yohimbine (10 nM-1 μM). In contrast, yohimbine (1 μM) did not prevent the enhancement of evoked [3H]NE overflow induced by H2O2 (300 μM). In conclusion, excitatory effects of peroxides on sympathetic neurotransmission in bovine irides are not mediated by prejunctional α2-adrenoceptors.
AB - Peroxides can enhance field-stimulated [3H]norepinephrine ([3H]NE) release in isolated irides from several mammalian species. In the present study, we investigated the role of prejunctional α2-adrenoceptors in peroxide-induced potentiation of sympathetic neurotransmission in bovine isolated irides. Isolated hemi-irides were incubated in a Krebs buffered- solution containing [3H]NE and prepared for studies of neurotransmitter release using the superfusion method. α2-Adrenoceptor agonists, oxymetazoline, UK-14304 and clonidine inhibited field-stimulated [3H]NE overflow without affecting basal tritium efflux. Pretreatment of tissues with H2O2 (300 μM) had no effect on inhibition of evoked [3H]NE release caused by the α2-adrenergic agonists. However, H2O2 (300 μM) caused significant (P <0.01) leftward shifts of excitatory concentration-response curves to yohimbine (10 nM-1 μM). In contrast, yohimbine (1 μM) did not prevent the enhancement of evoked [3H]NE overflow induced by H2O2 (300 μM). In conclusion, excitatory effects of peroxides on sympathetic neurotransmission in bovine irides are not mediated by prejunctional α2-adrenoceptors.
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U2 - 10.1023/A:1020764220449
DO - 10.1023/A:1020764220449
M3 - Article
C2 - 9704599
AN - SCOPUS:0031593694
VL - 23
SP - 1093
EP - 1098
JO - Neurochemical Research
JF - Neurochemical Research
SN - 0364-3190
IS - 8
ER -