Electrophysiological effects of locally applied noradrenergic agents at cerebellar Purkinje neurons: receptor specificity
Identifieur interne : 001595 ( Main/Exploration ); précédent : 001594; suivant : 001596Electrophysiological effects of locally applied noradrenergic agents at cerebellar Purkinje neurons: receptor specificity
Auteurs : Karen D. Parfitt [États-Unis] ; Robert Freedman [États-Unis] ; Paula C. Bickford-Wimer [États-Unis]Source :
- Brain Research [ 0006-8993 ] ; 1988.
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Abstract
Abstract: We have investigated the receptor subtype(s) mediating the noradrenergic inhibition of cerebellar Purkinje cell spontaneous firing rate using local application of specific agonists and antagonists, in situ, via pressure microejection. Extracellular action potentials were recorded from Purkinje neurons in anesthetized Fischer 344 rats. Timolol, a β-receptor antagonist, did not affect norepinephrine (NE)-induced inhibition in 9 of 12 cells studied. Phentolamine, a α-receptor antagonist, blocked the effect of NE in 8 of 11 cells. To further determine the subtype of α-receptor involved, the effects of the α1-antagonist prazosin and α2-antagonists idazoxan and yohimbine were examined. While prazosin had no effect on NE-mediated inhibition, both idazoxan and yohimbine blocked NE effects. Idazoxan was also successful in blocking phencyclidine (PCP), an indirect noradrenergic agonist. The inhibitory action of NE upon Purkinje cell firing rate was mimicked by the selective α2-agonist clonidine; whis action of clonidine was blocked by idazoxan but not by timolol or prazosin. In addition, the α1-adrenergic agonist phenylephrine and the β-adrenergic agonist isoproterenol inhibited Purkinje cell firing rate. Phenylephrine effects were blocked by prazosin but not by timolol or idazoxan. Isoproterenol-induced inhibition was blocked by timolol but not phentolamine. Taken together, these studies suggest that both α and β-receptors alter Purkinje cell firing rate; the depressat action of locally applied NE, however, seems to be mediated primarily via an α2-adrenergic receptor.
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DOI: 10.1016/0006-8993(88)90552-5
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Extracellular action potentials were recorded from Purkinje neurons in anesthetized Fischer 344 rats. Timolol, a β-receptor antagonist, did not affect norepinephrine (NE)-induced inhibition in 9 of 12 cells studied. Phentolamine, a α-receptor antagonist, blocked the effect of NE in 8 of 11 cells. To further determine the subtype of α-receptor involved, the effects of the α1-antagonist prazosin and α2-antagonists idazoxan and yohimbine were examined. While prazosin had no effect on NE-mediated inhibition, both idazoxan and yohimbine blocked NE effects. Idazoxan was also successful in blocking phencyclidine (PCP), an indirect noradrenergic agonist. The inhibitory action of NE upon Purkinje cell firing rate was mimicked by the selective α2-agonist clonidine; whis action of clonidine was blocked by idazoxan but not by timolol or prazosin. In addition, the α1-adrenergic agonist phenylephrine and the β-adrenergic agonist isoproterenol inhibited Purkinje cell firing rate. Phenylephrine effects were blocked by prazosin but not by timolol or idazoxan. Isoproterenol-induced inhibition was blocked by timolol but not phentolamine. Taken together, these studies suggest that both α and β-receptors alter Purkinje cell firing rate; the depressat action of locally applied NE, however, seems to be mediated primarily via an α2-adrenergic receptor.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Colorado</li></region></list><tree><country name="États-Unis"><region name="Colorado"><name sortKey="Parfitt, Karen D" sort="Parfitt, Karen D" uniqKey="Parfitt K" first="Karen D." last="Parfitt">Karen D. Parfitt</name></region><name sortKey="Bickford Wimer, Paula C" sort="Bickford Wimer, Paula C" uniqKey="Bickford Wimer P" first="Paula C." last="Bickford-Wimer">Paula C. Bickford-Wimer</name><name sortKey="Bickford Wimer, Paula C" sort="Bickford Wimer, Paula C" uniqKey="Bickford Wimer P" first="Paula C." last="Bickford-Wimer">Paula C. 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