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- W2029679905 abstract "The α2-adrenoceptor agonist, clonidine (0.001–1 mg/kg, IP), dose-dependently induced mydriasis in conscious rats (ED50 0.088 mg/kg). This response was maximal when measured 10 min after clonidine injection and was of about 30-min duration. The noradrenaline releasing agent, methamphetamine (0.75 mg/kg, IP), also increased pupil diameter. Clonidine (0.03 mg/kg, IP)-induced mydriasis was inhibited in a dose-related fashion by the α2-adrenoceptor antagonists, idazoxan (0.03–3 mg/kg, IP) and yohimbine (0.03–3 mg/kg, IP), but was unaltered by the α1- or β-adrenergic antagonists, prazosin (1 and 3 mg/kg, IP) or pindolol (1 and 3 mg/kg, IP). Methamphetamine (0.75 mg/kg, IP)-induced mydriasis was similarly inhibited by idazoxan (1 mg/kg, IP) and yohimbine (1 mg/kg, IP). These data argued strongly that central α2-adrenoceptors are involved in the mediation of mydriasis. The synaptic location of these receptors was determined using DSP-4 (50 mg/kg × 2, IP) to lesion noradrenergic neurones: this produced a 64% depletion of noradrenaline in the midbrain (containing the Edinger-Westphal nucleus responsible for mydriasis) and reduced the mydriatic effect of methamphetamine (0.75 mg/kg, IP) to a similar extent (72%), whereas clonidine mydriasis remained unaltered. Therefore, these results show that the mydriasis responses induced by either clonidine or methamphetamine are mediated by central postsynaptic α2-adrenoceptors." @default.
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- W2029679905 date "1997-01-01" @default.
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- W2029679905 title "Modulation of dopamine by norepinephrine in the prefrontal cortex" @default.
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