• O L Pudovkina, Y Kawahara, J de Vries, and B H Westerink.
• Department of Biomonitoring and Sensoring, University Center for Pharmacy, University of Groningen, Deusinglaan 1, 9712 AV Groningen, The Netherlands. o.pudovkina@farm.rug.nl
• Brain Res. 2001 Jul 6;906(1-2):38-45.

AbstractThe present study was undertaken to investigate and compare the properties of noradrenaline release in the locus coeruleus (LC) and prefrontal cortex (PFC). For that aim the dual-probe microdialysis technique was applied for simultaneous detection of noradrenaline levels in the LC and PFC in conscious rats. Calcium omission in the LC decreased noradrenaline levels in the LC, but increased its levels in the PFC. Novelty increased noradrenaline levels in both structures. Infusion of the alpha(2)-adrenoceptor agonist clonidine decreased extracellular noradrenaline in the LC as well as in the PFC. Infusion of the alpha(2A)-adrenoceptor antagonist BRL44408, or the alpha(1)-adrenoceptor agonist cirazoline into the LC or PFC caused a similar dose-dependent increase in both structures. When BRL44408 or cirazoline were infused into the LC, few effects were seen in the PFC. Infusion of the 5-HT(1A)-receptor agonist flesinoxan into the LC or the PFC decreased the release of noradrenaline in both structures. When flesinoxan was infused into the LC, no effects were seen in the PFC. When the GABA(A) antagonist bicuculline was applied to the LC, noradrenaline increased in the LC as well as in the PFC. It is concluded that the release of noradrenaline from somatodendritic sites and nerve terminals responded in a similar manner to presynaptic receptor modulation. The possible existence of dendritic noradrenaline release is discussed.

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