ULTRASTRUCTURAL EVIDENCE FOR PROMINENT POSTSYNAPTIC LOCALIZATION OF ALPHA(2C)-ADRENERGIC-RECEPTORS IN CATECHOLAMINERGIC DENDRITES IN THE RAT NUCLEUS LOCUS-COERULEUS
A. Lee et al., ULTRASTRUCTURAL EVIDENCE FOR PROMINENT POSTSYNAPTIC LOCALIZATION OF ALPHA(2C)-ADRENERGIC-RECEPTORS IN CATECHOLAMINERGIC DENDRITES IN THE RAT NUCLEUS LOCUS-COERULEUS, Journal of comparative neurology, 394(2), 1998, pp. 218-229
Alpha-8-adrenergic receptor (alpha(2)-AR) agonists potently inhibit th
e activity of noradrenergic neurons of the locus coeruleus (LC), an ef
fect that may be mediated by the A- and/or C-subtypes of alpha(2)-AR (
alpha(2A)- and alpha(2C)-AR). To gain insight into the functional sign
ificance of these alpha(2)-AR subtypes in the LC, we have examined the
ir ultrastructural localization by using subtype-specific antibodies.
We recently demonstrated that alpha(2A)-ARs are localized prominently
in axon terminals and catecholaminergic dendrites in the LC. In the pr
esent study, we sought to identify the subcellular substrates underlyi
ng alpha(2C)-AR actions in the LC by analyzing the ultrastructural dis
tribution of alpha(2C)-AR immunoreactivity (alpha(2C)-AR-IR) in sectio
ns that were dually labeled far the catecholamine-synthesizing enzyme
tyrosine hydroxylase (TH). Alpha-2C-AR-IR was predominantly localized
in dendrites, most of which also contained immunolabeling far TR. With
in such dendrites, alpha(2C)-AR-IR was associated with the plasma memb
rane and occasionally Golgi cisternae and tubulovesicles. The vast maj
ority of dendrites containing alpha(2C)-AR-IR received asymmetric (exc
itatory) contacts from unlabeled axon terminals that often contained d
ense core vesicles. Alpha-2C-AR-IR was observed in some unmyelinated a
xons and astrocytic processes that were apposed to TH-immunoreactive d
endrites but was rarely associated with axon terminals. These results
provide the first ultrastructural evidence that alpha(2C)-ARs (1) are
localized postsynaptically in catecholaminergic neurons of the LC and
(2) may be strategically situated to modulate the activation of LC neu
rons by excitatory inputs. (C) 1998 Wiley-Liss, Inc.