Ta. Milner et al., Cellular relations between mu-opioid receptive, GABAergic and reticulospinal neurons in the rostral ventrolateral medulla, BRAIN RES, 917(1), 2001, pp. 1-14
Physiological studies have suggested that mu -opioid receptor (MOR) activat
ion can both excite and inhibit reticulospinal neurons in the rostral ventr
olateral medulla (RVL), possibly via influences on GABAergic neurons. Thus,
to determine the cellular relationships of MORs to GABAergic neurons in th
e RVL, two experimental approaches were used. First, single sections throug
h the RVL were labeled for MOR using immunoperoxidase detection and for GAB
A using immunogold detection and examined by electron microscopy. These stu
dies revealed that MOR-immunoreactive (IR) terminals were smaller on averag
e than GABA-IR terminals and formed both asymmetric and symmetric synapses,
whereas GABA-IR terminals formed exclusively symmetric synapses. MOR and G
ABA immunoreactivities rarely co-localized. Interactions between axons and
terminals containing MOR or GABA immunoreactivity were primarily: (1) direc
t appositions with each other; or (2) convergence onto a common dendritic t
arget that sometimes contained either MOR or GABA immunoreactivity. Since t
he identity of these target dendrites mostly was unknown, a second study wa
s designed to determine if they might be reticulospinal neurons. For this s
tudy, reticulospinal neurons were identified with a retrograde tracer and b
oth MOR and GABA were localized in the same sections of the RVL. These stud
ies revealed that numerous GABA-IR terminals formed symmetric synapses on t
he perikarya and proximal dendrites of reticulospinal neurons. In contrast,
few MOR-IR terminals contacted reticulospinal perikarya and large dendrite
s although they were often found nearby. These results provide anatomical e
vidence that MOR activation by endogenous or exogenous agonists may indirec
tly alter GABAergic neurotransmission in the RVL either through presynaptic
interactions between cells or through competing influences on postsynaptic
targets. (C) 2001 Elsevier Science B.V. All rights reserved.