D. Krizsanagbas et al., PRESYNAPTIC ADRENERGIC FACILITATION OF PARASYMPATHETIC NEUROTRANSMISSION IN SYMPATHECTOMIZED RAT SMOOTH-MUSCLE, Journal of physiology, 512(3), 1998, pp. 841-849
1. Parasympathetic innervation of rat eyelid tarsal smooth muscle norm
ally inhibits sympathetic neurotransmission prejunctionally without si
gnificant direct postjunctional effects. Following surgical sympathect
omy, parasympathetic stimulation elicits smooth muscle contraction. Th
is study examined the relative contributions of cholinergic and adrene
rgic mechanisms mediating these contractions. 2. Electrical stimulatio
n of the superior salivatory nucleus, which activates tarsal muscle pa
rasympathetic nerves, elicited large contractions at 2 days postsympat
hectomy, which were abolished by atropine and were decreased by 65% by
alpha(1)-adrenoceptor blockade or spinal cord transection. 3. Contrac
tions in response to direct cholinergic stimulation by bethanechol at
2 days postsympathectomy were increased following spinal cord transect
ion (C2) and suppressed by the alpha(1)-adrenoceptor agonist phenyleph
rine, indicating that adrenoceptors on smooth muscle attenuate choline
rgic contractions. However, phenylephrine infusion enhanced contractil
e responses to parasympathetic stimulation. 4. Reverse transcription-p
olymerase chain reaction revealed alpha(1D)-adrenoceptor mRNA within p
terygopalatine ganglia. 5. At 5 weeks and 14 months postsympathectomy,
adrenergic facilitation was significantly less than at 2 days, wherea
s prazosin-insensitive muscarinic contraction was increased. 6. We con
clude that degeneration of sympathetic :innervation is followed rapidl
y by adrenoceptor-mediated prejunctional enhancement of parasympatheti
c nerve-smooth muscle neurotransmission, which occurs prior to neuroef
fector junction formation as determined previously by electron microsc
opy. Subsequently, noradrenergic enhancement is diminished as choliner
gic neurotransmission becomes established.