Dj. Watkins et al., LOSS OF [I-125] PINDOLOL BINDING TO BETA-ADRENOCEPTORS ON RAT NODOSE GANGLION AFTER CHRONIC ISOPRENALINE TREATMENT, Journal of the autonomic nervous system, 60(1-2), 1996, pp. 12-16
The nodose ganglion contains the cell bodies of afferent nerves which
convey predominantly sensory information from the viscera to the centr
al nervous system (CNS). Autoradiographic studies show binding sites f
or beta-adrenoceptor ligands are present on sections of the rat nodose
ganglion and also on the corresponding inferior vagal ganglion in hum
ans, indicating the presence of beta-adrenoceptors in these ganglia. S
ince prolonged stimulation of beta-adrenoceptors in rats with the nons
elective beta-adrenoceptor agonist isoprenaline (400 mu g kg(-1) day(-
1) s.c.) for 14 days results in desensitisation and/or down-regulation
of receptors in peripheral tissues, such as heart, kidney and blood v
essels, the effects of this treatment on the p-adrenoceptor population
on the nodose ganglion have been examined. Using [I-125]-pindolol as
a radioligand, autoradiographic studies revealed that specific binding
was reduced by 74% in ganglia from isoprenaline-pretreated rats compa
red to that in ganglia from vehicle-pretreated rats, demonstrating dow
n-regulation of receptors by isoprenaline. [I-125]-Pindolol binding wa
s sensitive to inhibition by ICI 118,551 (selective beta(2)-adrenocept
or antagonist) but not to atenolol (selective beta(1)-adrenoceptor ant
agonist), indicating receptors are predominantly of the beta(2)-adreno
ceptor subtype. No change in binding was apparent over the vagus nerve
. The nodose ganglion appears to be an additional site at which beta(2
)-adrenoceptors may be down-regulated in vivo, possibly interfering wi
th normal baro-, chemo- and sensory reflexes.