Altered α1-adrenoceptor binding in intact and adrenalectomized obese Zucker rats ( fa fa)

Barry E. Levin, Barbara Planas, Vanessa H. Routh, Jock Hamilton, Judith S. Stern, Barbara A Horwitz

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

While many autonomic and metabolic defects associated with genetic obesity in the Zucker rat are corrected by adrenalectomy (Adx), brain adrenoceptor function has not been examined in this context. Here, 3 weeks after Adx or sham surgery, brains of 11 weeks old lean ( Fa Fa) and obese ( fa fa) male Zucker rats were assayed for α1-([3H]prazosin; [3H]PRZ) and α2-adrenoceptor ([3H]paraminoclonidine; [3H]PAC) binding by autoradiography. By genotype, obese rats had 19-256% higher [3H]PRZ binding than lean rats in the amygdala (central [ACN], basolateral [ABL], basomedial [ABM] and medial [MAN] nuclei [n.]), hypothalamus (dorsomedial n. [DMN] and lateral [LH]) and somatosensory cortex. In the ABL and ACN, increased maximal binding(Bmax) in obese rats was associated with decreased affinity (increased Kd). Three weeks after surgery, sham-operated obese rats gained 27% more weight than lean rats but lean and obese Adx rats gained the same amount of weight. Adx reduced [3H]PRZ binding in both lean and obese rats by 37-70% in the amygdala (ABM, ACN, MAN) compared to sham-operated rats. But, Adx selectively reduced [3H]PRZ binding only in lean rats in the ABL, DMN, ventromedial hypothalamic n. (VMN) and ventroposteromedial thalamic n. In most areas, decreases in maximal binding (Bmax) associated with Adx were accompanied by decreases in Kd. Unlike [3H]PRZ binding, there was no consistent genotype difference in [3H]PAC binding although Adx was followed by increased binding in obese and decreased binding in lean rats in the ABL. In only the VMN, obese rats had a 21% higher α2- to α1-adrenoceptor ratio than lean White widespread differences in brain α1-adrenoceptor binding between lean and obese rats may be important, the selectively higher VMN α2-/α1- ratio may be critical to the pathogenesis of obesity.

Original languageEnglish (US)
Pages (from-to)146-154
Number of pages9
JournalBrain Research
Volume614
Issue number1-2
DOIs
StatePublished - Jun 18 1993

Fingerprint

Zucker Rats
Adrenergic Receptors
Brain
Obesity
Genotype
Weights and Measures
Somatosensory Cortex
Prazosin
Adrenalectomy
Amygdala
Autoradiography
Hypothalamus

Keywords

  • Adrenalectomy
  • Adrenoceptor
  • Catecholamine
  • Corticosterone
  • Norepinephrine
  • Obesity

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Levin, B. E., Planas, B., Routh, V. H., Hamilton, J., Stern, J. S., & Horwitz, B. A. (1993). Altered α1-adrenoceptor binding in intact and adrenalectomized obese Zucker rats ( fa fa). Brain Research, 614(1-2), 146-154. https://doi.org/10.1016/0006-8993(93)91028-Q

Altered α1-adrenoceptor binding in intact and adrenalectomized obese Zucker rats ( fa fa). / Levin, Barry E.; Planas, Barbara; Routh, Vanessa H.; Hamilton, Jock; Stern, Judith S.; Horwitz, Barbara A.

In: Brain Research, Vol. 614, No. 1-2, 18.06.1993, p. 146-154.

Research output: Contribution to journalArticle

Levin, BE, Planas, B, Routh, VH, Hamilton, J, Stern, JS & Horwitz, BA 1993, 'Altered α1-adrenoceptor binding in intact and adrenalectomized obese Zucker rats ( fa fa)', Brain Research, vol. 614, no. 1-2, pp. 146-154. https://doi.org/10.1016/0006-8993(93)91028-Q
Levin, Barry E. ; Planas, Barbara ; Routh, Vanessa H. ; Hamilton, Jock ; Stern, Judith S. ; Horwitz, Barbara A. / Altered α1-adrenoceptor binding in intact and adrenalectomized obese Zucker rats ( fa fa). In: Brain Research. 1993 ; Vol. 614, No. 1-2. pp. 146-154.
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abstract = "While many autonomic and metabolic defects associated with genetic obesity in the Zucker rat are corrected by adrenalectomy (Adx), brain adrenoceptor function has not been examined in this context. Here, 3 weeks after Adx or sham surgery, brains of 11 weeks old lean ( Fa Fa) and obese ( fa fa) male Zucker rats were assayed for α1-([3H]prazosin; [3H]PRZ) and α2-adrenoceptor ([3H]paraminoclonidine; [3H]PAC) binding by autoradiography. By genotype, obese rats had 19-256{\%} higher [3H]PRZ binding than lean rats in the amygdala (central [ACN], basolateral [ABL], basomedial [ABM] and medial [MAN] nuclei [n.]), hypothalamus (dorsomedial n. [DMN] and lateral [LH]) and somatosensory cortex. In the ABL and ACN, increased maximal binding(Bmax) in obese rats was associated with decreased affinity (increased Kd). Three weeks after surgery, sham-operated obese rats gained 27{\%} more weight than lean rats but lean and obese Adx rats gained the same amount of weight. Adx reduced [3H]PRZ binding in both lean and obese rats by 37-70{\%} in the amygdala (ABM, ACN, MAN) compared to sham-operated rats. But, Adx selectively reduced [3H]PRZ binding only in lean rats in the ABL, DMN, ventromedial hypothalamic n. (VMN) and ventroposteromedial thalamic n. In most areas, decreases in maximal binding (Bmax) associated with Adx were accompanied by decreases in Kd. Unlike [3H]PRZ binding, there was no consistent genotype difference in [3H]PAC binding although Adx was followed by increased binding in obese and decreased binding in lean rats in the ABL. In only the VMN, obese rats had a 21{\%} higher α2- to α1-adrenoceptor ratio than lean White widespread differences in brain α1-adrenoceptor binding between lean and obese rats may be important, the selectively higher VMN α2-/α1- ratio may be critical to the pathogenesis of obesity.",
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N2 - While many autonomic and metabolic defects associated with genetic obesity in the Zucker rat are corrected by adrenalectomy (Adx), brain adrenoceptor function has not been examined in this context. Here, 3 weeks after Adx or sham surgery, brains of 11 weeks old lean ( Fa Fa) and obese ( fa fa) male Zucker rats were assayed for α1-([3H]prazosin; [3H]PRZ) and α2-adrenoceptor ([3H]paraminoclonidine; [3H]PAC) binding by autoradiography. By genotype, obese rats had 19-256% higher [3H]PRZ binding than lean rats in the amygdala (central [ACN], basolateral [ABL], basomedial [ABM] and medial [MAN] nuclei [n.]), hypothalamus (dorsomedial n. [DMN] and lateral [LH]) and somatosensory cortex. In the ABL and ACN, increased maximal binding(Bmax) in obese rats was associated with decreased affinity (increased Kd). Three weeks after surgery, sham-operated obese rats gained 27% more weight than lean rats but lean and obese Adx rats gained the same amount of weight. Adx reduced [3H]PRZ binding in both lean and obese rats by 37-70% in the amygdala (ABM, ACN, MAN) compared to sham-operated rats. But, Adx selectively reduced [3H]PRZ binding only in lean rats in the ABL, DMN, ventromedial hypothalamic n. (VMN) and ventroposteromedial thalamic n. In most areas, decreases in maximal binding (Bmax) associated with Adx were accompanied by decreases in Kd. Unlike [3H]PRZ binding, there was no consistent genotype difference in [3H]PAC binding although Adx was followed by increased binding in obese and decreased binding in lean rats in the ABL. In only the VMN, obese rats had a 21% higher α2- to α1-adrenoceptor ratio than lean White widespread differences in brain α1-adrenoceptor binding between lean and obese rats may be important, the selectively higher VMN α2-/α1- ratio may be critical to the pathogenesis of obesity.

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