Abstract
Rat sweat glands provide an interesting model system for a developmental study of adrenergic receptor expression because their sympathetic innervation undergoes a switch from a noradrenergic to cholinergic and peptidergic phenotype. α1B, α2B, and β2 receptors are expressed in rat footpads; α1 and β2 receptors are localized specifically to sweat glands, and α2 receptors also are expressed in other tissues. α1 and, to a lesser extent, β2 receptors decrease during development, whereas α2 levels remain relatively constant. Decreased receptor expression is accompanied by the loss of α1-stimulated inositol phosphate accumulation, but no change in β- stimulated cAMP production. The number of α1 and β2 receptors decreases after P21, when the sympathetic innervation no longer produces catecholamines. Neonatal sympathectomy causes a partial failure of α1 downregulation, but has no effect on β2 or α2 receptor levels. Therefore, at least two distinct mechanisms regulate development of adrenergic receptors in sweat glands. Innervation-independent processes control developmental expression of α1, β2, and α2 receptors, and an additional, innervation- dependent mechanism influences expression of α1 receptors. Denervation at postnatal day 20, when the sympathetic innervation is cholinergic and peptidergic, results in retention of α1 receptors, but cholinergic blockade begun at P20 does not. These results indicate that regulation of receptor expression in sweat glands is complex, and suggest that the innervation- dependent factors that decrease α1 levels during development act through a nonadrenergic, noncholinergic mechanism.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 229-237 |
| Number of pages | 9 |
| Journal | Journal of Neuroscience |
| Volume | 16 |
| Issue number | 1 |
| State | Published - Jan 1 1996 |
| Externally published | Yes |
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Keywords
- adrenergic receptors
- anterograde regulation
- autonomic nervous system
- developmental regulation
- neurotransmitter phenotype
- sweat glands
- sympathetic development
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Differential regulation of adrenergic receptor development by sympathetic innervation. / Habecker, Beth; Malec, Neil M.; Landis, Story C.
In: Journal of Neuroscience, Vol. 16, No. 1, 01.01.1996, p. 229-237.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Differential regulation of adrenergic receptor development by sympathetic innervation
AU - Habecker, Beth
AU - Malec, Neil M.
AU - Landis, Story C.
PY - 1996/1/1
Y1 - 1996/1/1
N2 - Rat sweat glands provide an interesting model system for a developmental study of adrenergic receptor expression because their sympathetic innervation undergoes a switch from a noradrenergic to cholinergic and peptidergic phenotype. α1B, α2B, and β2 receptors are expressed in rat footpads; α1 and β2 receptors are localized specifically to sweat glands, and α2 receptors also are expressed in other tissues. α1 and, to a lesser extent, β2 receptors decrease during development, whereas α2 levels remain relatively constant. Decreased receptor expression is accompanied by the loss of α1-stimulated inositol phosphate accumulation, but no change in β- stimulated cAMP production. The number of α1 and β2 receptors decreases after P21, when the sympathetic innervation no longer produces catecholamines. Neonatal sympathectomy causes a partial failure of α1 downregulation, but has no effect on β2 or α2 receptor levels. Therefore, at least two distinct mechanisms regulate development of adrenergic receptors in sweat glands. Innervation-independent processes control developmental expression of α1, β2, and α2 receptors, and an additional, innervation- dependent mechanism influences expression of α1 receptors. Denervation at postnatal day 20, when the sympathetic innervation is cholinergic and peptidergic, results in retention of α1 receptors, but cholinergic blockade begun at P20 does not. These results indicate that regulation of receptor expression in sweat glands is complex, and suggest that the innervation- dependent factors that decrease α1 levels during development act through a nonadrenergic, noncholinergic mechanism.
AB - Rat sweat glands provide an interesting model system for a developmental study of adrenergic receptor expression because their sympathetic innervation undergoes a switch from a noradrenergic to cholinergic and peptidergic phenotype. α1B, α2B, and β2 receptors are expressed in rat footpads; α1 and β2 receptors are localized specifically to sweat glands, and α2 receptors also are expressed in other tissues. α1 and, to a lesser extent, β2 receptors decrease during development, whereas α2 levels remain relatively constant. Decreased receptor expression is accompanied by the loss of α1-stimulated inositol phosphate accumulation, but no change in β- stimulated cAMP production. The number of α1 and β2 receptors decreases after P21, when the sympathetic innervation no longer produces catecholamines. Neonatal sympathectomy causes a partial failure of α1 downregulation, but has no effect on β2 or α2 receptor levels. Therefore, at least two distinct mechanisms regulate development of adrenergic receptors in sweat glands. Innervation-independent processes control developmental expression of α1, β2, and α2 receptors, and an additional, innervation- dependent mechanism influences expression of α1 receptors. Denervation at postnatal day 20, when the sympathetic innervation is cholinergic and peptidergic, results in retention of α1 receptors, but cholinergic blockade begun at P20 does not. These results indicate that regulation of receptor expression in sweat glands is complex, and suggest that the innervation- dependent factors that decrease α1 levels during development act through a nonadrenergic, noncholinergic mechanism.
KW - adrenergic receptors
KW - anterograde regulation
KW - autonomic nervous system
KW - developmental regulation
KW - neurotransmitter phenotype
KW - sweat glands
KW - sympathetic development
UR - http://www.scopus.com/inward/record.url?scp=0030065622&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030065622&partnerID=8YFLogxK
M3 - Article
C2 - 8613789
AN - SCOPUS:0030065622
VL - 16
SP - 229
EP - 237
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 1
ER -