Differential regulation of adrenergic receptor development by sympathetic innervation

Habecker, Beth A.; Malec, Neil M.; Landis, Story C.

doi:10.1523/jneurosci.16-01-00229.1996

Cited by 20 publications

(17 citation statements)

References 34 publications

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“…Thus, not only are catecholamines required for secretory responsiveness, but the time of onset and the extent of secretory responsiveness depend on catecholamine levels. Developing and mature sweat gland cells possess at least two adrenergic receptors, ␣ 1 and ␤ 2 (Habecker et al, 1996). Each receptor activates the predicted second messenger system: ␣ 1 receptors stimulate phospholipase C, and ␤ 2 receptors stimulate adenylyl cyclase activity.…”

Section: Discussionmentioning

confidence: 99%

“…Scale bar : a, c, 10 m; b, 20 m. et al, 1984). Not only does gland morphogenesis occur normally in 6-OHDA-treated rat pups, but so does the development of adrenergic and muscarinic receptors and their coupling to second messenger systems Habecker et al, 1996). Despite the fact that glands appear to develop normally in albino TH null mice and 6-OHDA-treated rats, in neither case are the sweat glands competent to produce sweat droplets in response to treatment with a muscarinic agonist; i.e., they fail to mature functionally.…”

Section: Discussionmentioning

confidence: 99%

“…In culture sweat glands require adrenergic receptor activation to produce cholinergic differentiation factor, which in turn induces cholinergic properties in the sympathetic neurons innervating them (Habecker et al, 1996(Habecker et al, , 1997. It is possible that the absence of a secretory response in albino TH null mice was a consequence of the absence of cholinergic function in the gland innervation, which is essential for secretory responsiveness (Grant et al, 1995).…”

Section: Catecholamines Are Not Required For the Appearance Of Cholinmentioning

confidence: 99%

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Catecholamines Are Required for the Acquisition of Secretory Responsiveness by Sweat Glands

et al. 2000

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The sympathetic innervation of sweat glands undergoes a developmental change in transmitter phenotype from catecholaminergic to cholinergic. Acetylcholine elicits sweating and is necessary for development and maintenance of secretory responsiveness, the ability of glands to produce sweat after nerve stimulation or agonist administration. To determine whether catecholamines play a role in the development or function of this system, we examined the onset of secretory responsiveness in two transgenic mouse lines, one albino and the other pigmented, that lack tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine synthesis. Although both lines lack TH, their catecholamine levels differ because tyrosinase in pigmented mice serves as an alternative source for catecholamine synthesis (Rios et al., 1999). At postnatal day 21 (P21), 28 glands on average are active in interdigital hind footpads of albino TH wild-type mice. In contrast, fewer than one gland is active in albino TH null mice, which lack catecholamines in gland innervation. Treatment of albino TH null mice with DOPA, a catecholamine precursor, from P11 to P21 increases the number of active glands to 14. Pigmented TH null mice, which have faint catecholamine fluorescence in the developing gland innervation, possess 12 active glands at P21, indicating that catecholamines made via tyrosinase, albeit reduced from wild-type levels, support development of responsiveness. Gland formation and the appearance of cholinergic markers occur normally in albino TH null mice, suggesting that catecholamines act directly on gland cells to trigger their final differentiation and to induce responsiveness. Thus, catecholamines, like acetylcholine, are essential for the development of secretory responsiveness.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Catecholamines Are Not Required For the Appearance Of Cholinmentioning

confidence: 99%

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Catecholamines Are Required for the Acquisition of Secretory Responsiveness by Sweat Glands

et al. 2000

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“…The morphological development of sweat glands, as well as the molecular and pharmacological properties of muscarinic cholinergic and adrenergic receptors of sweat glands are independent of innervation Habecker et al, 1996). However, innervation is essential for a late step of sweat gland maturation, the development and maintenance of secretory responsiveness, i.e.…”

Section: Functions Of Cholinergic Sympathetic Innervationmentioning

confidence: 99%

Target-dependent specification of the neurotransmitter phenotype:cholinergic differentiation of sympathetic neurons is mediated in vivo by gp130 signaling

et al. 2006

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Sympathetic neurons are generated through a succession of differentiation steps that initially lead to noradrenergic neurons innervating different peripheral target tissues. Specific targets, like sweat glands in rodent footpads, induce a change from noradrenergic to cholinergic transmitter phenotype. Here, we show that cytokines acting through the gp130 receptor are present in sweat glands. Selective elimination of the gp130 receptor in sympathetic neurons prevents the acquisition of cholinergic and peptidergic features (VAChT, ChT1, VIP) without affecting other properties of sweat gland innervation. The vast majority of cholinergic neurons in the stellate ganglion, generated postnatally, are absent in gp130-deficient mice. These results demonstrate an essential role of gp130-signaling in the target-dependent specification of the cholinergic neurotransmitter phenotype.

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“…Much of this process must depend on gene regulation and new protein synthesis. For example, developing sympathetic neurons switch their neurotransmitter phenotype from noradrenergic to cholinergic and peptidergic after innervation of the sweat gland and periosteum (42,43), a process induced by target-derived retrograde factors. Although the switching of transmitter type requires the expression of a set of new enzymes for transmitter metabolism, possibly affecting the entire presynaptic neuron, retrograde determination of other more subtle presynaptic phenotypes can be restricted only to a subset of presynaptic nerve terminals.…”

Section: Retrograde Signaling During Synaptogenesismentioning

confidence: 99%

Retrograde signaling at central synapses

Tao

Poo

2001

Proc. Natl. Acad. Sci. U.S.A.

124

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Transcellular retrograde signaling from the postsynaptic target cell to the presynaptic neuron plays critical roles in the formation, maturation, and plasticity of synaptic connections. We here review recent progress in our understanding of the retrograde signaling at developing central synapses. Three forms of potential retrograde signals-membrane-permeant factors, membrane-bound factors, and secreted factors-have been implicated at both developing and mature synapses. Although many of these signals may be active constitutively, retrograde factors produced in association with activity-dependent synaptic plasticity, e.g., long-term potentiation and long-term depression, are of particular interest, because they may induce modification of neuronal excitability and synaptic transmission, functions directly related to the processing and storage of information in the nervous system. N eural information coded by the action potential is transmitted through a chemical synapse in the anterograde direction by release of neurotransmitters, neuropeptides, and other protein factors from the presynaptic terminal. These molecules produce immediate changes in the membrane potential as well as long-term structural and metabolic changes in the postsynaptic cell. Over the past several decades, it has become increasingly clear that information exchange at the synapse is bidirectional: the postsynaptic cell also provides a variety of retrograde signals to the presynaptic neuron. This reciprocal interaction is crucial for the differentiation and maintenance of the presynaptic cell as well as the formation and maturation of the synapse. The general notion of retrograde signaling involves postsynaptic production of a signal, either constitutively or triggered by synaptic activity, that acts on the presynaptic neuron through the following mechanisms. First, the retrograde signal can be carried by a membrane-permeant molecule that diffuses across the plasma membranes from the postsynaptic cell directly into the presynaptic nerve terminal. Second, membraneimpermeant but soluble factors can be packaged and secreted via exocytotic vesicles by the postsynaptic cell and exert the retrograde action by binding and activation of receptors on the presynaptic membrane. Third, direct signaling through the synaptic cleft may be accomplished through mediation of physically coupled pre-and postsynaptic membrane-bound proteins, including transmembrane proteins as well as those secreted and immobilized in the extracellular matrix within the synaptic cleft. This review will summarize recent progress in the study of retrograde regulation at central synapses, with a focus on the role of retrograde interaction in the formation and activitydependent plasticity of synapses. Some aspects of this subject have been more extensively reviewed elsewhere (1). An excellent review of signaling at developing neuromuscular junctions (NMJs) has also appeared recently (2). Retrograde Signaling During SynaptogenesisOur present understanding of the process of synaptogenesis...

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Differential regulation of adrenergic receptor development by sympathetic innervation

Cited by 20 publications

References 34 publications

Catecholamines Are Required for the Acquisition of Secretory Responsiveness by Sweat Glands

Catecholamines Are Required for the Acquisition of Secretory Responsiveness by Sweat Glands

Target-dependent specification of the neurotransmitter phenotype:cholinergic differentiation of sympathetic neurons is mediated in vivo by gp130 signaling

Retrograde signaling at central synapses

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