Sympathetic activation of sweat glands

In wild-type mice, a cholinergic innervation of adjacent sweat gland fields was undetectable in P1, although VAChT immunoreactivity was readily detectable in neuromuscular junctions Fig.

The presence of a sympathetic innervation, however, was confirmed by TH staining around sweat gland coils at this age Fig. Similar to the previous analyses in rats and mice Schafer et al. TH immunoreactivity also intensified from P3 Fig. A VAChT immunoreactivity is present in neuromuscular endplates arrow , but undetectable in an adjacent sweat gland territory asterisks of a P1 WT mouse.

B TH immunoreactivity labels sympathetic sweat gland innervation on an adjacent section to A , but is absent from the cholinergic neuromuscular junctions.

F TH immunoreactivity labels exclusively sympathetic sweat gland innervation on an adjacent section to E. The arrow points to a neuromuscular endplate. TH staining is comparable to P3 WT. EGFP appears to be a less valuable marker compared with VAChT for labeling distal nerve fibers and terminals during development, perhaps because of relative VAChT protein concentrations in small synaptic vesicles in distal forming nerve terminals, compared with EGFP expression in their relatively scanty cytoplasm.

Finally, we confirmed that VAChT and TH were co-expressed in sympathetic fibers by performing a double immunofluorescence analysis. At P4, both in wild type Fig. Other noradrenergically innervated sympathetic targets, e.

Two possible mechanisms could account for the developmental acquisition of the cholinergic phenotype in peripheral sympathetic neurons. In one, the peripheral target structure, e. A second mechanism is based on the assumption that most, if not all, genes encoding proteins required for classic neurotransmission in a given class of neurons, are expressed prior to target innervation, and that with new target selection a pre-existing phenotype is enhanced and shifted to a preferential and target-specific neurotransmitter choice Schafer et al.

Introduction of several copies of the CGL into mice increased the sensitivity of the detection of cholinergic nerve cell bodies and fibers through EGFP over-expression from the ChAT promoter.

While EGFP-based fluorescence turned out to be a valuable marker for central cholinergic neurons von Engelhardt et al. We found that VAChT mRNA and protein expression was indeed proportionately higher, and present in many SG neurons around birth, indicating that in addition to a small number of purely cholinergic neurons Guidry and Landis, ; Masliukov and Timmermans, , many additional postganglionic sympathetic neurons in the SG transiently have a cholinergic phenotype, albeit weak, during development Masliukov and Timmermans, ; Weihe and Eiden, Thus, from embryonic stages on and into adulthood, the sympathetic cholinergic phenotype passes through a successive stabilization in expression, rather than through a target-dependent induction.

This indicates that pioneering sudomotor axons that express a cholinergic phenotype successfully connect cholinergically committed neuronal cell bodies with their appropriate target without being instructed to switch from a noradrenergic phenotype. According to the target-dependent instruction mode one would expect to see a significant increase in the number of cholinergic neurons between the initial noradrenergic target innervation and the subsequent appearance of cholinergic markers, leaving a time window for a target-dependent switch of just a few days.

Thus, a detailed analysis of cholinergic neuron numbers in the sympathetic ganglion of interest across the critical developmental time points is highly informative. This postnatal increase was interpreted in favor of the target-dependent mode of cholinergic phenotype aquisition.

According to Stanke and colleagues this proportion would be expected to increase significantly until P If it does not control acquisition of the neurotransmitter phenotype per se, what then is the specific function of the target in this process? One function of the target organ could be the generation of an innervation factor Glebova and Ginty, Developing sweat glands have been found to express neurturin mRNA shortly after birth in mice Hiltunen and Airaksinen, This study suggested that single cholinergic nerve fiber plexus arborization and final target innervation may require neurturin signaling.

The target may also release classic neurotransmitter-selective neurotrophins, that not only function as survival factors Glebova and Ginty, , but also preferentially regulate the sorting of vesicle-type-specific proteins, e.

VMAT2, VAChT and their subsequent selective delivery to the synapse, thus influencing the type of neurotransmitter released at the varicose ending Felder and Dechant, All the previously proposed sweat gland factors, e. Enhancement of the expression of cholinergic genes and thus generation of larger amounts of cholinergic-specific proteins may also be driven by the synaptic interaction between neuron and target.

Moreover, differential sensitivities of cholinergic vs. Discrepancies in the ability to detect the cholinergic phenotype on the ganglionic vs. Finally, the target might also be responsible for influencing the acquisition of additional neuropeptides in the cholinergic neurons, since interfering with the expression of leukemia inhibitory factor receptor beta, a protein that forms heterodimers with gp, strongly reduced the developmental expression of the VIP gene in chick sympathetic neurons Duong et al.

While maintenance, trophic support, anterograde transport of neurotransmitter-specific proteins and survival of these neurons may all be regulated in a target-dependent manner Hippenmeyer et al. We thank H. Hlawaty, P. Lattermann, R. Weber, and M. Schneider for technical assistance. National Center for Biotechnology Information , U. Author manuscript; available in PMC Jun 2. Author information Copyright and License information Disclaimer. E-mail address: ed. Copyright notice. The publisher's final edited version of this article is available at Neuroscience.

See other articles in PMC that cite the published article. Abstract Classic neurotransmitter phenotypes are generally predetermined and develop as a consequence of target-independent lineage decisions. Keywords: acetylcholine, development, transgene, vesicular transporter.

Open in a separate window. VAChT and TH immunoreactive nerve fibers appear simultaneously in nerve fibers around developing forepaw sweat glands in ChAT-EGFP transgenic mice We next analyzed if the increased mRNA expression and immunohistochemical detection of VAChT in the SG at birth resulted in a proportionately enhanced detectability in the developing sweat gland terminal field and other sympathetic targets.

Acknowledgments We thank H. The GDNF family: signalling, biological functions and therapeutic value. Nat Rev Neurosci. How many types of cholinergic sympathetic neuron are there in the rat stellate ganglion?

Illicitinga parasympathetic response will not stimulate these neurons and therefore sweating is not a parasympathetic side effect. However, as post-synaptic sweat glands contain Muscarinic receptors and not adrenoceptors the administration of a non-selective Muscarinic agonist would result in both a parasympathetic response such as constriction of the pupil or decreased heart rate as well as sweating due to the activation of these sympathetic post-synaptic MAChR in the sweat glands.

That is a good question! Sweat glands get the nerve supply from the sympathetic trunk. So anatomically they get sympathetic nerve supply. But the neurotransmitter at the target cells is acetylcholine. So functionally or physiologically, the sweat glands get the parasympathetic nerve supply.

Your sweat glands are controlled by autonomic nervous system. They get the nervous supply through the sympathetic nerves. But functionally they are parasympathetic nerves, because the acetylcholine is secreted over there at the terminal end. Sympathetic fibers innervate sweat glands. The sympathetic division innervates the sweat glands and hair follicles. Sympathetic stimulation of your salivary glands suppresses the activity of the glands and salivation decreases.

During parasympathetic stimulation you to salivate. Sympathetic fibers convey impulses that stimulate our "fight or flight" response. Parasympathetic are just the opposite, you might say they are for "rest and digest". They are both firing at the same time but depending on your environment and emotional state, one will dominate over the other. Sympathetic and parasympathetic fibers release different neurotransmitters, which bind to different receptors.

Three structures that receive sympathetic innervation are the adrenal glands, arrector pilli muscles, and sweat glands. Organs innervated by the parasympathetic nervous system. One addition to that are sweat glands. They are innervated by sympathetic nervous system, however, they have muscarinic receptors, NOT adrenergic receptors. They are neither sympathetic nor parasympathetic.

Parasympathetic decrease the heart rate while sympathetic increase it. The sympathetic and parasympathetic nervous systems are subdivisions of the autonomic nervous system. No, post-ganglionic sympathetic fibers mostly release norepinephrine.

But they do release some ACh to the sweat glands, which causes concurrent vasodilation of surrounding blood vessels paired with release of bradykinin from sweat glands. The sympathetic division of the autonomic nervous system controls eccrine sweat glands.

Log in. Preganglionic neurons communicate with the chromaffin cells and stimulate them to release epinephrine and norepinephrine directly into your blood. The sympathetic nervous system releases two hormones within the body in response to stress, resulting in an "adrenaline rush", or a sense of urgency that occurs during stressful conditions.

These hormones are called epinephrine and norepinephrine, which help your body perform optimally during such events. Upon activation of your system, norepinephrine is released to prepare the body for the initial stages of stress. If the stress is quickly resolved, the body functions return to normal. However, if the stressful event persists, your body produces epinephrine to increase these effects and activate various parts of the body to react accordingly.

When one faces a dangerous or stressful situation, the sympathetic nervous system is automatically activated without conscious control.

Various body functions are activated almost simultaneously such as:. These are just some of the common functions involved in the fight-or-flight response regulated by your sympathetic nervous system. Because of such body reactions, your body is prepared to run, fight, lift heavy weights or react according to the need, depending on specific threatening situations.

When the situation is resolved, the sympathetic functions return to its resting state, allowing your heart rate to go back to normal, your breathing to slow down, and your other body functions to return to a balanced state. Copyright WWW. Last Updated 14 January, What Is the Sympathetic Nervous System?