Guanethidine-sensitive release of neuropeptide Y-like immunoreactivity in the cat spleen by sympathetic nerve stimulation

doi:10.1016/0304-3940(84)90370-7

Neuroscience Letters

Volume 52, Issues 1–2, 23 November 1984, Pages 175-180

https://doi.org/10.1016/0304-3940(84)90370-7 Get rights and content

Abstract

Splenic nerve stimulation (10 Hz for 2 min) caused a perfusion-pressure increase, a volume reduction and an increase in the output of neuropeptide Y-like immunoreactivity (NPY-LI) from the isolated blood-perfused cat spleen. Gel-filtration HPLC analysis revealed that plasma NPY-LI collected during nerve stimulation was similar to the NPY-LI in the spleen and synthetic porcine NPY. Combined propranolol and phenoxybenzamine pretreatment enhanced NPY output upon nerve stimulation by about 60%. Forty percent of the perfusion-pressure increase and 25% of the volume reduction seen during control stimulations remained after adrenoceptor blockade. Guanethidine abolished the release of NPY-LI, the perfusion-pressure increase and the volume reduction normally seen upon splenic nerve stimulation. Infusion of synthetic porcine NPY caused a long-lasting increase in perfusion pressure and a relatively moderate volume reduction. Noradrenaline (NA) both increased perfusion pressure and induced a marked volume reduction. The NPY effects were resistant to adrenoceptor antagonists in doses which abolished the NA response. In conclusion, the present data show that NPY-LI is released upon sympathetic nerve stimulation by a guanethidine-sensitive mechanism. Furthermore, the sympathetic response is partially resistant to adrenoceptor antagonists and NPY has powerful vasoconstrictor effects. This provides further evidence for a role of NPY in sympathetic vascular control.

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Specifically, low-frequency EA instigates the release of many neuropeptides, including nerve growth factor (NGF) and neuropeptide Y (NPY) that are distributed in the peripheral and central nerve systems, and are essential for inducing functional changes in different organ systems [15–17]. Furthermore, NPY can be released from sympathetic nerves via electrical stimulation [6,18,19]. It seems reasonable that NPY could be involved in the working principles of EA treatment in OHSS model rat.
Electroacupuncture (EA) is an effective and safe therapeutic method widely used for treating clinical diseases. Previously, we found that EA could decrease serum hormones and reduce ovarian size in ovarian hyperstimulation syndrome (OHSS) rat model. Nevertheless, the mechanisms that contribute to these improvements remain unclear.
HE staining was used to count the number of corpora lutea (CL) and follicles. Immunohistochemical and ELISA were applied to examine luteal functional and structural regression. Immunoprecipitation was used for analyzing the interaction between NPY (neuropeptide Y) and COX-2; western blotting and qRT-PCR were used to evaluate the expressions of steroidogenic enzymes and PKA/CREB pathway.
EA treatment significantly reduced the ovarian weight and the number of CL, also decreased ovarian and serum levels of PGE2 and COX-2 expression; increased ovarian PGF2α levels and PGF2α/PGE2 ratio; decreased PCNA expression and distribution; and increased cyclin regulatory inhibitor p27 expression to have further effect on the luteal formation, and promote luteal functional and structural regression. Moreover, expression of COX-2 in ovaries was possessed interactivity increased expression of NPY. Furthermore, EA treatment lowered the serum hormone levels, inhibited PKA/CREB pathway and decreased the expressions of steroidogenic enzymes. Hence, interaction with COX-2, NPY may affect the levels of PGF2α and PGE2 as well as impact the proliferation of granulosa cells in ovaries, thus further reducing the luteal formation, and promoting luteal structural and functional regression, as well as the ovarian steroidogenesis following EA treatment.
EA treatment could be an option for preventing OHSS in ART.
Pathway specific expression of neuropeptides and autonomic control of the vasculature
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Studies by Lundberg and colleagues have been instrumental in demonstrating the release of NPY from vasoconstrictor neurons in a range of vascular beds and species. NPY is released together with noradrenaline (NA) and adenosine-5′-triphosphate (ATP) [103–107], although there is preferential release of NPY with higher frequencies and intermittence of stimulation [106,108]. Release of NPY from vasoconstrictor neurons clearly occurs in vivo in response to moderate or intense, but not mild, reflex activation of sympathetic pathways [109–111].
In this article, we review the immunohistochemical evidence for the pathway-specific expression of co-existing neuropeptides in autonomic vasomotor neurons, and examine the functional significance of these expression patterns for the autonomic regulation of the vasculature. Most final motor neurons in autonomic vasomotor pathways contain neuropeptides in addition to non-peptide co-transmitters such as catecholamines, acetylcholine and nitric oxide. Neuropeptides also occur in preganglionic vasomotor neurons. The precise combinations of neuropeptides expressed by neurons in vasomotor pathways vary with species, vascular bed, and the level within the vascular bed. This applies to both vasoconstrictor and vasodilator pathways. There is a similar degree of variation in the expression of neuropeptide receptors in the vasculature. Consequently, the contributions of different peptides to autonomic vasomotor control are closely matched to the functional requirements of specific vascular beds. This arrangement allows for a high degree of precision in vascular control in normal conditions and has the potential for considerable plasticity under pathophysiological conditions.
Changes in the expression of neuropeptide Y (NPY) during maturation of human sympathetic ganglionic neurons: Correlation with tyrosine hydroxylase immunoreactivity
2000, Annals of Anatomy
Developmental patterns of neuropeptide (NPY) and tyrosine hydroxylase (TH)-immunoreactivities (IR) were investigated using the method of indirect immunohistochemistry in the stellate and thoracic sympathetic ganglia of human neonates ranging in gestational age from 24 to 27 weeks (premature group) and from 38 to 41 weeks (mature group). In the paravertebral ganglia of premature neonates a small (up to 7%) population of NPY-IR nerve cells was revealed. With the gestational age increase (a mature group), a marked elevation of the number of NPY-IR ganglionic neurons (up to 41%) was noted. In contrast, in the sympathetic ganglia of premature neonates almost all the neurons were tyrosine hydroxylase immunoreactive and any change in pattern during maturation was insignificant.
The results demonstrate an age-related increase of neuropeptide Y-immunoreactivity in human paravertebral ganglia during maturation, and suggest that peptidergic co-transmission arises later in development than do the classical autonomic messengers. Adaptability of the fetus to a new external environment at birth demands a qualitatively new activity level of the autonomic nervous system, and this is provided side by side with the classical messengers noradrenaline and acetylcholine by the cotransmitter and modulating role of the neuropeptides. The appearance of neuropeptide Y in the principal sympathetic ganglionic neurons defines not only a qualitatively new level in the functional regulation of target organs at birth, but serves as an index of neonatal maturity.
Neuropeptide Y actions and the distribution of Ca<sup>2+</sup>-dependent Cl<sup>-</sup> conductance in rat dorsal root ganglion neurons
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Neuropeptide Y (NPY) increases the excitability of `small', nociceptive, dorsal root ganglion (DRG) neurons. This effect, which may contribute to the etiology of `neuropathic' pain, has been attributed to attenuation of Ca²⁺-sensitive K⁺ conductance(s) (g_K,Ca) following suppression of Ca²⁺ entry via N-type Ca²⁺ channels. A problem arises with this conclusion because rat DRG neurons normally contain high intracellular Cl⁻ and some of them express a Ca²⁺-dependent Cl⁻ conductance (g_Cl,Ca). In this study, we find that in rat DRG neurons increasing intracellular Cl⁻ does not attenuate the effect of 1 μM NPY because g_Cl,Ca is not found in `small' DRG cells and the peptide failed to affect the g_Cl,Ca found in `large' cells. Thus, the presence of g_Cl,Ca in a subpopulation of `large' DRG neurons does not alter the conclusion that excitatory effects of NPY result from attenuation of g_K,Ca.
Nerve injury increases an excitatory action of neuropeptide Y and Y<inf>2</inf>- agonists on dorsal root ganglion neurons
1999, Neuroscience
Damage to sensory nerves invokes the expression of neuropeptide Y in the cell bodies of sensory neurons in dorsal root ganglia. We therefore compared the action of this peptide on control dorsal root ganglia neurons with its action on neurons from animals in which the sciatic nerve had been cut. Neuropeptide Y (0.1–1.0 μM) increased the excitability of 24% of control neurons and its effect was stronger and more cells (56%) were affected after axotomy. Increased excitability was mediated via a Y₂-receptor and resulted from attenuation of Ca²⁺-sensitive K⁺-conductance(s) secondary to suppression of N-type Ca²⁺ channel current. Y₁-agonists potentiated L-type Ca²⁺ channel current in control neurons without altering excitability. This Y₁-effect was attenuated whereas effects mediated via Y₂-receptors were enhanced after axotomy. No evidence was found for involvement of Y₄- or Y₅-receptor subtypes in the actions of neuropeptide Y either on control or on axotomized dorsal root ganglion neurons.
It is concluded that neuropeptide Y increases the excitability of sensory neurons by interacting with a Y₂-receptor and thereby decreasing N-type Ca²⁺ channel current and Ca²⁺-sensitive K⁺-conductance(s). When peripheral nerves are damaged, dorsal root ganglion neurons start to express neuropeptide Y and its excitatory Y₂-excitatory effects are enhanced. The peptide may therefore contribute to the generation of aberrant sensory activity and perhaps to the etiology of injury-induced neuropathic pain.
Neuropeptide Y Y<inf>1</inf> receptors in vascular pharmacology
1998, European Journal of Pharmacology
The existence of neurogenic mediator candidates apart from noradrenaline and acetylcholine involved in the control of vascular tone has attracted enormous attention during the past few decades. One such mediator is neuropeptide Y (NPY), which is co-localized with noradrenaline in sympathetic perivascular nerves. Stimulation of sympathetic nerves in vitro and in vivo causes non-adrenergic vasoconstriction which can be blocked by experimental manipulations that inhibit NPY mechanisms. Thus, the vasopressor response to stimulation of sympathetic nerves can be attenuated by chemical or surgical sympathectomy, treatment with reserpine or other pharmacological agents, and tachyphylaxis to NPY or by NPY antagonists. The NPY field was long plagued by a lack of specific antagonists, but with the recently developed, selective, non-peptide and stable NPY antagonists it has now become possible to study subtypes of this receptor family. For instance, it has become clear that the NPY Y₁ receptor mediates most of the direct peripheral effects of NPY on vascular tone. These antagonists promise to stimulate NPY research and will likely unravel the true significance of NPY in cardiovascular control under physiological conditions as well as in pathophysiological states.

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Guanethidine-sensitive release of neuropeptide Y-like immunoreactivity in the cat spleen by sympathetic nerve stimulation

Abstract

Neurosci. Lett.

The response of the spleen to nerve stimulation in relation to the frequency of splenic nerve discharge

The effect of neuronal rest on the output of sympathetic transmitter from the spleen

J. Physiol. (Lond.)

Vascular responses and noradrenaline overflows in the isolated blood perfused cat spleen: some effects of cocaine normetanephrine and α-blocking agents

J. Physiol. (Lond.)

The effects of graded doses of phenoxybenzamine on the vascular and capsular responses of the isolated, blood-perfused dog's spleen to sympathetic nerve stimulation and catecholamines

Arch. Int. Pharmacodyn.

A specific sympathomimetic ergone in adrenergic nerve fibers (sympathin) and its relations to adrenaline and noradrenaline

Acta Physiol. Scand.