Dataset Information

Neuromodulation of the Pineal Gland via Electrical Stimulation of Its Sympathetic Innervation Pathway.

ABSTRACT: Stimulation of the pineal gland via its sympathetic innervation pathway results in the production of N-acetylserotonin and melatonin. Melatonin has many therapeutic roles and is heavily implicated in the regulation of the sleep-wake cycle. In addition, N-acetylserotonin has recently been reported to promote neurogenesis in the brain. Upregulation of these indoleamines is possible via neuromodulation of the pineal gland. This is achieved by electrical stimulation of structures or fibres in the pineal gland sympathetic innervation pathway. Many studies have performed such pineal neuromodulation using both invasive and non-invasive methods. However, the effects of various experimental variables and stimulation paradigms has not yet been reviewed and evaluated. This review summarises these studies and presents the optimal experimental protocols and stimulation parameters necessary for maximal upregulation of melatonin metabolic output.

SUBMITTER: Lumsden SC

PROVIDER: S-EPMC7145358 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Neuromodulation of the Pineal Gland via Electrical Stimulation of Its Sympathetic Innervation Pathway.

Lumsden Susannah C SC Clarkson Andrew N AN Cakmak Yusuf Ozgur YO

Frontiers in neuroscience 20200402

Stimulation of the pineal gland via its sympathetic innervation pathway results in the production of N-acetylserotonin and melatonin. Melatonin has many therapeutic roles and is heavily implicated in the regulation of the sleep-wake cycle. In addition, N-acetylserotonin has recently been reported to promote neurogenesis in the brain. Upregulation of these indoleamines is possible via neuromodulation of the pineal gland. This is achieved by electrical stimulation of structures or fibres in the pi ...[more]

PMID: 32300290

Similar Datasets

Project description:ObjectiveThe unraveling of the elaborate brain networks that control glucose metabolism presents one of the current challenges in diabetes research. Within the central nervous system, the hypothalamus is regarded as the key brain area to regulate energy homeostasis. The aim of the present study was to investigate the hypothalamic mechanism involved in the hyperglycemic effects of the neuropeptide pituitary adenylyl cyclase-activating polypeptide (PACAP).Research design and methodsEndogenous glucose production (EGP) was determined during intracerebroventricular infusions of PACAP-38, vasoactive intestinal peptide (VIP), or their receptor agonists. The specificity of their receptors was examined by coinfusions of receptor antagonists. The possible neuronal pathway involved was investigated by 1) local injections in hypothalamic nuclei, 2) retrograde neuronal tracing from the thoracic spinal cord to hypothalamic preautonomic neurons together with Fos immunoreactivity, and 3) specific hepatic sympathetic or parasympathetic denervation to block the autonomic neuronal input to liver.ResultsIntracerebroventricular infusion of PACAP-38 increased EGP to a similar extent as a VIP/PACAP-2 (VPAC2) receptor agonist, and intracerebroventricular administration of VIP had significantly less influence on EGP. The PACAP-38 induced increase of EGP was significantly suppressed by preinfusion of a VPAC2 but not a PAC1 receptor antagonist, as well as by hepatic sympathetic but not parasympathetic denervation. In the hypothalamus, Fos immunoreactivity induced by PACAP-38 was colocalized within autonomic neurons in paraventricular nuclei projecting to preganglionic sympathetic neurons in the spinal cord. Local infusion of PACAP-38 directly into the PVN induced a significant increase of EGP.ConclusionsThis study demonstrates that PACAP-38 signaling via sympathetic preautonomic neurons located in the paraventricular nucleus is an important component in the hypothalamic control of hepatic glucose production.

Project description:Purpose:Perineural invasion (PNI) is reported to correlate with local recurrence and poor prognosis of salivary adenoid cystic carcinoma (SACC). However, the pathogenesis of PNI remains unclear. The aims of this study were to investigate the correlation between sympathetic innervation and SACC PNI and to elucidate how the sympathetic neurotransmitter norepinephrine (NE) regulates the PNI process. Materials and methods:Sympathetic innervation and ?2-adrenergic receptor (?2-AR) expression in SACC tissues were evaluated by immunohistochemistry. The NE concentrations in SACC tissues and dorsal root ganglia (DRG) coculture models were measured by ELISA. ?2-AR expression in SACC cells was detected by performing quantitative real-time polymerase chain reaction (qRT-PCR) and immunofluorescence assay. SACC cells were treated with NE, the nonselective ?-AR blocker phentolamine, the ?2-AR antagonist ICI118,551, or were transfected with ?2-AR small interfering RNA (siRNA). Proliferation was evaluated in methyl thiazolyl tetrazolium assay, and migration was evaluated in Transwell assay and wound-healing assay. PNI was tested through both Transwell assay and a DRG coculture model. The expressions of epithelial-mesenchymal transition (EMT) markers and matrix metalloproteinases (MMPs) were measured by performing qRT-PCR and Western blot assay. Results:Sympathetic innervation and ?2-AR were highly distributed in SACC tissues and correlated positively with PNI (P=0.035 and P=0.003, respectively). The sympathetic neurotransmitter NE was overexpressed in SACC tissues and DRG coculture models. Exogenously added NE promoted proliferation, migration, and PNI of SACC cells via ?2-AR activation. NE/?2-AR signaling may promote proliferation, migration, and PNI by inducing EMT and upregulating MMPs. However, ?2-AR inhibition with either an antagonist or siRNA abrogated NE-induced PNI. Conclusion:Collectively, our findings reveal the supportive role of sympathetic innervation in the pathogenesis of SACC PNI and suggest ?2-AR as a potential therapeutic target for treating PNI in SACC.

Dataset Information

Neuromodulation of the Pineal Gland via Electrical Stimulation of Its Sympathetic Innervation Pathway.

Publications

Neuromodulation of the Pineal Gland via Electrical Stimulation of Its Sympathetic Innervation Pathway.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets