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

Lumsden, Susannah C.; Clarkson, Andrew N.; Cakmak, Yusuf Özgür

doi:10.3389/fnins.2020.00264

Cited by 20 publications

(11 citation statements)

References 231 publications

(331 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increase in the activity of nervi conarii initiated by the suprachiasmatic nucleus of the hypothalamus stimulates the synthesis of melatonin during night time. 112 Day time melatonin levels are low. Optimal levels of melatonin is a powerful free-radical scavenger and combats oxidative stress.…”

Section: Sleep Deprivation and Melatoninmentioning

confidence: 99%

Effects of Sleep Deprivation on the Tryptophan Metabolism

Bhat

Pires

Tan

et al. 2020

Int J�Tryptophan�Res

View full text Add to dashboard Cite

Sleep has a regulatory role in maintaining metabolic homeostasis and cellular functions. Inadequate sleep time and sleep disorders have become more prevalent in the modern lifestyle. Fragmentation of sleep pattern alters critical intracellular second messengers and neurotransmitters which have key functions in brain development and behavioral functions. Tryptophan metabolism has also been found to get altered in SD and it is linked to various neurodegenerative diseases. The kynurenine pathway is a major regulator of the immune response. Adequate sleep alleviates neuroinflammation and facilitates the cellular clearance of metabolic toxins produced within the brain, while sleep deprivation activates the enzymatic degradation of tryptophan via the kynurenine pathway, which results in an increased accumulation of neurotoxic metabolites. SD causes increased production and accumulation of kynurenic acid in various regions of the brain. Higher levels of kynurenic acid have been found to trigger apoptosis, leads to cognitive decline, and inhibit neurogenesis. This review aims to link the impact of sleep deprivation on tryptophan metabolism and associated complication in the brain.

show abstract

Section: Sleep Deprivation and Melatoninmentioning

confidence: 99%

Effects of Sleep Deprivation on the Tryptophan Metabolism

Bhat

Pires

Tan

et al. 2020

Int J�Tryptophan�Res

View full text Add to dashboard Cite

show abstract

“…The SPNs from the IML project out to the postganglionic neurons located within the cervical sympathetic chain (Bowers et al, 1984). The postganglionic sympathetic neurons directly innervate the pineal gland and release norepinephrine during dark cycles of the circadian rhythm to stimulate melatonin synthesis (Huang and Lin, 1984;Lumsden et al, 2020).…”

Section: Pineal Glandmentioning

confidence: 99%

“…Increasing levels of melatonin has been explored as a means to treat able-bodied individuals with perturbed sleep patterns. Interestingly, it has been found that following SCI, the pineal gland is able to produce melatonin again with electrical stimulation of the sympathetic pathway responsible for innervating the pineal gland (Lumsden et al, 2020), identifying a possible means to treat sleep disorders after SCI (Scheer et al, 2006).…”

Section: Pineal Glandmentioning

confidence: 99%

Consequences of spinal cord injury on the sympathetic nervous system

Wulf

Tom

2023

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Spinal cord injury (SCI) damages multiple structures at the lesion site, including ascending, descending, and propriospinal axons; interrupting the conduction of information up and down the spinal cord. Additionally, axons associated with the autonomic nervous system that control involuntary physiological functions course through the spinal cord. Moreover, sympathetic, and parasympathetic preganglionic neurons reside in the spinal cord. Thus, depending on the level of an SCI, autonomic function can be greatly impacted by the trauma resulting in dysfunction of various organs. For example, SCI can lead to dysregulation of a variety of organs, such as the pineal gland, the heart and vasculature, lungs, spleen, kidneys, and bladder. Indeed, it is becoming more apparent that many disorders that negatively affect quality-of-life for SCI individuals have a basis in dysregulation of the sympathetic nervous system. Here, we will review how SCI impacts the sympathetic nervous system and how that negatively impacts target organs that receive sympathetic innervation. A deeper understanding of this may offer potential therapeutic insight into how to improve health and quality-of-life for those living with SCI.

show abstract

“…The pineal gland receives sympathetic innervation from the superior cervical ganglion (SCG). The suprachiasmatic nucleus (SCN) is involved in the control of circadian rhythms and, via sympathetic innervation from the SCG, activates arylalkylamine N-acetyltransferase (AA-NAT) in the pineal gland, which is the main enzyme regulating melatonin synthesis (Lumsden et al, 2020).…”

Section: Norepinephrine Transporter Expression In the Sympathetic Ner...mentioning

confidence: 99%

Schizophrenia Hypothesis: Autonomic Nervous System Dysregulation of Fetal and Adult Immune Tolerance

Carnac¹

2022

Front. Syst. Neurosci.

View full text Add to dashboard Cite

The autonomic nervous system can control immune cell activation via both sympathetic adrenergic and parasympathetic cholinergic nerve release of norepinephrine and acetylcholine. The hypothesis put forward in this paper suggests that autonomic nervous system dysfunction leads to dysregulation of immune tolerance mechanisms in brain-resident and peripheral immune cells leading to excessive production of pro-inflammatory cytokines such as Tumor Necrosis Factor alpha (TNF-α). Inactivation of Glycogen Synthase Kinase-3β (GSK3β) is a process that takes place in macrophages and microglia when a toll-like receptor 4 (TLR4) ligand binds to the TLR4 receptor. When Damage-Associated Molecular Patterns (DAMPS) and Pathogen-Associated Molecular Patterns (PAMPS) bind to TLR4s, the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) pathway should be activated, leading to inactivation of GSK3β. This switches the macrophage from producing pro-inflammatory cytokines to anti-inflammatory cytokines. Acetylcholine activation of the α7 subunit of the nicotinic acetylcholine receptor (α7 nAChR) on the cell surface of immune cells leads to PI3K/Akt pathway activation and can control immune cell polarization. Dysregulation of this pathway due to dysfunction of the prenatal autonomic nervous system could lead to impaired fetal immune tolerance mechanisms and a greater vulnerability to Maternal Immune Activation (MIA) resulting in neurodevelopmental abnormalities. It could also lead to the adult schizophrenia patient’s immune system being more vulnerable to chronic stress-induced DAMP release. If a schizophrenia patient experiences chronic stress, an increased production of pro-inflammatory cytokines such as TNF-α could cause significant damage. TNF-α could increase the permeability of the intestinal and blood brain barrier, resulting in lipopolysaccharide (LPS) and TNF-α translocation to the brain and consequent increases in glutamate release. MIA has been found to reduce Glutamic Acid Decarboxylase mRNA expression, resulting in reduced Gamma-aminobutyric acid (GABA) synthesis, which combined with an increase of glutamate release could result in an imbalance of glutamate and GABA neurotransmitters. Schizophrenia could be a “two-hit” illness comprised of a genetic “hit” of autonomic nervous system dysfunction and an environmental hit of MIA. This combination of factors could lead to neurotransmitter imbalance and the development of psychotic symptoms.

show abstract

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

Cited by 20 publications

References 231 publications

Effects of Sleep Deprivation on the Tryptophan Metabolism

Effects of Sleep Deprivation on the Tryptophan Metabolism

Consequences of spinal cord injury on the sympathetic nervous system

Schizophrenia Hypothesis: Autonomic Nervous System Dysregulation of Fetal and Adult Immune Tolerance

Contact Info

Product

Resources

About