Physostigmine effects on serotonin uptake in human blood platelets

Rausch, Jeffrey L.; Janowsky, David S.; Risch, S. Craig; Huey, Leighton Y.

doi:10.1016/0014-2999(85)90543-6

Cited by 29 publications

(14 citation statements)

References 22 publications

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“…Thus, the assessment of the peripheral circulating ACh levels would not afford a useful tool for the understanding of the pathophysiological and/or clinical disorders. Besides, a close cooperation between the peripheral ACh and serotonin neurotransmitters has been demonstrated [2, 125,130,131]. This factor affords additional complexity to the management of this circulating neurotransmitter as a useful tool to the understanding of the peripheral ANS mechanisms, as is the case of circulating catecholamines and indolamines.…”

Section: Physiological Evidencementioning

confidence: 99%

“…This neurotransmitter is not detectable at the peripheral blood because it is fastly destroyed by the acetyl cholinesterase enzyme. Moreover, this neurotransmitter is uptaked by platelets [2,125]. However, ACh released from parasympathetic nerves is able to act at the nicotinic and muscarinic receptors located at the visceral and muscle levels.…”

Section: Physiological Evidencementioning

confidence: 99%

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Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Lechín¹,

Dijs²

2008

TONEURJ

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Abstract:The assessment of circulating neurotransmitters: noradrenaline, adrenaline, dopamine, platelet serotonin, plasma serotonin and plasma tryptophan before and after many types of stressor agents and neuropharmacological drugs carried out over the last thirty years allowed us to accumulate information dealing with the central nervous system (CNS) versus the peripheral autonomic nervous system (ANS) interactions in healthy as well as diseased mammals. Furthermore, the accurate knowledge about the CNS circuitry disorders which underlie both the CNS and peripheral clinical syndromes, has allowed us to prescribe successful neuropharmacological therapeutical strategies for many types of illnesses. In addition, the demonstration that the clinical improvement was always paralleled by the normalization of the neurochemical, hormonal, immunological and clinical profiles affords strong support to our point of view. According to all the above, the authors postulate the existence of two types of diseases: type A and Type N, which are underlain by two opposite CNS + ANS disorders. Type A diseases should be associated with the "uncoping stress" syndrome and are underlain by hyperactivity of the adrenocortical glands plus the CNS disorder characterized by the predominance of the C1(adrenergic) + DR(serotonergic) axis over the A5(noradrenergic) + MR(serotonergic) binomial, whereas the type N diseases depends on the opposite profile: "endogenous depression" syndrome. Finally, we quoted exhaustive evidence showing that the well known fading of both the A6(noradrenergic) + C1(adrenergic) CNS nuclei activity occurring during aging is responsible for the ANS + CNS disorder which is similar to that underlying psychosis, Alzheimer, post-traumatic stress disorder and deficit-attention hyperactive disorder.

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Section: Physiological Evidencementioning

confidence: 99%

Section: Physiological Evidencementioning

confidence: 99%

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Lechín¹,

Dijs²

2008

TONEURJ

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“…These activities were minimized throughout the OGTT + tianeptine test because of the fall of f5-HT. With respect to this, it should be known that both circulating Ad and ACh are able to increase f5-HT, the former because it triggers platelet aggregation, whereas the latter throughout the interference with the platelet uptake of serotonin [42].…”

Section: Peripheral Mechanismsmentioning

confidence: 99%

Effect of Tianeptine on Glucose Tolerance with Insulin Secretion in Human: Potential Anti-Diabetic Effect of the Drug

Lechín¹,

Dijs²,

Maldonado³

et al. 2009

TONEUROEJ

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Due to the fact that drugs which interfere with the serotonin (5-HT) uptake (doxepin, sertraline, fluvoxamine and fluoxetine), were able to minimize the insulin release from islet beta-cells and counteract hypoglycemia, we investigated the effects of tianeptine, a drug which enhances 5-HT uptake during the oral glucose tolerance test. We found that the drug triggered significant and sustained insulin rises which were opposite to the plasma glucose decreases. The fact that significant noradrenaline/adrenaline (NA/Ad) plasma ratio paralleled insulin rises throughout the test is consistent with the excitatory role played by the peripheral neural sympathetic activity. Additionally, the positive correlations registered between NA versus DA (dopamine) plasma levels indicate that the latter arose from sympathetic nerves rather than the adrenal glands. Furthermore, the significant reductions of both platelet and plasma 5-HT registered throughout the OGTT plus tianeptine test support the postulation that reduction of the parasympathetic drives is occurring. This parasympathetic drive is responsible for the secretion of 5-HT from the enterochromaffin cells. Finally, considering that circulating 5-HT excites alpha-cells and modulates beta-cells, it is possible to infer that minimization of this factor contributed to the insulinogenic effect displayed by the association of this drug to an oral glucose load. We also discussed the peripheral and central nervous system mechanisms responsible for the insulinogenic effect registered throughout the test.

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“…Furthermore, taking into account that circulating 5-HT is stored into platelets, f5-HT is increased because of deficit uptake and/or platelet aggregation. Platelet aggregation depends on the epinephrine overflow [13 -15] and from parasympathetic over-activity [16], which enhances circulating 5-HT by excitation of enterochromaffin cells [17,18].…”

Section: Central Nervous System (Cns) + Peripheral Neuroautonomic + Nmentioning

confidence: 99%

Pathophisiological and Neuropharmacological Mechanisms Under- lying the Therapeutical Effects of Tianeptine

Lechín¹,

Dijs²

2017

MEDJ

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Background:Tianeptine, a drug that enhances rather than inhibits serotonin uptake by platelets and serotonergic axons, is able to act as an antidepressant and/or anti-stress drug. Methods:The former effect should be attributed to its ability to reduce neural sympathetic over activity, whereas the latter to the interference by the drug to the hypothalamic stress cascade which includes corticotropin releasing factor + ACTH + cortisol secretion. Conclusion:This singular mechanism should be taken into account when the drug is prescribed as a therapeutic agent.

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Physostigmine effects on serotonin uptake in human blood platelets

Cited by 29 publications

References 22 publications

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Effect of Tianeptine on Glucose Tolerance with Insulin Secretion in Human: Potential Anti-Diabetic Effect of the Drug

Pathophisiological and Neuropharmacological Mechanisms Under- lying the Therapeutical Effects of Tianeptine

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