Autonomic actions of cocaine

1989 ◽  
Vol 67 (9) ◽  
pp. 1168-1176 ◽  
Author(s):  
D. K. Pitts ◽  
J. Marwah
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Adrenergic Receptor ◽  
Monoamine Neurotransmitter ◽  
Autonomic Nervous ◽  
In Situ Techniques ◽  
Receptor Sites ◽  
The Impact

The development of our knowledge of the physiological, pharmacological, and biochemical actions of cocaine has in essence occurred in parallel with the development of our knowledge about the function of the autonomic nervous system. Cocaine is a sympathomimetic compound with potent local anesthetic properties. The principal hypothesis accepted to date to explain the sympathomimetic effects of cocaine is that this drug inhibits neuronal monoamine neurotransmitter reuptake by binding to a transporter or uptake site thereby increasing the effective concentration of neurotransmitter at adrenergic receptor sites. Much of the available evidence for this hypothesis has come from studies utilizing in vitro or in situ techniques. There have been relatively fewer studies examining the impact of cocaine on the autonomic nervous system in the intact animal. In addition, few studies have examined the effects of cocaine on central autonomic function. Past studies concerning the mechanism of action of cocaine are reviewed and recent data addressing the cardiovascular, respiratory, and central autonomic effects of cocaine are discussed.Key words: cocaine, autonomic nervous system.

Evaluation of the Impact of Short Duration Music Listening on Autonomic State (Preprint)

2021 ◽  
Author(s):  
Garry Elvin ◽  
Paras Patel ◽  
Petia Sice ◽  
Chirine Riachy ◽  
Nigel Osborne ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Short Duration ◽  
System Response ◽  
Time Interval ◽  
Music Listening ◽  
Autonomic Nervous ◽  
The Impact ◽  
Change In Mean

BACKGROUND Heart rate variability (HRV), or the variation in the time interval between consecutive heartbeats, is a proven measure for assessing changes in autonomic activity. An increase in variability suggests an upregulation of the parasympathetic nervous system (PNS). Music was shown to have an effect on the limbic system, respiratory rate, and blood pressure. However, there have been relatively few empirical investigations on the effect of music on HRV compared to mean heart rate (HR). Also, the majority of studies have been experimental rather than interventional, reporting significant changes in HRV as a function of musical characteristics, such as tempo, genre, and valence. OBJECTIVE The aim of this pilot study is to evaluate the impact of short duration music listening on the autonomic nervous system response of healthy adults. METHODS Six participants (three males and three females) were tested to investigate the effect of listening to music on HR and HRV. Electrocardiographic (ECG) data was recorded at a sampling rate of 1000 Hz using an eMotion Faros 360 device produced by Bittium Biosignals. The data was collected while the participants listened to four pre-selected songs in a random order separated by a relaxation period of 5 minutes. Data was then cleaned and processed through Kubious HRV 2.0 software. Statistical analysis using Wilcoxon signed rank test was carried out for the time and frequency domains. RESULTS For all but one song that is shorter than 3 minutes (song 1), we observed a statistically significant increase in Standard Deviation of the RR intervals (SDRR) (song 1: P=.125, r=.333; song 2: P=.023, r=.575; song 3: P=.014, r=.635; song 4: P=.014, r=.635) and in the Low Frequency (LF) component of the cardiac spectrogram (song 1: P=.300, r=.151; song 2: P=.038, r=.514; song 3: P=.014, r=.635; song 4: P=.014, r=.635) with a large effect size r, indicating increased HRV. No significant change in mean HR was observed (song 1: P=.173 r=-.272; song 2: P=.058, r=-.454; song 3: P=.125, r=-.333; song 4: P=.232. r=-.212). CONCLUSIONS Listening to pre-selected songs of longer duration than 3 minutes 30 seconds is associated with significant increases in HRV measures, especially SDRR and LF. Music thus has the potential to overcome autonomic nervous system (ANS) dysregulation and thereby benefit health and wellbeing.

α2B-Adrenergic receptor deletion polymorphism and cardiac autonomic nervous system responses to exercise in obese women

2005 ◽  
Vol 30 (2) ◽  
pp. 214-220 ◽  
Author(s):  
L M Ueno ◽  
E S T Frazzatto ◽  
L T Batalha ◽  
I C Trombetta ◽  
M do Socorro Brasileiro ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Adrenergic Receptor ◽  
Obese Women ◽  
Deletion Polymorphism ◽  
Cardiac Autonomic Nervous System ◽  
Autonomic Nervous

scholarly journals Brain permeable AMPK activator R481 raises glycemia by autonomic nervous system activation and amplifies the counterregulatory response to hypoglycemia in rats

2019 ◽  
Author(s):  
Ana M. Cruz ◽  
Yasaman Malekizadeh ◽  
Julia M. Vlachaki Walker ◽  
Paul G. Weightman Potter ◽  
Katherine Pye ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Ventromedial Hypothalamus ◽  
Whole Body ◽  
Ampk Activation ◽  
Autonomic Nervous ◽  
Glucose Levels

ABSTRACTAMP-activated protein kinase (AMPK) is a critical cellular and whole body energy sensor activated by energy stress, including hypoglycemia, which is frequently experienced by people with diabetes. Previous studies using direct delivery of an AMPK activator to the ventromedial hypothalamus (VMH) in rodents increased hepatic glucose production. Moreover, recurrent glucoprivation in the hypothalamus leads to blunted AMPK activation and defective hormonal responses to subsequent hypoglycemia. These data suggest that amplifying AMPK activation may prevent or reduce frequency hypoglycemia in diabetes. We used a novel brain-permeable AMPK activator, R481, which potently increased AMPK phosphorylation in vitro. R481 significantly increased peak glucose levels during glucose tolerance tests in rats, which were attenuated by treatment with AMPK inhibitor SBI-0206965 and completely abolished by blockade of the autonomic nervous system. This occurred without altering insulin sensitivity measured by hyperinsulinemic-euglycemic clamps. Endogenous insulin secretion was not altered by R481 treatment. During hyperinsulinemic-hypoglycemic clamp studies, R481 treatment reduced exogenous glucose requirements and amplified peak glucagon levels during hypoglycemia. These data demonstrate that peripheral administration of the brain permeable AMPK activator R481 amplifies the counterregulatory response to hypoglycemia in rats, which could have clinical relevance for prevention of hypoglycemia.

scholarly journals Biallelic MADD variants cause a phenotypic spectrum ranging from developmental delay to a multisystem disorder

Brain ◽  
2020 ◽  
Vol 143 (8) ◽  
pp. 2437-2453
Author(s):  
Pauline E Schneeberger ◽  
Fanny Kortüm ◽  
Georg Christoph Korenke ◽  
Malik Alawi ◽  
René Santer ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Developmental Delay ◽  
Autonomic Nervous ◽  
Organ Systems ◽  
Tnf Α ◽  
Epidermal Growth ◽  
The Impact

Abstract In pleiotropic diseases, multiple organ systems are affected causing a variety of clinical manifestations. Here, we report a pleiotropic disorder with a unique constellation of neurological, endocrine, exocrine, and haematological findings that is caused by biallelic MADD variants. MADD, the mitogen-activated protein kinase (MAPK) activating death domain protein, regulates various cellular functions, such as vesicle trafficking, activity of the Rab3 and Rab27 small GTPases, tumour necrosis factor-α (TNF-α)-induced signalling and prevention of cell death. Through national collaboration and GeneMatcher, we collected 23 patients with 21 different pathogenic MADD variants identified by next-generation sequencing. We clinically evaluated the series of patients and categorized the phenotypes in two groups. Group 1 consists of 14 patients with severe developmental delay, endo- and exocrine dysfunction, impairment of the sensory and autonomic nervous system, and haematological anomalies. The clinical course during the first years of life can be potentially fatal. The nine patients in Group 2 have a predominant neurological phenotype comprising mild-to-severe developmental delay, hypotonia, speech impairment, and seizures. Analysis of mRNA revealed multiple aberrant MADD transcripts in two patient-derived fibroblast cell lines. Relative quantification of MADD mRNA and protein in fibroblasts of five affected individuals showed a drastic reduction or loss of MADD. We conducted functional tests to determine the impact of the variants on different pathways. Treatment of patient-derived fibroblasts with TNF-α resulted in reduced phosphorylation of the extracellular signal-regulated kinases 1 and 2, enhanced activation of the pro-apoptotic enzymes caspase-3 and -7 and increased apoptosis compared to control cells. We analysed internalization of epidermal growth factor in patient cells and identified a defect in endocytosis of epidermal growth factor. We conclude that MADD deficiency underlies multiple cellular defects that can be attributed to alterations of TNF-α-dependent signalling pathways and defects in vesicular trafficking. Our data highlight the multifaceted role of MADD as a signalling molecule in different organs and reveal its physiological role in regulating the function of the sensory and autonomic nervous system and endo- and exocrine glands.

Role of the autonomic nervous system in the development of hyperinsulinemia by high-carbohydrate formula feeding to neonatal rats

2007 ◽  
Vol 292 (4) ◽  
pp. E1069-E1078 ◽  
Author(s):  
Paul Mitrani ◽  
Malathi Srinivasan ◽  
Catherine Dodds ◽  
Mulchand S. Patel
Keyword(s):  
Nervous System ◽  
Insulin Secretion ◽  
Autonomic Nervous System ◽  
Dietary Intervention ◽  
Neonatal Rat ◽  
Milk Formula ◽  
Autonomic Nervous ◽  
High Carbohydrate

An early dietary intervention in the form of a high-carbohydrate (HC) milk formula in neonatal rat pups results in immediate onset of hyperinsulinemia. While increased insulin secretion in HC rats has been shown to be related to hypersensitivity to glucose, the immediate onset of hyperinsulinemia and its persistence throughout the suckling period suggest involvement of multiple systems that enhance insulin secretion in response to increased demand. Evidence presented here in 12-day-old HC rats indicates that altered activity of the autonomic nervous system contributes to enhanced insulin secretory responses to glucose stimulation through increased parasympathetic and decreased sympathetic signaling. Both in vivo and in vitro studies have shown that HC rats secrete significantly higher levels of insulin in response to glucose in the presence of acetylcholine, a cholinergic agonist, while sensitivity to inhibition of insulin secretion by oxymetazoline, an α2a-adrenergic receptor (α2aAR) agonist, was reduced. In addition, HC rats showed increased sensitivity to blockade of cholinergic-induced insulin secretion by the muscarinic type 3 receptor (M3R) antagonist 4-diphenylacetoxy- N-methylpiperidine methobromide, as well as increased potentiation of glucose-stimulated insulin secretion by treatment with yohimbine. Increases in islets levels of M3R, phospholipase C-β1, and protein kinase Cα mRNAs, as well as decreased α2aAR mRNA, in 12-day-old HC rats provide a mechanistic connection to the changes in insulin secretion seen in HC rats. In conclusion, altered autonomic regulation of insulin secretion, due to the HC nutritional intervention, contributes to the development of hyperinsulinemia in 12-day-old HC rats.

scholarly journals The Association between Trp64Arg Polymorphism of the β3-Adrenergic Receptor and Autonomic Nervous System Activity1

1999 ◽  
Vol 84 (5) ◽  
pp. 1623-1627
Author(s):  
Nobuyuki Shihara ◽  
Koichiro Yasuda ◽  
Toshio Moritani ◽  
Hidetoshi Ue ◽  
Tetsuya Adachi ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Adrenergic Receptor ◽  
Autonomic Nervous ◽  
Trp64arg Polymorphism
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