scholarly journals GABA-induced facilitation of the periodic bursting activity of oxytocin neurones in suckled rats.

1995 ◽  
Vol 488 (1) ◽  
pp. 103-114 ◽  
Author(s):  
F C Moos
Keyword(s):  
Bursting Activity ◽  
Oxytocin Neurones

ACUTE α1-ADRENERGIC ANTAGONISM INHIBITS MORPHINE-WITHDRAWAL EXCITATION OF OXYTOCIN NEURONES

Analgesia ◽  
1995 ◽  
Vol 1 (4) ◽  
pp. 335-338
Author(s):  
Colin H. Brown ◽  
Niall P. Murphy ◽  
Gareth Leng ◽  
John A. Russell
Keyword(s):  
Morphine Withdrawal ◽  
Oxytocin Neurones

GnRH neurons and episodic bursting activity

2002 ◽  
Vol 13 (10) ◽  
pp. 409-410 ◽  
Author(s):  
Martin J Kelly ◽  
Edward J Wagner
Keyword(s):  
Gnrh Neurons ◽  
Bursting Activity

scholarly journals Intracellular Na+ Modulates Pacemaking Activity in Murine Sinoatrial Node Myocytes: An In Silico Analysis

2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Membrane Potential ◽  
In Silico ◽  
Sinoatrial Node ◽  
In Silico Analysis ◽  
Ankyrin B ◽  
Deficient Mice ◽  
Silico Analysis ◽  
Bursting Activity

Background: The mechanisms underlying dysfunction in the sinoatrial node (SAN), the heart’s primary pacemaker, are incompletely understood. Electrical and Ca2+-handling remodeling have been implicated in SAN dysfunction associated with heart failure, aging, and diabetes. Cardiomyocyte [Na+]i is also elevated in these diseases, where it contributes to arrhythmogenesis. Here, we sought to investigate the largely unexplored role of Na+ homeostasis in SAN pacemaking and test whether [Na+]i dysregulation may contribute to SAN dysfunction. Methods: We developed a dataset-specific computational model of the murine SAN myocyte and simulated alterations in the major processes of Na+ entry (Na+/Ca2+ exchanger, NCX) and removal (Na+/K+ ATPase, NKA). Results: We found that changes in intracellular Na+ homeostatic processes dynamically regulate SAN electrophysiology. Mild reductions in NKA and NCX function increase myocyte firing rate, whereas a stronger reduction causes bursting activity and loss of automaticity. These pathologic phenotypes mimic those observed experimentally in NCX- and ankyrin-B-deficient mice due to altered feedback between the Ca2+ and membrane potential clocks underlying SAN firing. Conclusions: Our study generates new testable predictions and insight linking Na+ homeostasis to Ca2+ handling and membrane potential dynamics in SAN myocytes that may advance our understanding of SAN (dys)function.

Sodium Currents in Neurons From the Rostroventrolateral Medulla of the Rat

2003 ◽  
Vol 90 (3) ◽  
pp. 1635-1642 ◽  
Author(s):  
Ilya A. Rybak ◽  
Krzysztof Ptak ◽  
Natalia A. Shevtsova ◽  
Donald R. McCrimmon
Keyword(s):  
Sodium Channels ◽  
Sodium Current ◽  
Cell Voltage ◽  
Kinetic Properties ◽  
Persistent Sodium Current ◽  
Sodium Currents ◽  
Bötzinger Complex ◽  
Window Current ◽  
Bursting Activity

Rapidly inactivating and persistent sodium currents have been characterized in acutely dissociated neurons from the area of rostroventrolateral medulla that included the pre-Bötzinger Complex. As demonstrated in many studies in vitro, this area can generate endogenous rhythmic bursting activity. Experiments were performed on neonate and young rats (P1-15). Neurons were investigated using the whole cell voltage-clamp technique. Standard activation and inactivation protocols were used to characterize the steady-state and kinetic properties of the rapidly inactivating sodium current. Slow depolarizing ramp protocols were used to characterize the noninactivating sodium current. The “window” component of the rapidly inactivating sodium current was calculated using mathematical modeling. The persistent sodium current was revealed by subtraction of the window current from the total noninactivating sodium current. Our results provide evidence of the presence of persistent sodium currents in neurons of the rat rostroventrolateral medulla and determine voltage-gated characteristics of activation and inactivation of rapidly inactivating and persistent sodium channels in these neurons.

Effects of Time Delay on Burst Synchronization Transition of Neuronal Networks

2018 ◽  
Vol 28 (12) ◽  
pp. 1850143 ◽  
Author(s):  
Xiaojuan Sun ◽  
Tianshu Xue
Keyword(s):  
Time Delay ◽  
Neuronal Network ◽  
Coupling Strength ◽  
Neuronal Networks ◽  
The Other ◽  
Electrical Synapses ◽  
Synchronization Transition ◽  
Burst Synchronization ◽  
Chemical Synapses ◽  
Bursting Activity

In this paper, we focus on investigating the effects of time delay on burst synchronization transitions of a neuronal network which is locally modeled by Hindmarsh–Rose neurons. Here, neurons inside the neuronal network are connected through electrical synapses or chemical synapses. With the numerical results, it is revealed that burst synchronization transitions of both electrically and chemically coupled neuronal networks could be induced by time delay just when the coupling strength is large enough. Meanwhile, it is found that, in electrically and excitatory chemically coupled neuronal networks, burst synchronization transitions are observed through change of spiking number per burst when coupling strength is large enough; while in inhibitory chemically coupled neuronal network, burst synchronization transitions are observed for large enough coupling strength through changing fold-Hopf bursting activity to fold-homoclinic bursting activity and vice versa. Namely, two types of burst synchronization transitions are observed. One type of burst synchronization transitions occurs through change of spiking numbers per burst and the other type of burst synchronization transition occurs through change of bursting types.

scholarly journals The importance of oxytocin mechanisms in the control of mouse parturition

Reproduction ◽  
2002 ◽  
pp. 543-552 ◽  
Author(s):  
AJ Douglas ◽  
G Leng ◽  
JA Russell
Keyword(s):  
Red Light ◽  
Endogenous Opioids ◽  
Beta Agonist ◽  
Early Gene ◽  
Opioid Antagonist ◽  
Dependent Manner ◽  
Birth Process ◽  
Opioid Agonist ◽  
Adrenergic Antagonist ◽  
Oxytocin Neurones

The role of oxytocin in parturition in mice was investigated. Pup birth profiles, blood samples and brains were collected from parturient mice observed under red light conditions in a reversed light:dark photoperiod. Peripheral administration of an oxytocin antagonist in a dose-dependent manner delayed the birth of subsequent pups, indicating that oxytocin is required for a normal pup birth profile. Oxytocin neurones were activated during birth as shown by both increased immediate early gene ( Fos) expression in oxytocin neurones in the supraoptic nucleus and increased plasma oxytocin concentrations during birth. In addition, the nucleus of the tractus solitarius and the olfactory bulbs, sites that process inputs to oxytocin neurones, become activated during parturition. Exposure to stress during parturition halted subsequent deliveries; at this stage plasma oxytocin concentrations were not higher than those of virgin mice, and birth was restored by administration of oxytocin. Administration of beta-adrenergic antagonist (propranolol) also restored stress-delayed birth, whereas administration of ritrodrine (beta-agonist) delayed birth in non-stressed mice, indicating that adrenergic mechanisms contribute to stress-delayed births in mice. Administration of morphine (mu-opioid agonist) delayed births transiently, but naloxone (opioid antagonist) did not prevent stress-delayed birth, indicating that endogenous opioids do not appear to contribute to neuroendocrine or uterine mechanisms that promote birth in mice. Therefore, despite evidence in oxytocin knockout mice that oxytocin is not essential for parturition in this species, the results of the present study indicate that oxytocin neurone activity and secretion contribute to the birth process in normal mice.

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