scholarly journals Synchronization transition from bursting to spiking and bifurcation mechanism of the pre-Bötzinger complex

2020 ◽  
Vol 69 (4) ◽  
pp. 040501
Author(s):  
Yong-Xia Yang ◽  
Yu-Ye Li ◽  
Hua-Guang Gu
Keyword(s):  
Bifurcation Mechanism ◽  
Synchronization Transition ◽  
Bötzinger Complex

scholarly journals Release of ATP by pre-Bötzinger complex astrocytes contributes to the hypoxic ventilatory response via a Ca2+ -dependent P2Y1 receptor mechanism

2017 ◽  
Vol 596 (15) ◽  
pp. 3245-3269 ◽  
Author(s):  
Vishaal Rajani ◽  
Yong Zhang ◽  
Venkatesh Jalubula ◽  
Vladimir Rancic ◽  
Shahriar SheikhBahaei ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
P2y1 Receptor ◽  
Hypoxic Ventilatory Response ◽  
Bötzinger Complex

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.

Botzinger complex region role in phrenic-to-phrenic inhibitory reflex of cat

1989 ◽  
Vol 67 (4) ◽  
pp. 1364-1370 ◽  
Author(s):  
D. F. Speck
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Inhibitory Response ◽  
Phrenic Nerve Stimulation ◽  
Bötzinger Complex ◽  
Before And After ◽  
Pass Through ◽  
Bilateral Lesions ◽  
Decerebrate Cats ◽  
Inhibitory Reflex

Neuronal recordings, microstimulation, and electrolytic and chemical lesions were used to examine the involvement of the Botzinger Complex (BotC) in the bilateral phrenic-to-phrenic inhibitory reflex. Experiments were conducted in decerebrate cats that were paralyzed, ventilated, thoracotomized, and vagotomized. Microelectrode recordings within the BotC region revealed that some neurons were activated by phrenic nerve stimulation (15 of 69 expiratory units, 9 of 67 inspiratory units, and 19 nonrespiratory-modulated units) at average latencies similar to the onset latency of the phrenic-to-phrenic inhibition. In addition, microstimulation within the BotC caused a short latency transient inhibition of phrenic motor activity. In 17 cats phrenic neurogram responses to threshold and supramaximal (15 mA) stimulation of phrenic nerve afferents were recorded before and after electrolytic BotC lesions. In 15 animals the inhibitory reflex was attenuated by bilateral lesions. Because lesion of either BotC neurons or axons of passage could account for this attenuation, in eight experiments the phrenic-to-phrenic inhibitory responses were recorded before and after bilateral injections of 5 microM kainic acid (30–150 nl) into the BotC. After chemical lesions, the inhibitory response to phrenic nerve stimulation remained; however, neuronal activity typical of the BotC could not be located. These results suggest that axons important in producing the phrenic-to-phrenic reflex pass through the region of the BotC, but that BotC neurons themselves are not necessary for this reflex.

scholarly journals Voltage-Dependent Rhythmogenic Property of Respiratory Pre-Bötzinger Complex Glutamatergic, Dbx1-Derived, and Somatostatin-Expressing Neuron Populations Revealed by Graded Optogenetic Inhibition

eNeuro ◽  
2016 ◽  
Vol 3 (3) ◽  
pp. ENEURO.0081-16.2016 ◽  
Author(s):  
Hidehiko Koizumi ◽  
Bryan Mosher ◽  
Mohammad F. Tariq ◽  
Ruli Zhang ◽  
Naohiro Koshiya ◽  
...  
Keyword(s):  
Neuron Populations ◽  
Bötzinger Complex ◽  
Voltage Dependent

DISTRIBUTION OF GABA TRANSPORTER (GAT1) LEVELS IN THE BÖTZINGER COMPLEX AT THE EARLY STAGES OF POSTNATAL DEVELOPMENT IN RATS WITH PRENATAL SEROTONIN DEFICIENCY

2020 ◽  
pp. 7-12
Author(s):  
Л. И. Хожай
Keyword(s):  
Postnatal Development ◽  
Tryptophan Hydroxylase ◽  
Polyclonal Antibodies ◽  
Gaba Transporter ◽  
Early Stages ◽  
Bötzinger Complex ◽  
Neuronal Processes ◽  
Serotonin Deficiency ◽  
Gaba Transporter 1 ◽  
Primary Rabbit

Цель работы - исследование распределения уровня GAT-транспортера ГАМК в комплексе Бетцингера на разных сроках раннего постнатального развития крыс в норме и при пренатальном дефиците серотонина. Материал и методы. Работа проведена на лабораторных крысах линии Wistar. Снижение уровня эндогенного серотонина в эмбриональный период осуществляли методом ингибирования триптофан-гидроксилазы пара-хлорфенилаланином (пХФА). Выявление транспортного белка GAТпроводили посредством иммуногистохимической реакции с использованием первичных кроличьих поликлональных антител anti-GABA transporter1 (AbCam, Великобритания). Мозг исследовали на 5-, 10-е и 20-е сутки постнатального развития. Результаты. В комплексе Бетцингера на ранних сроках постнатального развития у контрольных животных отмечено колебание уровня GAT-транспортера ГАМК. На 1-й неделе жизни уровень GATбыл высоким как в сети отростков и терминалей, так и в синапсах. В течение 2-й недели жизни уровень GATснижался, а к концу 3-й недели - повышался вновь, достигая исходного уровня. Дефицит серотонина в пренатальный период вызывал у подопытных животных существенное увеличение уровня GATв нейропиле комплекса Бетцингера на всех изученных сроках постнатального развития. Выводы. Пренатальный дефицит серотонина приводит к существенному повышению уровня GAT-транспортера ГАМК в ранние сроки постнатального развития, что может приводить к изменению трансмиссии ГАМК и, как следствие, к нарушению баланса тормозных и возбуждающих эффектов в дыхательном ядре. Objective - to study the distribution of GABA transporter 1 (GAT) levels in the Bötzinger complex at the early stages of postnatal development in rats with prenatal serotonin deficiency. Materials and methods. The work was carried out on Wistar line laboratory rats. To reduce the level of endogenous serotonin in the embryonic period, the method of tryptophan hydroxylase inhibition by para-chlorophenylalanine (PCPA) (Sigma, USA) was used. The GAT1 transport protein was detected by immunohistochemical reaction with anti-GABA transporter1 primary rabbit polyclonal antibodies (AbCam, UK). The brain was examined on the 5, 10 and 20 day of postnatal development. Results. At the early stages of postnatal development, a fluctuation in the GAT1 level of the GABA transporter was noted in the Bötzinger complex of control animals. In the first postnatal week, the GAT level was high both in the network of neuronal processes and terminals, and in synapses. During the 2 week of life, the GAT1 level decreased, and by the end of the 3 week it increased again, reaching the initial level. Deficiency of serotonin in the prenatal period caused a significant increase in the level of GAT in the neuropil of the Bötzinger complex in experimental animals at all studied stages of postnatal development. Conclusions. Prenatal deficiency of serotonin leads to a significant increase in the GAT1 level at the early stages of postnatal development, which can lead to a change in the GABA transmission, and, as a result, to a disturbance in the balance of inhibitory and stimulatory effects in the respiratory nuclei.

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.

Sign in / Sign up

Export Citation Format

Share Document