Gap junction blockade with carbenoxolone differentially affects fictive breathing in larval and adult bullfrogs

Winmill, Rachel E.; Hedrick, Michael S.

doi:10.1016/j.resp.2003.08.005

Cited by 19 publications

(9 citation statements)

References 44 publications

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“…The changing role of NO in the amphibian respiratory network is similar to the developmental effects of NO in modulating the spinal rhythm generator for swimming in the amphibian spinal cord (McLean and Sillar, 2004). Gap junction regulation of lung burst activity is important in larval brainstems, but not in the adult brainstem (Winmill and Hedrick, 2003) similar to that shown in developing mammals (Bou-Flores and Berger, 2001;Solomon et al 2003). These studies suggest that a number of different neuromodulatory receptor systems increase their influence over lung burst activity throughout development.…”

Section: Role Of Non-nmda Receptors In Respiratory Rhythm Generationsupporting

confidence: 55%

Role of glutamate and substance P in the amphibian respiratory network during development

Chen

Hedrick

2008

Respiratory Physiology & Neurobiology

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This study tested the hypothesis that glutamatergic ionotropic (AMPA/kainate) receptors and neurokinin receptors (NKR) are important in the regulation of respiratory motor output during development in the bullfrog. The roles of these receptors were studied with in vitro brainstem preparations from pre-metamorphic tadpoles and post-metamorphic frogs. Brainstems were superfused with an artificial cerebrospinal fluid at 20-22 degrees C containing CNQX, a selective non-NMDA antagonist, or with substance P (SP), an agonist of NKR. Blockade of glutamate receptors with CNQX in both groups caused a reduction of lung burst frequency that was reversibly abolished at 5 microM (P<0.01). CNQX, but not SP, application produced a significant increase (P<0.05) in gill and buccal frequency in tadpoles and frogs, respectively. SP caused a significant increase (P<0.05) in lung burst frequency at 5 microM in both groups. These results suggest that glutamatergic activation of AMPA/kainate receptors is necessary for generation of lung burst activity and that SP is an excitatory neurotransmitter for lung burst frequency generation. Both glutamate and SP provide excitatory input for lung burst generation throughout the aquatic to terrestrial developmental transition in bullfrogs.

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Section: Role Of Non-nmda Receptors In Respiratory Rhythm Generationsupporting

confidence: 55%

Role of glutamate and substance P in the amphibian respiratory network during development

Chen

Hedrick

2008

Respiratory Physiology & Neurobiology

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“…The forebrain was exposed by opening a hole in the skull with a pair of sharp iris scissors, removed and placed in cold artificial cerebrospinal fluid (aCSF). The composition of aCSF was (in mmol·l -1 ): NaCl, 104.0; KCl 4.0; MgCl 2 , 1.4; NaHCO 3 , 25.0; CaCl 2 , 2.4; glucose, 10.0 (Winmill and Hedrick, 2003). Removal of the forebrain usually required less than 2·min to complete.…”

Section: Isolation Of Tadpole Forebrain Cellsmentioning

confidence: 99%

Intracellular calcium and survival of tadpole forebrain cells in anoxia

Hedrick

Fahlman

Bickler

2005

Journal of Experimental Biology

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SUMMARY The frog brain survives hypoxia with a slow loss of energy charge and ion homeostasis. Because hypoxic death in most neurons is associated with increases in intracellular calcium ([Ca2+]i), we examined the relationship between [Ca2+]i and survival of a mixed population of isolated cells from the forebrain of North American bullfrog Rana catesbeiana tadpoles. Forebrain cells from stage V-XV tadpoles were isolated by enzymatic digestion and loaded with one of three different calcium indicators (Fura-2, Fura 2-FF and BTC) to provide estimates of [Ca2+]i accurate at low and high[Ca2+]i. Propidium iodide (PI) fluorescence was used as an indicator of cell viability. Cells were exposed to anoxia (100%N2) and measurements of [Ca2+]i and cell survival made from 1 h to 18 h. Intracellular [Ca2+] increased significantly after 3-6 h anoxia (P<0.05), regardless of the type of Ca2+ indicator used; however, there were substantial differences in the measurements of [Ca2+]i with the different indicators, reflecting their varying affinities for Ca2+. Resting[Ca2+]i was approximately 50 nmol l-1 and increased to about 9-30 μmol l-1 after 4-6 h anoxia. The significant increase in [Ca2+]i during anoxia was not associated with significant increases in cell death, with 85-95% survival over this time period. Cells exposed to anoxia for 18 h, or those made anoxic for 4-6 and reoxygenated for 12 h to 16 h, had survival rates greater than 70%,but survival was significantly less than normoxic controls. These results indicate that large increases in [Ca2+]i are not necessarily associated with hypoxic cell death in vertebrate brain cells.

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“…In these studies, Solomon et al [25] demonstrated that pharmacological blockade of brainstem gap junctions reduces inspiratory-phase synchronization in the phrenic nerve in the adult rat while Bou-Flores and Berger [24] showed that on a short-time-scale, gap junction blockade increased inspiratory-phase synchronization in the hypoglossal and phrenic nerves in the neonatal rat. Additionally, Winmill and Hedrick [27] reported that fictive breathing was differentially affected by blockade of gap junctions in larval versus adult bullfrogs. While age-related differences in Cx expression and gap junction coupling are known to exist [4, 7, 9, 12, 16, 17, 20, 28] it is unclear how or why neuronal synchrony would be differentially affected by blockade of gap junctions in the above studies.…”

Section: Introductionmentioning

confidence: 99%

Analyzing the Effects of Gap Junction Blockade on Neural Synchrony via a Motoneuron Network Computational Model

Memelli

Horn

Wittie

et al. 2012

Computational Intelligence and Neuroscience

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In specific regions of the central nervous system (CNS), gap junctions have been shown to participate in neuronal synchrony. Amongst the CNS regions identified, some populations of brainstem motoneurons are known to be coupled by gap junctions. The application of various gap junction blockers to these motoneuron populations, however, has led to mixed results regarding their synchronous firing behavior, with some studies reporting a decrease in synchrony while others surprisingly find an increase in synchrony. To address this discrepancy, we employ a neuronal network model of Hodgkin-Huxley-style motoneurons connected by gap junctions. Using this model, we implement a series of simulations and rigorously analyze their outcome, including the calculation of a measure of neuronal synchrony. Our simulations demonstrate that under specific conditions, uncoupling of gap junctions is capable of producing either a decrease or an increase in neuronal synchrony. Subsequently, these simulations provide mechanistic insight into these different outcomes.

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Gap junction blockade with carbenoxolone differentially affects fictive breathing in larval and adult bullfrogs

Cited by 19 publications

References 44 publications

Role of glutamate and substance P in the amphibian respiratory network during development

Role of glutamate and substance P in the amphibian respiratory network during development

Intracellular calcium and survival of tadpole forebrain cells in anoxia

Analyzing the Effects of Gap Junction Blockade on Neural Synchrony via a Motoneuron Network Computational Model

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