scholarly journals Dynamics of Spiking Neurons with Electrical Coupling

2000 ◽  
Vol 12 (7) ◽  
pp. 1643-1678 ◽  
Author(s):  
Carson C. Chow ◽  
Nancy Kopell

We analyze the existence and stability of phase-locked states of neurons coupled electrically with gap junctions. We show that spike shape and size, along with driving current (which affects network frequency), play a large role in which phase-locked modes exist and are stable. Our theory makes predictions about biophysical models using spikes of different shapes, and we present simulations to confirm the predictions. We also analyze a large system of all-to-all coupled neurons and show that the splay-phase state can exist only for a certain range of frequencies.

1976 ◽  
Vol 22 (2) ◽  
pp. 427-434
Author(s):  
F. Mazet ◽  
J. Cartaud

The freeze-fracturing technique was used to characterize the junctional devices involved in the electrical coupling of frog atrial fibres. These fibres are connected by a type of junction which can be interpreted as a morphological variant of the “gap junction” or “nexus”. The most characteristic features are rows of 9-nm junctional particles forming single or anastomosed circular profiles on the inner membrane face, and corresponding pits on the outer membrane face. Very seldom aggregates consisting of few geometrically disposed 9-nm particles are found. The significance of the junctional structures in the atrial fibres is discussed, with respect to present knowledge about junctional features of gap junctions in various tissues, including embryonic ones.


2006 ◽  
Vol 67 (2) ◽  
pp. 300-303 ◽  
Author(s):  
Somayeh Mahdavi ◽  
Mostafa Rezaei-Tavirani ◽  
Shahriar Gharibzadeh ◽  
Farzad Towhidkhah

2020 ◽  
Author(s):  
William N Grimes ◽  
Didem Göz Aytürk ◽  
Mrinalini Hoon ◽  
Takeshi Yoshimatsu ◽  
Clare Gamlin ◽  
...  

AbstractAmacrine cells are interneurons comprising the most diverse cell type in the mammalian retina. They help encode visual features such as edges or directed motion by mediating excitatory and inhibitory interactions between input (i.e. bipolar) and output (i.e. ganglion) neurons in the inner plexiform layer (IPL). Like other brain regions, the retina also contains glial cells that contribute to neurotransmitter uptake, neurovascular control and metabolic regulation. Here, we report that a previously poorly characterized, but relatively abundant, inhibitory amacrine cell type in the mouse retina is coupled directly to Müller glia. Electron microscopic reconstructions of this amacrine type revealed extensive associations with Müller glia, whose processes often completely ensheathe the neurites of this amacrine cell type. Microinjections of small tracer molecules into the somas of these amacrine cells led to selective labelling of nearby Müller glia, leading us to suggest the name “Müller glia-coupled amacrine cell” or MAC. Our electrophysiological data also indicate that MACs release glycine at conventional chemical synapses with amacrine, bipolar and retinal ganglion cells (RGCs), and viral transsynaptic tracing showed connections to several known RGC types. Visually-evoked responses revealed a strong preference for light increments; these “ON” responses were primarily mediated by excitatory chemical synaptic input and direct electrical coupling to other cells. This initial characterization of the MAC provides the first evidence for neuron-glia coupling in the mammalian retina and identifies the MAC as a potential link between inhibitory processing and glial function.Significance StatementGap junctions between pairs of neurons or glial cells are commonly found throughout the nervous system, and play a myriad of roles including electrical coupling and metabolic exchange. In contrast, gap junctions between neurons and glia cells are rare and poorly understood. Here we report the first evidence for neuron-glia coupling in the mammalian retina, specifically between an abundant (but previously unstudied) inhibitory interneuron and Müller glia.


Development ◽  
1975 ◽  
Vol 33 (2) ◽  
pp. 403-417
Author(s):  
Brian P. Hayes ◽  
Alan Roberts

The distribution of intercellular junctions, other than synapses and their precursors, has beendescribed in the developing spinal cord of Xenopus laevis between the neurula andfree swimming tadpole stages. At the neurocoel, ventricular cells are joined in the apical contactzone by a sequence of junctions which usually has one or more intermediate junctions but often also includes close appositions, gap junctions and desmosomes. This apical complex is more diverse than that reported in other vertebrate embryos and between ependymal cells in the adult central nervous system. Gap junctions are also found between ventricular cells and their processes near the external cord surface. However, no other special junctions occur in this location under the basementlamella which surrounds the cord. Punctate intermediate junctions are generally distributed between undifferentiated and differentiating cells and their processes but were not found in neuropil after stage 28. These results are discussed in relation to cell movements during neural differentiation, possible effects on the freedom of movement of ions and molecules through extracellular pathways in the embryo, and possible intercytoplasmic pathways via gap junctions which may be responsible for the physiologically observed electrical coupling between neural tube cells.


2015 ◽  
Vol 43 (3) ◽  
pp. 513-518 ◽  
Author(s):  
Lisa McArthur ◽  
Lisa Chilton ◽  
Godfrey L. Smith ◽  
Stuart A. Nicklin

Gap junctions are channels which allow electrical signals to propagate through the heart from the sinoatrial node and through the atria, conduction system and onwards to the ventricles, and hence are essential for co-ordinated cardiac contraction. Twelve connexin (Cx) proteins make up one gap junction channel, of which there are three main subtypes in the heart; Cx40, Cx43 and Cx45. In the cardiac myocyte, gap junctions are present mainly at the intercalated discs between neighbouring myocytes, and assist in rapid electrical conduction throughout the ventricular myocardium. Fibroblasts provide the structural skeleton of the myocardium and fibroblast numbers significantly increase in heart disease. Fibroblasts also express connexins and this may facilitate heterocellular electrical coupling between myocytes and fibroblasts in the setting of cardiac disease. Interestingly, cardiac fibroblasts have been demonstrated to increase Cx43 expression in experimental models of myocardial infarction and functional gap junctions between myocytes and fibroblasts have been reported. Therefore, in the setting of heart disease enhanced cardiac myocyte: fibroblast coupling may influence the electrical activity of the myocyte and contribute to arrhythmias.


Zootaxa ◽  
2018 ◽  
Vol 4434 (1) ◽  
pp. 111
Author(s):  
JOSÉ G. PALACIOS-VARGAS ◽  
AILA SOARES FERREIRA ◽  
DOUGLAS ZEPPELINI

A new diagnosis of Denisiella is provided, based on the revision of most descriptions, including three new species from Brazil. New Brazilian taxa share the presence of 6 + 6 eyes, 4 + 4 serrate spine-like on tibiotarsi III and the polycarinate setae on tibiotarsi II but differ from each other by the shape and size of the sensilla of the tibiotarsi I. Denisiella rhizophorae sp. nov. has the combination of sensilla on tibiotarsi I of rhagidial type and C2 blunt on antennal segment III. Only D. betschi sp. nov. has barbulate spines on head and D. caatingae sp. nov. is the only which males present nasal organ. They are illustrated with drawings and scanning electron microscope photographs. Three different shapes of sensilla in the tibiotarsi I were observed and were compared with other species. 


2015 ◽  
Vol 146 (5) ◽  
pp. 387-398 ◽  
Author(s):  
Ana Santa Cruz ◽  
Gülistan Meşe ◽  
Laima Valiuniene ◽  
Peter R. Brink ◽  
Thomas W. White ◽  
...  

Gap junctions ensure the rapid propagation of the action potential throughout the myocardium. Three mutant forms of connexin40 (Cx40; A96S, M163V, and G38D), the primary component of the atrial gap junction channel, are associated with atrial fibrillation and retain the ability to form functional channels. We determined the biophysical properties of these mutant gap junctions in transiently transfected HeLa and N2A cells. All three mutants showed macroscopic junctional conductances over the range of 0.5 to 40 nS, and voltage dependences comparable to those of wild-type (WT) Cx40. However, the unitary conductance of G38D channels was ∼1.6-fold higher than that of WT Cx40 channels (∼220 vs. ∼135 pS), whereas the unitary conductances of the A96S and M163V mutants were similar to that of WT Cx40. Furthermore, the M163V and G38D channels exhibited approximately two- and approximately fivefold higher permeability to the anionic dye Lucifer yellow (LY) relative to K+ (LY/K+) compared with that of WT Cx40, whereas A96S LY transfer was similar to that of WT (G38D > M163V > A96S ≈ Cx40WT). In contrast, G38D channels were almost impermeable to cationic ethidium bromide (EtBr), suggesting that G38D alters channel selectivity. Conversely, A96S and M163V channels showed enhanced EtBr permeability relative to WT Cx40, with the following permeability order: M163V > A96S > Cx40WT > G38D. Altered conductive and permeability properties of mutant channels suggest an essential role for Cx40-mediated biochemical and electrical coupling in cardiac tissues. The altered properties of the three single-base substitution mutants may play a role in mechanisms of reentry arrhythmias.


1979 ◽  
Vol 57 (6) ◽  
pp. 578-580 ◽  
Author(s):  
Elane Zelcer ◽  
E. E. Daniel

Two distinct layers of circular muscle have previously been demonstrated in dog jejunum, the main circular layer containing many gap junction contacts, and an inner dense muscle layer where no gap junctions have been found. Length constants were determined for these muscle layers and no significant difference was found between these values. The main circular muscle cells had lower membrane potentials and may have had abnormally low space constants owing to injury. It was concluded that the absence of gap junctions in the inner dense layer does not reduce the spread of passive current as might be expected of electrically isolated cells, and it is suggested that an alternate pathway for passive current exists in this layer.


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