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Many electrophysiological experiments have shown that epileptic seizures often originate from the synchronous activities of abnormally excitable neurons. The dynamic process of epilepsy is very complex, and characterized by a seemingly rapid and dramatic birth of new oscillations, essentially leading to a propagation and amplification of the original aberrant activity. It is very difficult to thoroughly understand the mechanism from a theoretical standpoint, however some special work can prove helpful. Here we present a theoretical framework to investigate chaos and complexity in the synchrony of excitable neurons in an effort to study the collective oscillations within a neural network. As endogenous rhythms, oscillations arise because most cellular processes contain feedback. The Chay model of excitable neurons is chosen because the model describes the abnormal process, where spiking can be transformed into bursting via bifurcation.

In our study, the Chay model is regarded as an abnormal oscillator and coupled via a resistor representing the effect of gap junctions (electrical synapses). In this paper, we present some models developed from the original Chay model, for the synchrony of two cells and a 2D neural network. Lyapunov exponent and phase portrait are utilized to evaluate the chaotic dynamics. Finally, approximate entropy is utilized to measure its complexity. Our results show that the synchrony of abnormal oscillations can occur when the coupling strength of the gap junction is sufficiently large. It is also found that the concentration of Ca²⁺ ions does not synchronize. In the 2D network, approximate entropies of different oscillations with strong coupling strength are greater than those with weak coupling strength. It is indicated that synchronous neurons have greater ability to produce new oscillations than asynchronous ones. This work shows that nonlinear analytical methods may prove useful in elucidating the mechanisms of pathologic conditions, where new oscillations are born and propagated, such as in epilepsy.

The emergence of quantum consciousness stems from dynamic flows of hydrogen ions in brain liquid. This liquid contains vast areas of the fourth phase of water with hexagonal packing of its molecules, the so-called exclusion zone (EZ) of water. The hydrogen ion motion on such hexagonal lattices shows as the hopping of the ions forward and the holes (vacant places) backward, caused by the Grotthuss mechanism. By supporting this motion using external infrasound sources, one may achieve the appearance of the superfluid state of the EZ water. Flows of the hydrogen ions are described by the modified Navier–Stokes equation. It, along with the continuity equation, yields the nonlinear Schrödinger equation, which describes the quantum effects of these flows, such as the tunneling at long distances or the interference on gap junctions.

Inferior olive (IO) neurons project to the cerebellum and contribute to motor control. They can show intriguing spatio-temporal dynamics with rhythmic and synchronized spiking. IO neurons are connected to their neighbors via gap junctions to form an electrically coupled network, and so it is considered that this coupling contributes to the characteristic dynamics of this nucleus. Here, we demonstrate that a gap junction-coupled network composed of simple conductance-based model neurons (a simplified version of a Hodgkin–Huxley type neuron) reproduce important aspects of IO activity. The simplified phenomenological model neuron facilitated the analysis of the single cell and network properties of the IO while still quantitatively reproducing the spiking patterns of complex spike activity observed by simultaneous recording in anesthetized rats. The results imply that both intrinsic bistability of each neuron and gap junction coupling among neurons play key roles in the generation of the spatio-temporal dynamics of IO neurons.

Electrophysiological and ultrastructural studies have demonstrated that gap junctions connect diverse types of neurons in the central nervous system, permitting direct electrical and metabolic coupling. A member of gap junction channel subunit connexin36 (Cx36), is probed for the location of cell-to-cell communication in the mammalian retina, where gap junction networks of major classes of neurons are present. We present an analysis of the expression and localization of Cx36 protein in adult Wistar rat retina, using a newly generated polyclonal antibody against a sequence in the predicted cytoplasmic loop of the Cx36 amino acid alignment, deduced from the cDNA sequence. The affinity-purified antibody, recognizing a single 36-kDa protein, consistently labeled discrete puncta of subcellular structures likely to be associated with gap junctions in the inner plexiform layer, and also cytoplasm within somata and dendrites of retinal amacrine and ganglion cells, following examination with various fixation protocols and double labeling immuno-fluorescence. These results provide that prominent cell-to-cell communication appears in mature excitatory neurons such as retinal ganglion cells, in addition to inhibitory amacrine cells, mediated by gap junctions in the adult retina.

Alpha-type retinal ganglion cells (alpha cells) of the same class in mammalian retina are connected by gap junctions. Electrical synapses between alpha cells were examined using combined techniques of dual patch-clamp recordings, intracellular labeling and electron microscopy in the albino rat retina. In simultaneous dual whole-cell recordings from pairs of neighboring alpha cells, bidirectional electrical synapses with symmetrical junction conductance were observed in pairs with cells of the same morphological type. Regulatory domains of gap junction protein subunit connexins in electrical synapses between alpha cells by extracellular and intracellular ligands investigated by dual whole-patch clamp recordings. I examined how passage currents through electrical synapses between alpha cells are modulated by specific antibodies against connexin36 proteins, and extracellular or intracellular application of ligands. Control conditions led us to observe large passage currents between connected cells and adequate transjunctional conductance (Gj) (1.35$\pm$0.51nS). Experimental results show that high level of intracellular cyclic AMP within examined cells suppress electrical synapses between the neighboring cells. Gj between examined cells reduced to 0.15$\pm$0.04nS. Under application of dopamine (1.25$\pm$0.06nS) or intracellular cyclic GMP (0.98$\pm$0.23nS), however, Gj also remains as in the control level. Intracellular application of an antibody against the cytoplasmic loop of connexin36 reduced G_j (0.98$\pm$0.23nS). Cocktail of the antibody against cytoplasmic connexin36 and intracellular cyclic AMP leaves Gj as in the level by single involvement of the cytoplasmic antibody. The elimination of Gj by the cytoplasmic antibody was in a dose-dependent manner. These results suggest that binding domains against cyclic AMP may be present in the cytoplasmic sites of connexin proteins to regulate channel opening of gap junctions between mammalian retinal alpha ganglion cells.

Severe burn injuries are associated with chronic hypermetabolism. Through its metabolic, inflammatory, immune, and acute phase functions, the liver plays a central role in the creation and maintenance of prolonged hypermetabolism and ensuing muscle wasting. The objective here was to determine the effects of inhibiting gap junction communication in the liver on the acute phase response and prolonged hypermetabolic state after burn injury in both connexin 32 knockout mice and in wildtype mice dosed with a small molecule connexin 32 inhibitor shortly after burn injury. Male connexin 32 knockout mice received full-thickness 20% total body surface area burns or sham treatments and were euthanized at 24h for serum marker profiling and at 14 days for organ and muscle mass analysis. Wildtype mice receiving similar burns or sham treatments were injected 3h after injury with connexin 32 gap junction inhibitor 2-aminoethoxydiphenyl borate (2APB) or vehicle control and were euthanized after 24h for serum marker profiling. At 24h post-burn, lower serum levels of haptoglobin, serum amyloid P component, monocyte chemoattractant protein-1, interleukin-6, and alanine aminotransferase as assessed by ELISA were found in the knockout mice than in the wildtypes. Fourteen days post-burn, the increases in heart, spleen, and liver and decrease in calf muscle mass found in the wildtype mice were significantly mitigated in the knockouts. Further, the post-burn acute phase response was similarly diminished in the wildtype mice after 2APB administration. Interrupting detrimental post-burn hypermetabolism by inhibiting intercellular hepatocyte communication may provide novel therapeutic leverage during the initial systemic inflammatory response and improve clinical outcomes.