Application of the Catecholaminergic Neuron Electron Transport (CNET) Physical Substrate for Consciousness and Action Selection to Integrated Information Theory

A newly discovered physical mechanism involving incoherent electron tunneling in layers of the protein ferritin that are found in catecholaminergic neurons (catecholaminergic neuron electron transport or CNET) is hypothesized to support communication between neurons. Recent tests further confirm that these ferritin layers can also perform a switching function (in addition to providing an electron tunneling mechanism) that could be associated with action selection in those neurons, consistent with earlier predictions based on CNET. While further testing would be needed to confirm the hypothesis that CNET allows groups of neurons to communicate and act as a switch for selecting one of the neurons in the group to assist in reaching action potential, this paper explains how that hypothesized behavior would be consistent with Integrated Information Theory (IIT), one of a number of consciousness theories (CTs). While the sheer number of CTs suggest that any one of them alone is not sufficient to explain consciousness, this paper demonstrates that CNET can provide a physical substrate and action selection mechanism that is consistent with IIT and which can also be applied to other CTs, such as to conform them into a single explanation of consciousness.     

Retrieval and chaos in layeredQ-Ising neural networks

Using a probabilistic approach, we study the parallel dynamics of theQ-Ising layered networks for arbitraryQ. By introducing auxiliary thermal fields, we express the stochastic dynamics within the gain function formulation of the deterministic dynamics. Evolution equations are derived for arbitraryQ at both zero and finite temperatures. An explicit analysis of the fixed-point equations is carried out for bothQ=3 andQ. The retrieval properties are discussed in terms of the gain parameter, the storage capacity, and the temperature. Using the time evolution of the distance between two network configurations, we investigate the possibility of microscopic chaos. Chaotic behavior is always present for arbitrary finiteQ. However, in the limitQ the existence of chaos depends on the parameters of the system.     

Nitric oxide release during evoked neuronal activity in cerebellum slices: detection with platinized carbon-fiber microelectrodes.

Nitric oxide is an important biological messenger that particularly induces the relaxation of smooth muscle cells surrounding vessels, and, hence, controls the flow of blood. This mechanism is essential for brain function, and its fine control, termed functional hyperemia, is supposed to be realized by certain neurons that may release bursts of NO*. The aim of the present study is to examine the advantages of platinized carbon-fiber microelectrodes (5-7 microm tip diameter) for the direct and in situ electrochemical detection of NO* released by neurons into ex vivo cerebellum slices. After establishing the different analytical properties of the platinized carbon-fiber microelectrodes in vitro on NO* solutions at 50 nM to 1 mM concentration, they were characterized using DEA-NONOate solutions that chemically decompose into NO*, and therefore mimic the measurement of transient variations of NO* concentration in biological samples. This validated the present approach, so that direct, in situ ex vivo measurements of nitric oxide released by neurons in a rat cerebellar slice are presented and discussed.     

Effect of channel block on the collective spiking activity of coupled stochastic Hodgkin-Huxley neurons

Toxins, such as tetraethylammonium (TEA) and tetrodotoxin (TTX), can make potassium or sodium ion channels poisoned, respectively, and hence reduce the number of working ion channels and lead to the diminishment of conductance. In this paper, we have studied by numerical simulations the effects of sodium and potassium ion channel poisoning on the collective spiking activity of an array of coupled stochastic Hodgkin-Huxley (HH) neurons. It is found for a given number of neurons sodium or potas- sium ion channel block can either enhance or reduce the collective spiking regularity, depending on the membrane patch size. For a given smaller or larger patch size, potassium and sodium ion channel block can reduce or enhance the collective spiking regularity, but they have different patch size ranges for the transformation. This result shows that sodium or potassium ion channel block might have dif- ferent effects on the collective spiking activity in coupled HH neurons from the effects for a single neuron, which represents the interplay among the diminishment of maximal conductance and the in- crease of channel noise strength due to the channel blocks, as well as the bi-directional coupling be- tween the neurons.     

Endothelin 1 protects HN33 cells from serum deprivation-induced neuronal apoptosis through Ca(2+)-PKCalpha-ERK pathway

Endothelins (ETs), which were originally found to be potent vasoactive transmitters, were known to be implicated in nervous system, but the mode of mechanism remains unclear. ETs (ET-1, ET-2, and ET-3) were added to HN33 (mouse hippocampal neuron chi neuroblastoma) cells. Among the three types of ET, only ET-1 increased the intracellular calcium levels in a PLC dependent manner with the induction of ERK 1/2 activation. As the result of ET-1 exposure, the survival rate of HN33 cells and the PKCalpha translocation into the plasma membrane were increased. We suggest that ET-1 participated in the neuroprotective effect involving the calcium-PKCalpha-ERK1/2 pathway.     

利用VSV标记具有特定投射的特异类型神经元的精细结构

神经元是构成神经系统的基本单位之一，对其精细形态结构的研究是了解神经网络构筑和信息处理方式的基础，然而目前缺乏能够标记具有特定投射特征的特异类型神经元精细结构的有效方法.在糖蛋白基因缺失的水泡性口炎病毒（VSV）毒株基础上突变其核蛋白，我们获得了重组病毒VSV-△G-NR7A-EGFP，并发现该病毒在一定窗口期内可实现神经元形态的快速高亮度标记；我们进一步在此基础上构建了VSV-△G-EnvA-NR7A-EGFP病毒，并基于特定的转基因动物及辅助病毒rAAV-EF1α-Dio-Bfp-Tva，通过控制注射位点，分别实现了有NAc-LH投射特异性的D2R神经元和VTA-NAc投射特异性的多巴胺神经元的标记，展示了一种可用于稀疏、高亮地标记具有特定投射特征的特异类型神经元精细结构的新方法.     

The effects of rises in external K+ on the hyperpolarization-activated cation current Ih in rat dorsal root ganglion neurons

The effects of rises in external K⁺ (K_ext) were examined on the hyperpolarization-activated cation current (I _h) in rat dorsal root ganglion neurons using the whole-cell patch clamp technique. The results showed that K_ext increased I _h in a certain concentration and voltage-dependent manner. At the basal K_ext level (4 mmol/L), I _h had a maximal amplitude of 1085 ± 340 pA which was enhanced by ∼45% and ∼92% at 8 and 16 mmol/L K_ext, respectively. The midpoint activation voltage was significantly shifted from −98 mV in the hyperpolarizing direction by 8 and 12 mV at 8 and 16 mmol/L K_ext, respectively with alteration of the activation course of I _h. The short time constants of activation became longer with the increasing amplitude of the command potential upon rises in K_ext. The long time constants became shorter. The reversal potentials were shifted in the positive direction without significant alterations upon rises in K_ext. According to the functional role of I _h, K_ext increased I _h, resulting in an enhanced neuronal excitability, which might produce activation potential abnormality and perhaps neuropathic pain involved. Supported by the University of Science and Technology Foundation of Shanxi Province (Grant No. 200713010)     

Ultrastructural changes to rat hippocampus in pentylenetetrazol- and kainic acid-induced status epilepticus: A study using electron microscopy

A pentylenetetrazol (PTZ)-induced status epilepticus model in rats was used in the study. The brains were studied one month after treatment. Ultrastructural observations using electron microscopy performed on the neurons, glial cells, and synapses, in the hippocampal CA1 region of epileptic brains, demonstrated the following major changes over normal control brain tissue. (i) There is ultrastructural alterations in some neurons, glial cells and synapses in the hippocampal CA1 region. (ii) The destruction of cellular organelles and peripheral, partial or even total chromatolysis in some pyramidal cells and in interneurons are observed. Several astrocytes are proliferated or activated. Presynaptic terminals with granular vesicles and degenerated presynaptic profiles are rarely observed. (iii) The alterations observed are found to be dependent on the frequency of seizure activities following the PTZ treatment. It was observed that if seizure episodes are frequent and severe, the ultrastructure of hippocampal area is significantly changed. Interestingly, the ultrastructure of CA1 area is found to be only moderately altered if seizure episodes following the status epilepticus are rare and more superficial; (iv) alterations in mitochondria and dendrites are among the most common ultrastructural changes seen, suggesting cell stress and changes to cellular metabolism. These morphological changes, observed in brain neurons in status epilepticus, are a reflection of epileptic pathophysiology. Further studies at the chemical and molecular level of neurotransmitter release, such as at the level of porosomes (secretory portals) at the presynaptic membrane, will further reveal molecular details of these changes.     

Parallel Dynamics of Extremely Diluted Symmetric Q-Ising Neural Networks

The parallel dynamics of extremely diluted symmetric Q-Ising neural networks is studied for arbitrary Q using a probabilistic approach. In spite of the extremely diluted architecture the feedback correlations arising from the symmetry prevent a closed-form solution in contrast with the extremely diluted asymmetric model. A recursive scheme is found determining the complete time evolution of the order parameters taking into account all feedback. It is based upon the evolution of the distribution of the local field, as in the fully connected model. As an illustrative example an explicit analysis is carried out for the Q=2 and Q=3 model. These results agree with and extend the partial results existing for Q=2. For Q>2 the analysis is entirely new. Finally, equilibrium fixed-point equations are derived and a capacity-gain function diagram is obtained.