How Relations are Built within a SNS World: Social Network Analysis on Mixi

Our purpose here is to (1) investigate the structure of the personal networks developed on mixi, a Japanese social networking service (SNS), and (2) to consider the governing mechanism which guides participants of a SNS to form an aggregate network. Our findings are as follows:the clustering coefficient of the network is as high as 0.33 while the characteristic path lenght is as low as 5.5. A network among central users (over 300 edges) consist of two cliques, which seems to be very fragile. Community-affiliation network suggests there are several easy-entry communities which later lead users to more high-entry, unique-theme communities. The analysis on connectedness within a community reveals the importance of real-world interaction. Lastly, we depict a probable image of the entire ecology on mixi among users and communities, which contributes broadly to social systems on the Web

Traumatic alterations in GABA signaling disrupt hippocampal network activity in the developing brain

Severe head trauma causes widespread neuronal shear injuries and acute seizures. Shearing of neural processes might contribute to seizures by disrupting the transmembrane ion gradients that sub serve normal synaptic signaling. To test this possibility, we investigated changes in intracellular chloride concentration ([Cl -]i) associated with the widespread neural shear injury induced during preparation of acute brain slices. In hippo campal slices and intact hippo campal preparations from immature CLM-1 mice, increases in [Cl -]i correlated with disruption of neural processes and biomarkers of cell injury. Traumatized neurons with higher [Cl -]i demonstrated excitatory GABA signaling, remained synaptically active, and facilitated network activity as assayed by the frequency of extracellular action potentials and spontaneous network-driven oscillations. These data support a more inhibitory role for GABA in the unperturbed immature brain, demonstrate the utility of the acute brain slice preparation for the study of the consequences of trauma, and provide potential mechanisms for both GABA-mediated excitatory network events in the slice preparation and early post-traumatic seizures. © 2012 the authors

Neural Dynamics during Anoxia and the “Wave of Death”

Recent experiments in rats have shown the occurrence of a high amplitude slow brain wave in the EEG approximately 1 minute after decapitation, with a duration of 5–15 s (van Rijn et al, PLoS One 6, e16514, 2011) that was presumed to signify the death of brain neurons. We present a computational model of a single neuron and its intra- and extracellular ion concentrations, which shows the physiological mechanism for this observation. The wave is caused by membrane potential oscillations, that occur after the cessation of activity of the sodium-potassium pumps has lead to an excess of extracellular potassium. These oscillations can be described by the Hodgkin-Huxley equations for the sodium and potassium channels, and result in a sudden change in mean membrane voltage. In combination with a high-pass filter, this sudden depolarization leads to a wave in the EEG. We discuss that this process is not necessarily irreversible

High Brain Ammonia Tolerance and Down-Regulation of Na+:K+:2Cl- Cotransporter 1b mRNA and Protein Expression in the Brain of the Swamp Eel, Monopterus albus, Exposed to Environmental Ammonia or Terrestrial Conditions

10.1371/journal.pone.0069512PLoS ONE89-POLN

Neuroprotection by adenosine in the brain: From A1 receptor activation to A2A receptor blockade

Adenosine is a neuromodulator that operates via the most abundant inhibitory adenosine A1 receptors (A1Rs) and the less abundant, but widespread, facilitatory A2ARs. It is commonly assumed that A1Rs play a key role in neuroprotection since they decrease glutamate release and hyperpolarize neurons. In fact, A1R activation at the onset of neuronal injury attenuates brain damage, whereas its blockade exacerbates damage in adult animals. However, there is a down-regulation of central A1Rs in chronic noxious situations. In contrast, A2ARs are up-regulated in noxious brain conditions and their blockade confers robust brain neuroprotection in adult animals. The brain neuroprotective effect of A2AR antagonists is maintained in chronic noxious brain conditions without observable peripheral effects, thus justifying the interest of A2AR antagonists as novel protective agents in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease, ischemic brain damage and epilepsy. The greater interest of A2AR blockade compared to A1R activation does not mean that A1R activation is irrelevant for a neuroprotective strategy. In fact, it is proposed that coupling A2AR antagonists with strategies aimed at bursting the levels of extracellular adenosine (by inhibiting adenosine kinase) to activate A1Rs might constitute the more robust brain neuroprotective strategy based on the adenosine neuromodulatory system. This strategy should be useful in adult animals and especially in the elderly (where brain pathologies are prevalent) but is not valid for fetus or newborns where the impact of adenosine receptors on brain damage is different

Traumatic alterations in GABA signaling disrupt hippocampal network activity in the developing brain

Severe head trauma causes widespread neuronal shear injuries and acute seizures. Shearing of neural processes might contribute to seizures by disrupting the transmembrane ion gradients that sub serve normal synaptic signaling. To test this possibility, we investigated changes in intracellular chloride concentration ([Cl -]i) associated with the widespread neural shear injury induced during preparation of acute brain slices. In hippo campal slices and intact hippo campal preparations from immature CLM-1 mice, increases in [Cl -]i correlated with disruption of neural processes and biomarkers of cell injury. Traumatized neurons with higher [Cl -]i demonstrated excitatory GABA signaling, remained synaptically active, and facilitated network activity as assayed by the frequency of extracellular action potentials and spontaneous network-driven oscillations. These data support a more inhibitory role for GABA in the unperturbed immature brain, demonstrate the utility of the acute brain slice preparation for the study of the consequences of trauma, and provide potential mechanisms for both GABA-mediated excitatory network events in the slice preparation and early post-traumatic seizures. © 2012 the authors