Propagation Of Spontaneous Activity Research Articles

Changes in the spatiotemporal pattern of spontaneous activity across a cortical column after noise trauma.

In the auditory modality, noise trauma has often been used to investigate cortical plasticity as it causes cochlear hearing loss. One limitation of these past studies, however, is that the effects of noise trauma have been mostly documented at the granular layer, which is the main cortical recipient of thalamic inputs. Importantly, the cortex is composed of six different layers each having its own pattern of connectivity and specific role in sensory processing. The present study aims at investigating the effects of acute and chronic noise trauma on the laminar pattern of spontaneous activity (SA) in primary auditory cortex (A1) of the anesthetized guinea pig. We show that spontaneous activity is dramatically altered across cortical layers after acute and chronic noise-induced hearing loss. First, spontaneous activity was globally enhanced across cortical layers, both in terms of firing rate and amplitude of spike-triggered average of local field potentials. Second, current source density on (spontaneous) spike-triggered average of local field potentials indicates that current sinks develop in the supra- and infragranular layers. These latter results suggest that supragranular layers become a major input recipient and the propagation of spontaneous activity over a cortical column is greatly enhanced after acute and chronic noise-induced hearing loss. We discuss the possible mechanisms and functional implications of these changes.NEW & NOTEWORTHY The present study investigates the effects of acute and chronic noise trauma on the laminar pattern of spontaneous activity in the primary auditory cortex. Our study is first to report that noise trauma alters the sequence of cortical column activation during ongoing activity. In particular, we show that the supragranular layer becomes a major input recipient and the synaptic activity in the infragranular layers is enhanced.

Role of Pericytes in theInitiation and Propagation of Spontaneous Activity in theMicrovasculature.

The microvasculature is composed of arterioles, capillaries and venules. Spontaneous arteriolar constrictions reduce effective vascular resistance to enhance tissue perfusion, while spontaneous venular constrictions facilitate the drainage of tissue metabolites by pumping blood. In the venules of visceral organs, mural cells, i.e. smooth muscle cells (SMCs) or pericytes, periodically generate spontaneous phasic constrictions, Ca2+ transients and transient depolarisations. These events arise from spontaneous Ca2+ release from the sarco-endoplasmic reticulum (SR/ER) and the subsequent opening of Ca2+-activated chloride channels (CaCCs). CaCC-dependent depolarisation further activates L-type voltage-dependent Ca2+ channels (LVDCCs) that play a critical role in maintaining the synchrony amongst mural cells. Mural cells in arterioles or capillaries are also capable of developing spontaneous activity. Non-contractile capillary pericytes generate spontaneous Ca2+ transients primarily relying on SR/ER Ca2+ release. Synchrony amongst capillary pericytes depends on gap junction-mediated spread of depolarisations resulting from the opening of either CaCCs or T-type VDCCs (TVDCCs) in a microvascular bed-dependent manner. The propagation of capillary Ca2+ transients into arterioles requires the opening of either L- or TVDCCs again depending on the microvascular bed. Since the blockade of gap junctions or CaCCs prevents spontaneous Ca2+ transients in arterioles and venules but not capillaries, capillary pericytes appear to play a primary role in generating spontaneous activity of the microvasculature unit. Pericytes in capillaries where the interchange of substances between tissues and the circulation takes place may provide the fundamental drive for upstream arterioles and downstream venules so that the microvasculature network functions as an integrated unit.

The role of intra-striatal synaptic interactions for shaping cortico-striatal network dynamics

Event Abstract Back to Event The role of intra-striatal synaptic interactions for shaping cortico-striatal network dynamics Jovana Belić1*, Andreas Klaus2, Dietmar Plenz3 and Jeanette Hellgren Kotaleski4 1 Royal Institute of Technology (KTH), Stockholm and Bernstein Center Freiburg, Sweden 2 Karolinska Institutet (KI), Stockholm and National Institute of Mental Health (NIH), Bethesda, USA, United States 3 National Institute of Mental Health (NIH), Bethesda, USA, United States 4 Royal Institute of Technology (KTH), Stockholm and Karolinska Institutet (KI), Stockholm , Sweden The basal ganglia consist of several interconnected subcortical nuclei that are supposedly involved in many motor and cognitive functions. The striatum, the input stage of the basal ganglia, is a major recipient of massive glutamatergic inputs from the cerebral cortex and thalamus. Medium spiny neurons (MSNs) dominate in the striatum (up to 95% in rodents). They are inhibitory (GABAergic) and have membrane properties that give them a high threshold for activation [1]. MSNs interact with each other through weak recurrent inhibitory synapses and with low connection probability [2]. Fast-spiking GABAergic interneurons (FSNs) can delay or prevent the emission of an action potential in MSNs [3]. FSNs receive convergent inputs from a wider range of distinct cortical regions compared to nearby MSNs, and despite the fact that they are relatively sparse elements (1-2%) it seems that they have very prominent role in shaping the output of the striatum [4]. Neuronal avalanches are a type of spontaneous activity first observed in vitro by recording local field potentials in cortical neural networks using slices of rat cortex as well as cultured networks [5]. Propagation of spontaneous activity is balanced and shows a branching parameter close to 1. In addition, the number of electrodes driven over threshold during activity is distributed approximately like a power law with an exponent of -3/2 for event sizes suggesting a critical dynamics [5]. Neural avalanches have been shown to provide: optimal information transmission [5, 6], maximal information capacity [6] and maximal dynamic range [7]. We are studying simultaneously striatal and cortical activity in vitro. Preliminary results show that neuronal avalanches in cortex induce activity clusters in striatum whose size distribution can be approximated by a steeper power law than observed in cortex. Based on this we have developed network models in order to determine the impact of different striatal neurons on the more negative exponent. In particular, we are investigating whether FS or MS neurons have any roles in shaping the striatal dynamics.

Connexin-mediated communication controls cell proliferation and is essential in retinal histogenesis

Connexin (Cx) channels and hemichannels are involved in essential processes during nervous system development such as apoptosis, propagation of spontaneous activity and interkinetic nuclear movement. In the first part of this study, we extensively characterized Cx gene and protein expression during retinal histogenesis. We observed distinct spatio-temporal patterns among studied Cx and an overriding, ubiquitous presence of Cx45 in progenitor cells. The role of Cx-mediated communication was assessed by using broad-spectrum (carbenoxolone, CBX) and Cx36/Cx50 channel-specific (quinine) blockers. In vivo application of CBX, but not quinine, caused remarkable reduction in retinal thickness, suggesting changes in cell proliferation/apoptosis ratio. Indeed, we observed a decreased number of mitotic cells in CBX-injected retinas, with no significant changes in the expression of PCNA, a marker for cells in proliferative state. Taken together, our results pointed a pivotal role of Cx45 in the developing retina. Moreover, this study revealed that Cx-mediated communication is essential in retinal histogenesis, particularly in the control of cell proliferation.

Neuronal Avalanches in Neocortical Circuits

Networks of living neurons exhibit diverse patterns of activity, including oscillations, synchrony, and waves. Recent work in physics has shown yet another mode of activity in systems composed of many nonlinear units interacting locally. For example, avalanches, earthquakes, and forest fires all propagate in systems organized into a critical state in which event sizes show no characteristic scale and are described by power laws. We hypothesized that a similar mode of activity with complex emergent properties could exist in networks of cortical neurons. We investigated this issue in mature organotypic cultures and acute slices of rat cortex by recording spontaneous local field potentials continuously using a 60 channel multielectrode array. Here, we show that propagation of spontaneous activity in cortical networks is described by equations that govern avalanches. As predicted by theory for a critical branching process, the propagation obeys a power law with an exponent of -3/2 for event sizes, with a branching parameter close to the critical value of 1. Simulations show that a branching parameter at this value optimizes information transmission in feedforward networks, while preventing runaway network excitation. Our findings suggest that "neuronal avalanches" may be a generic property of cortical networks, and represent a mode of activity that differs profoundly from oscillatory, synchronized, or wave-like network states. In the critical state, the network may satisfy the competing demands of information transmission and network stability.

Effects of magnesium, oxytocin, and prostaglandin F2 alpha on the generation and propagation of excitation in the longitudinal muscle of rat myometrium during late pregnancy.

In order to find out the changes in myometrial properties towards parturition, effects of Mg, oxytocin, and prostaglandin F2 alpha (PGF2 alpha) were investigated on longitudinal muscle strips taken from rat uteri on Days 20 and 22 of pregnancy. With intracellular recording by microelectrode, membrane potential was 50.5 +/- 1.4 mV on Day 20, and 49.9 +/- 1.0 mV on Day 22 in the Mg-free Krebs solution. The slow potential was larger, and the spike potentials during a burst discharge exhibited variable amplitude on Day 20, whereas these were regular on Day 22. With extracellular recording by the rubber gap method, spike potentials discharged in a synchronized manner on Day 22, suggesting a better coordination between cell groups. When 1.2 mM Mg was applied, the spontaneous activity was depressed more strongly on Day 22. The excitatory effect of PGF2 alpha faded sooner, whereas that of oxytocin persisted. When the fading of PGF2 alpha had occurred, the excitatory effect of oxytocin was weaker than when it was given alone. Because propagation of spontaneous activity, occurring either in the Mg-free solution or in the presence of oxytocin and PGF2 alpha in normal Krebs solution, did not show a definite direction from ovarian to vaginal side of the longitudinal muscle, it was concluded that generation of spontaneous activity was not localized in a given site of the muscle, but originated anywhere in Days 20 and 22 preparations.