Same old

Friday, 26 October 2007

Synchronized spontaneous spikes on multi-electrode array show development of cultured neuronal network.

Synchronized spontaneous spikes on multi-electrode array show development of cultured neuronal network.

Conf Proc IEEE Eng Med Biol Soc. 2005;2:2134-7

Authors: Li X, Zhou W, Liu M, Luo Q

Spontaneous firing play an important role in development of neuronal network. Activity-dependent modification of synaptic efficacy is widely recognized as a cellular basis of learning, memory, and development plasticity. Little is known of the activity-dependent modification of the synchronized spontaneous firing of the hippocampal networks. Long-term recording of spontaneous activity in cultured hippocampal neuronal networks was carried out using substrates containing multi-electrode array (MEA). Spontaneous uncorrelated firing appeared within a week and transformed progressively into synchronized pattern. During the development, these synchronized firings became into oscillation pattern and the synchronization has little change. By paired stimulation from adjacent electrodes in the network, the synchronized firing form a larger network burst. These results suggest that synchronized spontaneous spikes show the development of neuronal network and electronical stimulation could change the development.

PMID: 17282651 [PubMed - in process]

Multiresolution bayesian detection of multiunit extracellular spike waveforms in multichannel neuronal recordings.

Multiresolution bayesian detection of multiunit extracellular spike waveforms in multichannel neuronal recordings.

Conf Proc IEEE Eng Med Biol Soc. 2005;1:141-4

Authors: Suhail Y, Oweiss K

We describe multiresolution Bayesian tests for spike detection in multielectrode recordings. We derive results for single channel and multi electrode data, and show that the use of the array model substantially improves the detection performance. The effect of signal and noise spatial correlation characteristics is also discussed. Our approach focuses on blind signal detection without any assumptions about the underlying signal parameters. It is therefore suitable for chronic recordings with electrode arrays where typically temporal and spatial nonstationarity of the extracellular waveforms complicates the estimation of the true action potential.

PMID: 17282131 [PubMed - in process]

Modeling the Nonlinear Dynamic Interactions of the Lateral and the Medial Perforant Path of the Hippocampal Dentate Gyrus.

Modeling the Nonlinear Dynamic Interactions of the Lateral and the Medial Perforant Path of the Hippocampal Dentate Gyrus.

Conf Proc IEEE Eng Med Biol Soc. 2006;1:5539-5542

Authors: Dimoka A, Courellis SH, Marmarelis VZ, Berger TW

We present a new method to characterize the nonlinearities resulting from the co-activity of two pathways that converge on a common postsynaptic element. We investigated the nonlinear dynamic interactions between the lateral perforant pathway (LPP) and the medial perforant pathway (MPP) of the hippocampal dentate gyms, and the effects of these cross-pathway interactions on granule cell output. A third order Volterra-Poisson modeling approach was implemented to capture the interactions between the two pathways. The kernels presented pathway specific signatures as they capture the nonlinear dynamics of each pathway individually in the form of self-kernels, and the nonlinear interactions between the two pathways in the form of cross-kernels. Data were collected in-vitro from acute slices of adult rats via a multi-electrode array recording system. The stimuli were dual-site random impulse trains with Poisson distributed inter-impulse intervals. The recorded responses from the granule cells were population spikes, simplified as discrete impulses with variable amplitudes. Our results indicated that the third order nonlinear interactions between the LPP and the MPP needs to be included in the model in order to achieve adequate predictive accuracy and indicate that this approach can be generalized to complex interactions between distinct inputs to the same set of neurons.

PMID: 17946313 [PubMed - as supplied by publisher]

Imaging of odor perception delineates functional disintegration of the limbic circuits in mesial temporal lobe epilepsy.

Imaging of odor perception delineates functional disintegration of the limbic circuits in mesial temporal lobe epilepsy.

Neuroimage. 2007 Sep 14;

Authors: Ciumas C, Lindström P, Bernard A, Savic I

Metabolic and neuro-receptor abnormalities within the extrafocal limbic circuits are established in mesial temporal lobe epilepsy (MTLE). However, very little is known about how these circuits process external stimuli. We tested whether odor activation can help delineate limbic functional disintegration in MTLE, and measured cerebral blood flow with PET during birhinal smelling of familiar and unfamiliar odors, using smelling of odorless air as the baseline condition. Patients with MTLE (13 left-sided, 10 right-sided) and 21 controls were investigated. In addition to odor activation, the analysis included functional connectivity, using right and left piriform cortex as seed regions. Healthy controls activated the amygdala, piriform, anterior insular, and cingulate cortices on both sides. Smelling of familiar odors engaged, in addition, the right parahippocampus, and the left Brodmann Area (BA) 44, 45, 47. Patients failed to activate the amygdala, piriform and the anterior insular cortex in the epileptogenic hemisphere. Furthermore, those with left MTLE did not activate the left BA 44, 45 and 47 with familiar odors, which they perceived as less familiar than controls. Congruent with the activation data each seed region was in patients functionally disconnected with the contralateral amygdala+piriform+insular cortex. The functional disintegration in patients exceeded the reduced activation, and included the contralateral temporal neocortex, and in subjects with right MTLE also the right orbitofrontal cortex. Imaging of odor perception may be used to delineate functional disintegration of the limbic networks in MTLE. It shows an altered response in several regions, which may underlie some interictal behavioral problems associated with this condition.

PMID: 17951077 [PubMed - as supplied by publisher]

Rhythmic Spontaneous Activity in the Piriform Cortex.

Rhythmic Spontaneous Activity in the Piriform Cortex.

Cereb Cortex. 2007 Oct 8;

Authors: Sanchez-Vives MV, Descalzo VF, Reig R, Figueroa NA, Compte A, Gallego R

Slow spontaneous rhythmic activity is generated and propagates in neocortical slices when bathed in an artificial cerebrospinal fluid with ionic concentrations similar to the ones in vivo. This activity is extraordinarily similar to the activation of the cortex in physiological conditions (e.g., slow-wave sleep), thus representing a unique in vitro model to understand how cortical networks maintain and control ongoing activity. Here we have characterized the activity generated in the olfactory or piriform cortex and endopiriform nucleus (piriform network). Because these structures are prone to generate epileptic discharges, it seems critical to understand how they generate and regulate their physiological rhythmic activity. The piriform network gave rise to rhythmic spontaneous activity consisting of a succession of up and down states at an average frequency of 1.8 Hz, qualitatively similar to the corresponding neocortical activity. This activity originated in the deep layers of the piriform network, which displayed higher excitability and denser connectivity. A remarkable difference with neocortical activity was the speed of horizontal propagation (114 mm/s), one order of magnitude faster in the piriform network. Properties of the piriform cortex subserving fast horizontal propagation may underlie the higher vulnerability of this area to epileptic seizures.

PMID: 17925296 [PubMed - as supplied by publisher]

Neuromodulation by Glutamate and Acetylcholine can Change Circuit Dynamics by Regulating the Relative Influence of Afferent Input and Excitatory Feedback.

Neuromodulation by Glutamate and Acetylcholine can Change Circuit Dynamics by Regulating the Relative Influence of Afferent Input and Excitatory Feedback.

Mol Neurobiol. 2007 Oct;36(2):184-200

Authors: Giocomo LM, Hasselmo ME

Substances such as acetylcholine and glutamate act as both neurotransmitters and neuromodulators. As neuromodulators, they change neural information processing by regulating synaptic transmitter release, altering baseline membrane potential and spiking activity, and modifying long-term synaptic plasticity. Slice physiology research has demonstrated that many neuromodulators differentially modulate afferent, incoming information compared to intrinsic and recurrent processing in cortical structures such as piriform cortex, neocortex, and the hippocampus. The enhancement of afferent (external) pathways versus the suppression at recurrent (internal) pathways could cause cortical dynamics to switch between a predominant influence of external stimulation to a predominant influence of internal recall. Modulation of afferent versus intrinsic processing could contribute to the role of neuromodulators in regulating attention, learning, and memory effects in behavior.

PMID: 17952661 [PubMed - in process]

The endocannabinoid system controls key epileptogenic circuits in the hippocampus.

The endocannabinoid system controls key epileptogenic circuits in the hippocampus.

Neuron. 2006 Aug 17;51(4):455-66

Authors: Monory K, Massa F, Egertová M, Eder M, Blaudzun H, Westenbroek R, Kelsch W, Jacob W, Marsch R, Ekker M, Long J, Rubenstein JL, Goebbels S, Nave KA, During M, Klugmann M, Wölfel B, Dodt HU, Zieglgänsberger W, Wotjak CT, Mackie K, Elphick MR, Marsicano G, Lutz B

Balanced control of neuronal activity is central in maintaining function and viability of neuronal circuits. The endocannabinoid system tightly controls neuronal excitability. Here, we show that endocannabinoids directly target hippocampal glutamatergic neurons to provide protection against acute epileptiform seizures in mice. Functional CB1 cannabinoid receptors are present on glutamatergic terminals of the hippocampal formation, colocalizing with vesicular glutamate transporter 1 (VGluT1). Conditional deletion of the CB1 gene either in cortical glutamatergic neurons or in forebrain GABAergic neurons, as well as virally induced deletion of the CB1 gene in the hippocampus, demonstrate that the presence of CB1 receptors in glutamatergic hippocampal neurons is both necessary and sufficient to provide substantial endogenous protection against kainic acid (KA)-induced seizures. The direct endocannabinoid-mediated control of hippocampal glutamatergic neurotransmission may constitute a promising therapeutic target for the treatment of disorders associated with excessive excitatory neuronal activity.

PMID: 16908411 [PubMed - indexed for MEDLINE]