Biomedical subjects

Gwendal Le Masson

Publications and source records attributed to Gwendal Le Masson.

6 recordsLinked to original sources

PubMed2005

Exploring spike transfer through the thalamus using hybrid artificial-biological neuronal networks.

We use dynamic clamp to construct "hybrid" thalamic circuits by connecting a biological neuron in situ to silicon- or software-generated "neurons" through artificial synapses. The purpose is to explore cellular sensory gating mechanisms that regulate the transfer efficiency of signals during different sleep-wake states. Hybrid technology is applied in vitro to different paradigms such as: (1) simulating interactions between biological thalamocortical neurons, artificial reticular thalamic inhibitory interneurons and a simulated sensory input, (2) grafting an artificial sensory input to a wholly biological thalamic network that generates spontaneous sleep-like oscillations, (3) injecting in thalamocortical neurons a background synaptic bombardment mimicking the activity of corticothalamic inputs. We show that the graded control of the strength of intrathalamic inhibition, combined with the membrane polarization and the fluctuating synaptic noise in thalamocortical neurons, is able to govern functional shifts between different input/output transmission states of the thalamic gate.

Action Potentials↗

PubMed2005

Synaptic background activity controls spike transfer from thalamus to cortex.

Characterizing the responsiveness of thalamic neurons is crucial to understanding the flow of sensory information. Typically, thalamocortical neurons possess two distinct firing modes. At depolarized membrane potentials, thalamic cells fire single action potentials and faithfully relay synaptic inputs to the cortex. At hyperpolarized potentials, the activation of T-type calcium channels promotes burst firing, and the transfer is less accurate. Our results suggest that this duality no longer holds if synaptic background activity is taken into account. By injecting stochastic conductances into guinea-pig thalamocortical neurons in slices, we show that the transfer function of these neurons is strongly influenced by conductance noise. The combination of synaptic noise with intrinsic properties gives a global responsiveness that is more linear, mixing single-spike and burst responses at all membrane potentials. Because in thalamic neurons, background synaptic input originates mainly from cortex, these results support a determinant role of corticothalamic feedback during sensory information processing.

Action Potentials↗

PubMed2003

A prospective evaluation of phrenic nerve conduction in multifocal motor neuropathy and chronic inflammatory demyelinating polyneuropathy.

The purpose of the study was to evaluate electrophysiologically phrenic nerve involvement in multifocal motor neuropathy (MMN) and chronic inflammatory demyelinating polyneuropathy (CIDP). The response latencies following phrenic nerve stimulation were increased in 11 of 14 (80%) patients in the CIDP group but in only 1 of 14 (8%) patients in the MMN group. The mean diaphragmatic compound muscle action potential (CMAP) was significantly lower in amplitude in the CIDP group compared to the MMN group and to a control group of 8 subjects (P < 0.001). There were no significant differences between the MMN and control groups. Only the reduction in CMAP amplitude correlated with the presence of restrictive lung function. Phrenic nerve conduction measurement should be performed more systematically, especially in CIDP and, when diaphragmatic CMAPs are reduced in amplitude, pulmonary function tests should be performed to look for a restrictive lung syndrome.

Adult↗

PubMed2003

Dynamic balance of metabotropic inputs causes dorsal horn neurons to switch functional states.

Sensory relay structures in the spinal cord dorsal horn are now thought to be active processing structures that function before supraspinal sensory integration. Dorsal horn neurons directly receive nociceptive (pain) signals from the periphery, express a high degree of functional plasticity and are involved in long-term sensitization and chronic pain. We show here that deep dorsal horn neurons (DHNs) in Wistar rats can switch their intrinsic firing properties from tonic to plateau or endogenous bursting patterns, depending upon the balance of control by metabotropic glutamate (mGlu) and GABA(B) receptors. We further show that this modulation acts on at least one common target, the inwardly rectifying potassium channel (Kir3). Finally, we found that these firing modes correspond to specific functional states of information transfer in which dorsal horn neurons can faithfully transmit, greatly enhance or block the transfer of nociceptive information.

Action Potentials↗

PubMed2003

Glutamatergic input governs periodicity and synchronization of bursting activity in oxytocin neurons in hypothalamic organotypic cultures.

During suckling, oxytocin (OT) neurons display a bursting electrical activity, consisting of a brief burst of action potentials which is synchronized throughout the OT neuron population and which periodically occurs just before each milk ejection in the lactating rat. To investigate the basis of such synchronization, we performed simultaneous intracellular recordings from pairs of OT neurons identified retrospectively by intracellular fluorescent labelling and immunocytochemistry in organotypic slice cultures derived from postnatal rat hypothalamus. A spontaneous bursting activity was recorded in 65% of OT neurons; the remaining showed only a slow, irregular activity. Application of OT triggered bursts in nonbursting neurons and accelerated bursting activity in spontaneously bursting cells. These cultures included rare vasopressinergic neurons showing no bursting activity and no reaction to OT. Bursts occurred simultaneously in all pairs of bursting OT neurons but, as in vivo, there were differences in burst onset, amplitude and duration. Coordination of firing was not due to electrotonic coupling because depolarizing one neuron in a pair had no effect on the membrane potential of its partner and halothane and proprionate did not desynchronize activity. On the other hand, bursting activity was superimposed on volleys of excitatory postsynaptic potentials (EPSPs) which occurred simultaneously in pairs of neurons. EPSPs, and consequently action potentials, were reversibly blocked by the non-NMDA glutamatergic receptor antagonist CNQX. Taken together, these data, obtained from organotypic cultures, strongly suggest that a local hypothalamic network governs synchronization of bursting firing in OT neurons through synchronous afferent volleys of EPSPs originating from intrahypothalamic glutamatergic inputs.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2002

Feedback inhibition controls spike transfer in hybrid thalamic circuits.

Sensory information reaches the cerebral cortex through the thalamus, which differentially relays this input depending on the state of arousal. Such 'gating' involves inhibition of the thalamocortical relay neurons by the reticular nucleus of the thalamus, but the underlying mechanisms are poorly understood. We reconstructed the thalamocortical circuit as an artificial and biological hybrid network in vitro. With visual input simulated as retinal cell activity, we show here that when the gain in the thalamic inhibitory feedback loop is greater than a critical value, the circuit tends towards oscillations -- and thus imposes a temporal decorrelation of retinal cell input and thalamic relay output. This results in the functional disconnection of the cortex from the sensory drive, a feature typical of sleep states. Conversely, low gain in the feedback inhibition and the action of noradrenaline, a known modulator of arousal, converge to increase input output correlation in relay neurons. Combining gain control of feedback inhibition and modulation of membrane excitability thus enables thalamic circuits to finely tune the gating of spike transmission from sensory organs to the cortex.

Action Potentials↗