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M Deschênes

Publications and source records attributed to M Deschênes.

At least 73 records · Page 4Linked to original sources
PubMed1987

Physiological characteristics of anterior thalamic nuclei, a group devoid of inputs from reticular thalamic nucleus.

This study tested the hypothesis that neurons of thalamic nuclei, which are normally devoid of inputs from the reticular thalamic nucleus, do not display spindle oscillations and related rhythmic spike bursts. This proposal derived from our recent studies indicating that the reticular nucleus is the generator of spindling rhythmicity. We used retrograde tracing methods, intracellular recordings in barbiturized cats, and extracellular recordings of single neurons and field potentials in anteroventral (AV), anteromedial (AM), ventroanterior (VA), ventrolateral (VL), and central lateral (CL) thalamic nuclei in cats with rostral brain stem transections (cerveau isolé preparations), before and after administration of barbiturates. The observation that AV and AM nuclei do not receive inputs from the reticular nucleus was confirmed by using injections of horseradish peroxidase conjugated to wheat germ agglutinin confined within the limits of anterior nuclei. Such injections led to massive retrograde labeling in mammillary nuclei and layer VI of the retrosplenial cortex but left free of labeling the neurons of the reticular thalamic nucleus. Intracellular recordings showed that AV-AM neurons discharge tonically in response to a depolarizing current applied at rest, whereas they give rise to a slow spike that underlies a burst of fast action potentials when the membrane is hyperpolarized by 5-12 mV. Despite the fact that they share similar properties with other thalamic neurons, intracellularly recorded AV-AM neurons do not exhibit spindle waves under barbiturate anesthesia, whereas VA-VL, CL, and other thalamocortical neurons that receive afferents from the reticular nucleus commonly display such oscillations. With extracellular recordings performed simultaneously in CL and AV or AM nuclei of the unanesthetized cerveau isolé preparation, focal spindle oscillations and related rhythmic high-frequency spike bursts of single CL cells contrasted with absence of spindles and spike bursts in AV or AM neurons. Spindling could be induced in AV-AM nuclei only after administration of barbiturates at doses exceeding 3 mg/kg, and it appeared approximately 35-40 s after the barbiturate effect was detected in the simultaneously recorded CL nucleus. Moreover, the spike bursts that were elicited in AV-AM neurons after barbiturate administration were not temporally related with focal spindles. Since spindle oscillations did not appear intracellularly in AV-AM neurons, the possibility was envisaged that barbiturate-induced spindles were the passive reflection of field potentials actively generated in neighboring thalamic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Morphology and electrophysiological properties of reticularis thalami neurons in cat: in vivo study of a thalamic pacemaker.

Reticularis thalami neurons (RE neurons) were identified morphologically, and their electrophysiological properties were studied in cat under barbiturate anesthesia. Intracellular HRP injections showed that RE neurons possessed very long dendrites bearing numerous filopodia-like appendages and that their axons were directed toward main thalamic nuclei. As a rule, small axonal branches were also emitted within the RE nucleus itself. At rest, the membrane potential of RE neurons displayed 2 types of oscillations: a slow 0.1-0.2 Hz oscillation and fast 7-12 Hz oscillations occurring on the positive phase of the former. Episodes of spindle (7-12 Hz) waves lasted for 2-3 sec and were characterized by rhythmic depolarizations and burst discharges. Intracellular injections of QX314 and current pulse analyses revealed the presence in RE cells of 2 distinct inward currents: a persistent current that promoted tonic firing and a low-threshold current deinactivated by hyperpolarization that generated burst discharges. The low-threshold current deinactivated with large somatic hyperpolarizations (up to 30 mV) and produced depolarizing responses that lasted for about 70 msec. In addition, low-threshold responses appeared rhythmically at intervals of about 150 msec after recovery of the membrane potential from hyperpolarization. Because of their duration, voltage dependence, and persistence after intracellular injections of QX314, it is suggested that these responses resulted from activation of a low-threshold Ca2+ current at the dendritic level. In QX314-injected cells, selective components of spontaneous oscillations were abolished, among them the positive phase of the slow oscillation and late depolarizing humps that followed burst discharges within spindle sequences. However, the rhythmic occurrence of spindle episodes at 0.1-0.2 Hz was never affected by DC currents or by QX314 or Cl- injections, suggesting that oscillations within a particular RE neuron partly reflected the oscillatory behavior of a network of cells. On the basis of these electrophysiological results and the known morphological and neurochemical features, a new hypothesis is proposed to account for the rhythmicity of RE neurons.

Animals↗
PubMed1985

Dendrodendritic synapses in the cat reticularis thalami nucleus: a structural basis for thalamic spindle synchronization.

Dendrodendritic synapses have been found between the dendrites of reticularis thalami neurons. These synapses were symmetric and the presynaptic element contained pleomorphic vesicles. A few cases of reciprocal dendrodendritic synapses were also observed. Given the morphological features of the synapses and the well-established GABAergic nature of reticularis neurons it is concluded that reticularis cell dendrites form a local inhibitory network. The functional implications of this type of organization for the synchronization of spindle oscillations are discussed and a new hypothesis is proposed.

Animals↗
PubMed1985

Absence of spindle oscillations in the cat anterior thalamic nuclei.

Intracellular recordings were performed in cat anterior thalamic nuclei (anterior ventral, medial and dorsal) which, according to a recent anatomical study, do not receive afferents from the reticularis thalami nucleus. Neurons of anterior nuclei did not display spontaneous membrane potential oscillations of the spindle type and such oscillations could neither be evoked in these cells by cortical stimulation. The absence of spontaneous and evoked spindling activity was observed despite that anterior thalamic cells displayed intrinsic membrane properties similar to those of thalamocortical cells in other nuclei. Electrographic recordings from cortical areas connected to anterior thalamic nuclei were also free of spindle activity. Taken together with the evidence that thalamic relay neurons deprived from their reticularis input by sections or kainic acid lesions lose their spindling activity, our results point to the essential role of the reticularis complex in the genesis of thalamic spindle waves.

Animals↗
PubMed1985

The effects of QX314 on thalamic neurons.

The effects of QX314 were studied in cat thalamic neurons recorded in vivo. Besides blocking Na+ spike electrogenesis, QX314 transformed spindle oscillations into a single long-lasting period of hyperpolarization that terminated with a rebound Ca2+ spike. Large sustained injections of the drug resulted in the occurrence of numerous fast prepotentials that had the characteristics of attenuated dendritic Ca2+ spikes. These effects are interpreted as resulting from the blockage by QX314 of a persistent Na+ current and a delayed rectifier K+ current which currents have already been disclosed in thalamic neurons recorded in vitro.

Animals↗
PubMed1985

Abolition of spindle oscillations in thalamic neurons disconnected from nucleus reticularis thalami.

The effects of depriving thalamic relay and intralaminar nuclei from their reticularis thalami (RE) inputs were investigated in acute and chronic experiments on cat. In acutely prepared animals, two (frontal and parasagittal) thalamic transections were made; extracellular and intracellular recordings were performed in RE-disconnected thalamic nuclei. In chronic experiments, the RE nuclear complex was lesioned by means of kainic acid injections; the activity of RE-deprived thalamocortical neurons was extracellularly studied during wakefulness and synchronized sleep. Two features distinguish RE-deprived nuclei from normal thalamic nuclei: absence of spindle-wave rhythmicity and all-burst activity of neurons. The abolition of spindle-related rhythms (sequences of 7- to 14-Hz waves recurring periodically with a rhythm of 0.1-0.2 Hz) in RE-disconnected thalamic nuclei and ipsilateral neocortical areas contrasted with normal spindling rhythmicity in contralateral EEG leads. Spontaneously occurring, rhythmic, long-lasting inhibitory postsynaptic potentials (IPSPs), as observed in intact preparations, were no longer observed in RE-disconnected thalamic neurons. The remaining inhibitory events consisted of short-duration IPSPs. The possibility that RE nucleus is a pacemaker for spindling rhythms, imposing them through inhibitory projections to target thalamic areas, is supported by our concurrent experiments that indicate RE neurons preserve their rhythmicity after disconnection from their major (cortical and thalamic) input sources. RE-deprived thalamocortical neurons exclusively exhibit high-frequency spike bursts whose intrinsic structure is identical to that of intact thalamic relay cells. Instead of the spindle-related sequences of bursts seen in normal animals, the bursts of RE-disconnected thalamocortical neurons are single events, with a dramatic rhythmicity at 1-2 Hz. The presumed mechanism of this rhythmicity is the periodic activation of a low-threshold somatic conductance whose deinactivation is brought about by temporal integration of short-lasting IPSPs. It is known that high-frequency spike bursts of thalamic relay neurons result from hyperpolarization of cell membrane. We blocked the underlying inhibitory events by bicuculline and reversibly changed the all-burst activity of RE-disconnected neurons into a tonic mode. Since the only activity of RE-deprived thalamocortical neurons consists of burst discharges, we hypothesize that local-circuit GABAergic neurons are released from inhibition after RE disconnection or lesion.

Action Potentials↗
PubMed1984

Electrophysiology of neurons of lateral thalamic nuclei in cat: resting properties and burst discharges.

Intracellular and extracellular recordings were performed in lateral thalamic nuclei (ventroanterior-ventrolateral, ventroposterolateral, centralis, lateralis, and reticularis) of cats under barbiturate anesthesia. Neurons were driven antidromically and/or synaptically by stimulating cortical projection areas and prethalamic afferent pathways. Three neuronal populations were identified on the basis of electrophysiological and anatomical criteria: thalamic relay neurons, local interneurons, and reticularis thalami neurons. At rest, two coexistent rhythms were observed in thalamic neurons. Brief episodes (1-2 s) of membrane-potential oscillations at frequencies of 8-12 Hz appeared with a periodicity of about 10 s. In relay neurons, each episode was characterized by a sequence of hyperpolarizations and burst discharges. These rhythmic episodes of hyperpolarization recurring about every 10 s could be reversed in sign by hyperpolarizing currents or by Cl injection, hence suggesting that they were mainly composed of rhythmic inhibitory postsynaptic potentials (IPSPs). This result also indicated that the slow 0.1-Hz rhythm was imposed on relay neurons by other neuronal pools. Following a complete isolation of the thalamus by cortical and high brain stem lesions, the slow 0.1-Hz rhythm was still present, and it was concluded that this rhythm was generated within the thalamus by inhibitory elements. In thalamic interneurons (identified by electrophysiological criteria) brief episodes (1-2 s) of repetitive depolarizations (8-12 Hz) and burst discharges recurred every 10 s. In the interval, the membrane potential of interneurons slowly hyperpolarized, contrasting with the rhythmic phasic hyperpolarizations observed in relay neurons. Electrophysiological properties shared by most relay neurons included a) afterspike hyperpolarizing potentials of long duration, which were blocked by injections of a Ca chelator; b) a pacemaker potential in the vicinity of the spike trigger level; and c) a low-threshold somatic Ca conductance that underlies burst discharges. As a general rule, prethalamic volleys induced faster rising and shorter lasting EPSPs than cortical volleys. Moreover prethalamic afferent-evoked responses could be associated with production of fast prepotentials, some of which appeared to result from dendritic spiking. It appears that synaptic and intrinsic membrane properties of thalamic neurons allow them to function under two modes: a relay mode and an oscillatory mode; the oscillatory mode being intrinsic to the thalamus and the relay mode being commanded and maintained by cortical and brain stem structures.

Animals↗
PubMed1984

Electrophysiology of neurons of lateral thalamic nuclei in cat: mechanisms of long-lasting hyperpolarizations.

Intracellular recordings were performed in the lateral thalamic nuclei of cats under barbiturate anesthesia. The nature of cyclic hyperpolarizations triggered in relay cells by cortical stimulation was analyzed. These long-lasting hyperpolarizations were made of three different components. The early component, which was reversed by current and Cl injections, was identified as a Cl-dependent inhibitory postsynaptic potential (IPSP). A depolarizing hump was usually present in the depth of the long-lasting hyperpolarization. This intermediate component was identified as a voltage-dependent dendritic Ca conductance on the basis of recordings and ethylene glycol tetraacetic acid (EGTA) injections performed in relay cell dendrites. The late phase of hyperpolarization was dissociated from the early IPSP by its differential sensitivity to current and Cl injections and to conditioning tetanic stimulation. This late component was abolished by EGTA and, thus, was interpreted as a Ca-dependent K conductance increase. Activation of intrinsic somatic or dendritic conductances by current pulses never generated rhythmic hyperpolarizations in thalamic relay neurons. Oscillations appear to be imposed on these cells by synaptic inputs. It is then proposed that other thalamic neurons would have pacemaker properties and/or that oscillations would be produced in thalamic cellular pools by feedback interconnections.

Animals↗
PubMed1982

Thalamic bursting mechanism: an inward slow current revealed by membrane hyperpolarization.

Hyperpolarization of the ventrolateral thalamic cell membrane reveals a slow inward current which is not normally observed at the resting membrane potential. The response evoked by depolarizing synaptic potentials or depolarizing current pulses from a hyperpolarized potential consists of a burst of action potentials superimposed upon a slow voltage response, in contrast to the single active response evoked without the background polarization. We propose that such behavior is caused by a slow inward current that is activated at subthreshold potentials and inactivated or masked at resting potential.

Afferent Pathways↗
PubMed1982

Geometry and orientation of thalamocortical arborizations in the cat somatosensory cortex as revealed by computer reconstruction.

The geometry of the intracortical arborization of single neurons from the ventroposterolateral thalamic nucleus in cat was studied with computer reconstruction after intraaxonal injections of horseradish peroxidase in fibers whose receptive field had been identified. The terminal arbors of slowly (SA) and rapidly (RA) adapting thalamocortical neurons were often (60%) composed of two separated bushes of 300-600 microns in diameter separated by a region of about the same size containing much less terminal ramifications. The bushes were aligned mainly along the mediolateral axis of the brain. It is proposed that this structural feature underlies the RA-SA banding already described in the somatosensory areas by physiological experiments.

Afferent Pathways↗
PubMed1982

Anterograde tracer and field potential analysis of the neocortical layer I projection from nucleus ventralis medialis of the thalamus in cat.

The projection of the ventromedial nucleus of the thalamus to the neocortex was studied in cat by means of anterograde and retrograde transport of horseradish peroxidase, by the depth profile of evoked thalamocortical field potentials, and by superfusion of the cortex with manganese to block transmitter release. Horseradish peroxidase injected into the ventromedial nucleus was anterogradely transported to the outer third of layer I in the neocortex, extending from the depth of the cruciate sulcus anterior to the olfactory bulb and tract. The region of projection from the ventromedial nucleus extended mediolaterally from the medial wall of the proreus gyrus to the ventral tip of the coronal gyrus. Horseradish peroxidase injections or applications in these areas of the neocortex resulted in the retrograde labeling of neurons in the ventromedial nucleus. Injections in many other cortical areas did not result in labeled neurons in this nucleus. Stimulation of the ventromedial nucleus with single pulses elicited surface-negative waves in the medial part of the precruciate region that had superficial isoelectric points. Superfusion of the precruciate area with manganese resulted in the suppression of the ventromedial-evoked wave, whereas control extracellular waves in deeper layers were unaffected. An additional additional finding was that horseradish peroxidase injections in the ventromedial nucleus led to a dense reciprocal retrograde labeling of neurons in layer VI of that part of the cortex to which the ventromedial nucleus projects. We conclude that, in cat, (1) the ventromedial nucleus projects to layer I of the cerebral cortex anterior to the cruciate sulcus and receives a dense reciprocal projection from layer VI; (2) stimulation of neurons in the ventromedial nucleus causes depolarization of structures in layer I and these neurons are responsible for recruiting responses in the anterior cortex.

Action Potentials↗
PubMed1982

A reanalysis of the ventrolateral input in slow and fast pyramidal tract neurons of the cat motor cortex.

In deeply anesthetized cats the temporal characteristics of ventro-lateral (thalamic) excitatory postsynaptic potentials (EPSPs) induced in pyramidal tract cells were studied with an averaging technique. Stimulation of the ventrolateral thalamus induced EPSPs in all pyramidal tract neurons at latencies of 1-5 ms. It was found that there was a positive relationship between the latency and rise time of stimulation-induced EPSPs and the latency of antidromic invasions of pyramidal tract neurons. In response to two closely spaced shocks the second EPSP had the same latency and amplitude as the first one in both slow and fast pyramidal tract neurons. Moreover, the span of antidromic latencies of ventrolateral thalamic relay cells to motor cortex stimulation showed that these thalamic neurons had the necessary conduction velocities to account for the distribution EPSP latencies recorded in pyramidal tract neurons. From these electrophysiological results, it has been concluded that slow and fast pyramidal tract morphological evidence, obtained at the electron-microscopic level, supporting this conclusion. Terminal degeneration induced by a lesion in the ventrolateral thalamus was found on the apical dendrite of a slow pyramidal tract neurons that had been injected with horseradish peroxidase. It is proposed that the matching between the latencies of EPSPs evoked from the ventrolateral thalamus and the latencies of antidromic invasions of pyramidal tract neurons may reflect a matching between the conduction velocity of thalamocortical and cortico-spinal neurons and/or it may be due to the electrotonic properties of the apical dendrites.

Animals↗
PubMed1981

Intracortical arborizations and receptive fields of identified ventrobasal thalamocortical afferents to the primary somatic sensory cortex in the cat.

The intracortical arborizations of neurons from the ventroposterolateral thalamic nucleus (VPL) in the cat were studied by intraaxonal injections of horseradish peroxidase (HRP) following identification of their receptive fields. In the primary somatic sensory cortex (SI) VPL cells terminated in different cytoarchitectonic areas according to their receptive field modality. Fibers excited by deep tissue or joint rotation arborized preferentially in area 3a. Those responding tonically to cutaneous stimuli were located in the anterior part of area 3b; hairdriven cells terminated in area 3b and in the rostral pole of area 1. All fibers had a similar laminar distribution within SI. Axons terminated mostly in layers VI, iV, and the lower part of layer III. None terminated in layers I and II. Most terminal arbors were oriented along the mediolateral axis of the brain. The main arborization of a single VPL cell formed a bush of about 500 micrometers in diameter. some fibers generated two such bushes with an uninvaded region of about 300 micrometer between them. It is proposed that this patchy organization underlies in part the columnar organization of areas SI. Many VPL cells had secondary projection sites in SI. These were issued from smaller-sized collaterals and were located in a different cytoarchitectonic area than that of the main terminal plexuses. A significant number of these collaterals projected to area 4, Insufficient filling of the collaterals by HRP prevented a more complete characterization of the secondary arbors.

Afferent Pathways↗
PubMed1981

Dendritic spikes induced in fast pyramidal tract neurons by thalamic stimulation.

In deeply anesthetized cats the synaptic events induced in fast pyramidal tract cells (Pt cells) by ventrolateral (VL) stimulation were analyzed with intracellular recordings. In 40% of the fastest conducting Pt neurons it was found that VL stimulation induced fast depolarizing potentials (FPPs) with or without underlying excitatory postsynaptic potentials (EPSPs). These FPPs were all or non fast rising events lasting about 2 ms. They could be induced by brachium conjunctivum stimulation or they could also occur spontaneously. Those occurring spontaneously had amplitude and time course similar to those evoked by VL stimulation suggesting that they were of thalamic origin. On the basis of their amplitude and lack of collision with antidromic action potentials FPPs were neither axonal nor IS events. Passage of hyperpolarizing currents could block them in an all or none manner. It is concluded that FPPs represent electronically attenuated dendritic spikes generated in small side branches (oblique ascending dendrites) or fast Pt neurons where VL terminals most probably establish their synaptic contacts.

Animals↗
PubMed1980

Intracortical distribution of axonal collaterals of pyramidal tract cells in the cat motor cortex.

Slow and fast pyramidal tract cells (Pt cells) from the cat motor cortex were identified antidromically and injected with horseradish peroxidase (HRP). The axonal collaterals of these cells were mapped following HRP histochemistry with benzidine di-hydrochloride. All cells, slow or fast, show a similar arrangement of their collaterals. A proximal axonal network of 0.5-0.8 mm in diameter delimits a local field of action for collaterals in layers V and VI. The tangential expansion of this local field corresponds to that of the basal dendritic domain of Pt neurons. Much longer collaterals running for millimeters in the lower gray or white matter were observed in all cells. They form at a cortical level a distal field of action for Pt neurons. Many of these long branches were traced to other regions of area 4 or toward other cytoarchitectonic areas. In one case a collateral was seen entering and dividing in area 3a. Due to limitations of the HRP technique most of these long branches could not be followed to their terminals. On the basis of the laminar distribution of Pt cell collaterals (mostly in layers V and VI) synaptic sites where recurrent excitation and inhibition are produced on Pt neurons are discussed.

Animals↗
PubMed1979

Morphological characterization of slow and fast pyramidal tract cells in the cat.

In adult cats the morphology of slow and fast pyramidal tract (Pt) neurons was studied following intracellular HRP injections and Golgi impregnation. Both types of neurons are pyramidal cells and their soma are all located in the fifth layer of the motor area. As a rule, fast Pt neurons have large somata and their basal and apical dendrites occupy a larger territory in the tangential plane. In layer I, terminal apical dendrites of fast Pt neurons are smooth and divide poorly while those of slow Pt neurons bear a moderate amount of spines and branch profusely. Midway between the pia and layer V, in the third layer, the apical shafts of both types of Pt cells run upward with little branching. These shafts are more numerous in fast Pt cells (7 to 16) and they are almost devoid of spines. Those of slow Pt cells in layer III number between 5 and 9 and are densely covered with spines. Oblique and horizontal branches of slow and fast Pt neurons extend in layer V and some of them invade the lower part of layer III. It is suggested that this zone corresponds to a true fourth layer in the motor area. In both types of cells oblique and lateral branches bear numerous spines. Within the basal dendritic territory of Pt cells, one has to distinguish two dendritic systems: a short and a long one. The former spreads downward obliquely and appears to remain within layer V. The latter is made up of long descending vertical (antiapical) and oblique dendrites (tap root). While both types of cells may have long antiapical dendrites that run down radially to the lower part of layer VI, tap root dendrites which expand laterally below the cell body for considerable distances are a distinctive feature of fast Pt neurons. Though basal dendrites of all Pt cells bear spines, their number, distribution and shape are very variable in fast Pt cells.

Animals↗