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Biomedical subjects

M Steriade

Publications and source records attributed to M Steriade.

At least 163 records · Page 9Linked to original sources
PubMed1984

Midbrain tegmental projections of nucleus reticularis thalami of cat and monkey: a retrograde transport and antidromic invasion study.

The projections of reticularis thalami (RE) neurons to midbrain reticular formation (MRF) and superior colliculus (SC) were studied in cat and monkey by using retrograde transport techniques and antidromic identification. The projections to MRF arise in rostral parts and lateral extent of RE nuclear complex whereas RE fibers to SC predominantly originate in the RE posteroventral district. Following injections of horseradish peroxidase (HRP) or fluorescent tracers into the MRF territory, retrogradely labeled neurons were always more numerous in the lateral hypothalamus and zona incerta than in the continuing RE wing. There were only very few doubly labeled RE cells following injections of fluorescent tracers into the midbrain tegmentum and thalamic nuclei, despite the fact that numerous doubly labeled cells occurred in the internal part of globus pallidum and pars reticulata of substantia nigra in the same animals. Control injections in the pons showed that RE labeling after midbrain injections was not due to uptake by fibers coursing more caudally. Antidromic identification experiments in cat confirmed the existence of a descending RE input to midbrain and further indicated that RE-midbrain projections consist of slow-conducting (congruent to 1 m/second) axons.

Afferent Pathways↗
PubMed1984

Bulbo-thalamic neurons related to thalamocortical activation processes during paradoxical sleep.

Neurons histologically localized in the gigantocellular (Gc) and magnocellular (Mc) fields of the bulbar reticular formation were tested for antidromic invasion by stimulating the ventromedial (VM) and intralaminar (centralis lateralis, CL, and centrum medianum, CM) thalamic nuclei, midbrain reticular formation (MRF), and reticulospinal tract. An overwhelming majority (94%) of antidromically identified cells projected either to rostral structures (MRF, medial and intralaminar thalamic nuclei) or to the spinal cord, while only 6% had bifurcating axons. Rostrally projecting bulbar reticular neurons were investigated during various wake-sleep behavioral states. (a) Phasic neurons were related to PGO waves, eye and head movements, and were localized in both Gc and Mc fields. (b) The majority of tonic neurons projected to MRF and VM and they were localized within Mc in a proportion of 85%. In order to test their possible role in activation of thalamocortical processes (as betrayed by EEG desynchronization), the activity of tonically discharging cells was separately evaluated in periods with and without phasic motor events. Half of the tonically discharging neurons had a high selectivity of discharge during paradoxical sleep without REM bursts (PS-); the ratio of their mean discharge rate during PS- to that in quiet wakefulness ( QW ) or slow-wave sleep (SWS) was 8 and 6, respectively. The other half of the tonic neurons equally increased firing rates from SWS to either QW or PS. The firing rate of rostrally projecting bulbar reticular neurons with tonic discharge patterns was analyzed during transitions from SWS to PS. An increase in discharge rate was found about 30 to 60 s prior to the first sign of EEG desynchronization in PS, during fully synchronized sleep with PGO waves (S-PGO). Statistical testing showed that the increased firing rate was not associated to PGO waves, but was temporally related to the appearance of EEG desynchronization at PS onset. We conclude, on the basis of these and other recent data, that tonically discharging bulbar reticular neurons with identified projections to the midbrain and thalamic nuclei act synergically with rostrally projecting MRF neurons as sources of thalamocortical activation.

Animals↗
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↗
PubMed1983

Slow rhythmic oscillations of EEG slow-wave amplitudes and their relations to midbrain reticular discharge.

The amplitude of anterior neocortical EEG slow-waves (0.5-4 Hz) measured during quiet waking, drowsy (WS) and synchronized sleep (S) states showed slow rhythmic oscillations in WS and S similar to those previously reported in midbrain reticular neurons (periods of 8-12 s). Abrupt changes in slow rhythms of unit discharge was reflected by similar changes in the amplitude of EEG slow-waves. Analyses on grouped data from many WS leads to S transitions showed no common phase relation between oscillations of EEG slow-wave amplitudes prior to S onset, but showed signs of a common phase relationship after. These findings, together with a significantly lower EEG synchronization level just before S onset in grouped data, suggest that the beginning of S is phase-related to oscillations of slow-wave amplitudes in WS.

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

Zona incerta and lateral hypothalamic afferents to the midbrain reticular core of cat--HRP and electrophysiological study.

The zona incerta (ZI) and lateral hypothalamic afferents to the midbrain reticular formation (MRF) of cat were investigated with the horseradish peroxidase (HRP) technique and by using antidromic identification in experiments on chronically implanted, behaving preparations. Following HRP injections restricted to the MRF territory (nucleus cuneiformis and central tegmental field), the largest number of retrogradely labeled cells appeared in the medial third of the ipsilateral ZI. Labeling extended medially to the adjacent lateral hypothalamus. The number of positive elements gradually diminished towards the lateral extremity of the ZI and continuing reticularis thalamic nucleus. Ventral lateral geniculate neurons were consistently labeled. No positive elements were found in ventrobasal, pulvinar-lateralis posterior and ventralis lateralis thalamic nuclei. The MRF-evoked antidromic invasion of ZI cells occurred with a sharp mode between 0.5 and 0.75 ms (median latency of the whole sample: 0.6 ms). The conduction velocity of the ZI leads to MRF axons is twice as high as the values found in the reciprocal MRF leads to ZI projection. In addition to the antidromically elicited discharges, MRF stimulated resulted in short-latency synaptic excitation, sometimes following the antidromic invasion of the same neuron. The difference between the discharge rates of ZI neurons during EEG-desynchronized and EEG-synchronized behavioral states was not significant. A statistically significant increase in firing rates was found in ZI neurons during waking periods with movements compared to quiet, motionless epochs of waking. The possible involvement of caudally projecting ZI cells in the preparation of postural and/or phasic motor functions is discussed.

Afferent Pathways↗
PubMed1982

Firing rates and patterns of midbrain reticular neurons during steady and transitional states of the sleep-waking cycle.

Spontaneous firing of midbrain reticular formation (MRF) neurons was recorded extracellularly in chronically implanted, behaving cats during steady and transitional states of the sleep-waking cycle. Physiological identification of receiver and/or projection MRF neurons was achieved through orthodromically elicited discharges. Discharge rates of MRF neurons were more than double in waking (W) and active sleep (D) without phasic motor events, as compared to synchronized sleep (S). During behavioral states associated with EEG activation, the increased firing was essentially due to cells exhibiting high discharge rates, located at relatively ventral levels of the midbrain core. MRF neurons with identified rostrally projecting axons were more active during W and D states; their discharge rates were significantly higher than those of caudally projecting cells. The discharge patterns of MRF neurons increasing their firing rates from S to W and D were of the tonic type. First-order analyses showed a negligible proportion of both very short and long interspike intervals in all states, large interval density around the mode especially in W and D, and the smallest variation coefficients in W. Rhythmic firing with a period near the modal interval was detected during W by autocorrelations. The increase in firing rate of MRF neurons from S to W or D took place before overt EEG desynchronization and behavioral manifestations that define stable W or D states. In our sample a statistically significant increase in discharge rate was found about 15 s before the end of S sleep epochs that developed into awakening. The differences between discharge features of MRF neurons during waking and sleep states and those of neurons in other brainstem reticular fields are emphasized. Taken together, these data support, at a cellular level, Moruzzi and Magoun's concept of a rostral reticular substrate that gives rise to impulses leading to tonic activation of the thalamocortical systems.

Animals↗
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

Discharge rate and excitability of cortically projecting intralaminar thalamic neurons during waking and sleep states.

Spontaneous firing and antidromically or synaptically evoked discharges of 89 single neurons in centralis lateralis-paracentralis (CL-Pc) intralaminar thalamic nuclei were examined during waking and sleep states in behaving cats with chronic pontine lesions. Twenty-four neurons were activated synaptically at short latencies from the midbrain reticular formation (MRF) after anterograde degeneration of passing fibers. Sixty-five neurons were identified antidromically as projecting to motor or parietal association cortical areas; of them, 23 also could be excited synaptically from the MRF. These neurons were regarded as possibly being involved in the transfer toward the neocortex of the tonic excitation from the MRF during EEG-desynchronized behavioral states. Rates of spontaneous discharge in CL-Pc neurons doubled from synchronized sleep (S) to either wakefulness (W) or desynchronized sleep (D). First order measures of discharge patterns indicated that interval modes in both W and D states (greater than 10 msec) are significantly different from those in S (2.5 msec). During S, the intervals found in the less than 5-msec class indicated the intraburst frequencies; a later minor mode (200 to 350 msec) reflected the interburst silent periods. All neurons tested for antidromic activation from cortical areas had enhanced responsiveness in both W and D states as compared to S sleep. In some cases, the enhanced antidromic excitability was observed in conjunction with a transformation from initial segment spikes during S to full spikes in EEG-desynchronized states. During both W and D states, compared to S sleep, the probability of monosynaptically elicited single discharges to MRF stimulation was increased, and the latency and duration of high frequency bursts evoked by MRF volleys were shortened. We conclude that the features of cortically projecting intralaminar neurons that relay MRF activity fit in well with their hypothesized role in the tonic activation processes that characterize both W and D states. Several lines of evidence suggest that sustained hyperpolarization prevails in intralaminar neurons during S sleep. This is the basic prerequisite for thalamic bursting. The effect of long lasting inhibitory potentials in thalamic neurons provides a mechanism for closing sensory channels during S sleep.

Afferent Pathways↗
PubMed1981

Development from primary to augmenting responses in the somatosensory system.

The development from primary to augmenting responses of somatosensory (SI) cortical area to low-frequency stimulation of the ventrobasal (VB) thalamus or white matter (WM) beneath SI in VB-lesioned preparations was studied by field potential analysis and extracellular unit recording. Compared to the major postsynaptic components of the primary field response, which reverse at 0.25--0.35 mm and whose sink extends from 0.6 to 1.8 mm, the augmenting potential reverses more superficially (0.1--0.15 mm) and its large depth-negativity is located in layers III and IV (0.4--1 mm). Augmentation is visible by the second shock of a 10/sec train; it grows from a late (15--20 msec) depth-negative wave in conjunction with the decrement of the early rapid components of the primary response. Out of 47 neurons that responded to the first shock in the 10/sec VB or WM train with early (less than 5 msec) discharges, 23 fulfilled stringent criteria for augmentation at the second shock: greater than 100% increased discharge probability and greater than 100% increased mean latency of response. The necessary condition for the generation of an augmented potential is a given temporal relation between the evoking stimulus and the declining phase of inhibition or the onset of rebound in the preceding response. The augmented potential cannot appear if the stimulus is delivered following the rebound of the preceding response. Not only this finding, but the similarity between the depth-profiles of the rebound and augmenting potential suggest that the same elements are responsible for both events. While the patterns of augmenting responses to WM stimulation in VB-lesioned preparations differ slightly from thalamically evoked augmenting waves, the intrinsic cortical organization is sufficient for the development of a primary potential into augmenting responses.

Animals↗
PubMed1981

Reticular influences on primary and augmenting responses in the somatosensory cortex.

The effects of brief, conditioning trains of high-frequency pulses to the midbrain reticular formation (RF) on primary and augmenting responses of somatosensory (SI) cortex were investigated. Testing stimulation was applied to the ventrobasal (VB) thalamus or to the white matter (WM) beneath SI in VB-lesioned animals. The RF-elicited EEG activation was associated with increased firing rates of SI neurons, enhanced probability of early synaptic discharges to VB or WM stimuli, and significantly reduced duration of the suppressed firing period following an afferent VB or WM volley. The diminished latency of the postinhibitory rebound under RF stimulation had the consequence that, within 10/sec shock-train, the second stimulus was delivered following completion of the rebound component and, instead of an augmented potential, generated a field response of primary-type. The dependence of the RF-induced change in augmenting potentials upon the sharpening effect exerted on the preceding inhibitory-rebound sequence was corroborated by analyzing the RF influence on neurons with different time-course of recovery from inhibition. The replacement of augmenting potentials by primary responses under RF stimulation is advanced as the mechanism behind the obliteration of spontaneously developing 'type I' spindle-waves during EEG arousal. The demonstration of RF influences on SI responses to WM stimulation in VB-lesioned animals points out the cortical level of the effects. The reticulo-thalamo-cortical pathways underlying these influences are discussed.

Animals↗
PubMed1981

Immediate behavioral effects of kainic acid injections into the midbrain reticular core.

Microinjections of kainic acid into the midbrain reticular core were performed in chronically implanted, unanesthetized cats. The immediate effects of kainate excitation were studied during the first 8 h, in animals without any behavioral or EEG signs of epilepsy. Animals displayed pupillary dilatation, piloerection, accelerated respiration, a frozen attitude with a complete lack of facial expression, and no or only very slight orienting reactions. The most structural syndrome was a hallucinatory-type behavior that began in the first hour following the injection. Animals moved forward in a crouched position as if stalking a prey, vocalizing and opening their mouth in an attacking attitude, or moved back as if defending themselves against as imaginary menacer, seeming virtually terrified. The EEG desynchronization began 20-30 sec after the onset of injection and lasted for 12-14 h without any trace of alpha rhythm, spindles or slow waves. Control injections of buffer solution into the midbrain core and kainic acid in other cerebral structures were followed neither by the hallucinatory defense-attack syndrome, nor by comparably long-lasting EEG desynchronization. The hallucinatory-type behavior elicited during the waking state in the present experiments is compared to the oneiric behavior described by Jouvet and Delorme [21] during paradoxical sleep in animals with suppression of muscular atonia, and possible common mechanisms are discussed.

Amygdala↗