Characteristics of spreading depression and of its propagation. Their possible role in migraine.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D Albe-Fessard.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Single unit activity of substantia nigra reticulata (SNr) neurons was recorded in normal rats and bilaterally in rats subjected to a unilateral 6-hydroxydopamine lesion of the substantia nigra compacta 2-4 weeks previously. Lesions were assessed by rotational behaviour to apomorphine. In normal rats the majority of neurons (63%) showed a regular firing pattern. Following lesion the percentage of these cells was similar in the SNr contralateral to the lesion but decreased on the lesioned side to 26%, whereas bursting activity developed (37% vs 5% in normal rats). The mean firing rate of reticulata neurons was slightly increased after lesion, but not statistically significant.
Explore the source record for details and available documents.
The sign and duration of corticofugal effects on the extracellularly recorded spontaneous activity of cuneate and gracile neurons were examined by means of the cortical spreading depression technique (CSD). Among the 40 units studied 22 showed changes in their spontaneous firing rate during the passage of a CSD. Changes were of either short (5-20 s) or long (greater than 20-140 s) duration. Increases and decreases in activity, as well as sequences of both types of alteration were observed. Short duration changes were more frequent and much more pronounced than those of long duration. From their time course and intensity the short duration effects seem to be related to the brief high frequency cortical neuron discharge that precedes the cortical silence due to CSD, whereas the long lasting effects seem related to the cortical block. It is concluded that the most important corticofugal effects on gracile and cuneate neurons are phasic in nature and the sensorimotor cortical regions were found to be responsible for these influences.
Recordings were performed in the thalamus of 13 patients suffering from either abnormal movements or intractable pain, with the aim of delimiting the region to be destroyed or stimulated in order to diminish the syndrome. In 11 of these patients averaged evoked potentials were recorded simultaneously from the scalp and specific thalamus (VP) hand area levels following median nerve stimulation. These recordings were done during the operation or afterwards when an electrode was left in place for a program of stimulation. The latencies of onsets and peaks on the scalp 'P15' were compared with those of the VP wave; a clear correspondence was found. Moreover, when increased stimulation was used, both waves began to develop in parallel. Thus in the contralateral 'P15' a component exists due to the field produced by the thalamic response. To explain the presence of an ipsilateral scalp 'P15' wave, we propose that a second wave having the same latency and a slightly shorter peak exists on the scalp due to a field produced by a brain-stem response. This double origin of 'P15' is also shown by the different changes which the ipsilateral and contralateral waves present during changes in alertness. The scalp 'N18-N20' is also composed of at least 2 components. The first peak appears on the scalp with a latency shorter than that of the negativity which develops in the thalamus. The N wave, moreover, increases in latency with rapid stimulus repetition. We propose with others that 'N18' is a cortical event reflecting the arrival of the thalamo-cortical volley. The second component, 'N20,' has a peak latency closely correlated to that of the thalamic negativity. This component was present alone in 'N' when rapid stimulation (greater than 4/sec) was used, which did not change the thalamic response. It must be a field produced by the thalamic negativity.
Explore the source record for details and available documents.
In rats which received section of 5 dorsal roots corresponding to the brachial plexus, self-mutilation of the forelimb develops during the first 2 months after deafferentation. The extent of self-mutilation was measured for 90 days in a control group of animals and in a group with an electrode implanted in the ventral tegmental area and which were allowed to self-stimulate at freedom. The animals which self-stimulated for 35 days did not develop the self-mutilation even after the self-stimulation was stopped.
The use of Leão's spreading depression for studying the action of connections between central structures is examined. Extracellular recordings of cortical and striatal spreading depressions with single microelectrodes are presented using both a DC channel and spike recordings systems. Striatal spreading depression was produced by peristaltic perfusion of a KC1 solution via a push-pull cannula system. The characteristics of cortical and striatal spreading depressions were studied and their effects on antidromically provoked cellular spikes. Using double microelectrode recordings modifications of spontaneous activity provoked by cortical spreading depression were examined in n. ventralis posterior (VP) and centralis lateralis (CL) of the thalamus. In both nuclei a silence corresponding to the block of spontaneous activity of a localised cortical area was observed. The controls originated from different cortical regions for each nucleus. The discharge preceeding the onset of the spreading depression slow wave is reflected by a similar discharge in VP but not in CL. The differences in the frequency following of CL and VP was examined in order to explain this discrepancy. The results just summarized can be explained if we accept that a tonic facilitatory control exists between localised cortical areas and the two thalamic nuclei studied. Similar experiments were performed to study the controls exerted by cortical areas on dorsal column nuclei. Only phasic transitory effects were observed which were either an increase or a decrease in activity. These facilitatory or depressive effects were attributed to the initial excitation signalling the propagation of a cortical spreading depression. No tonic effects were observed. Striatal spreading depression was not accompanied by a cortical effect but on the contrary the activity of cells in substantia nigra was significantly altered. In pars reticulata two populations could be distinguished. The first presented a phasic increase followed by a long period of decreased activity, they are proposed to be under the control of striatum via an excitatory pathway. The second was initially depressed then presented a long period of increased activity. This probably reflects the block of an inhibitory striato-nigral pathway. Both striato nigral effects were tonic in nature. The possibility of separating the effects due to cortical excitation or cortical block are discussed as well as the problems of interpretation of long distance changes in cellular activity.
The effects of a sural nerve conditioning stimulation (S2) were studied on nociceptive flexion reflexes (RIII) from the biceps femoris muscle elicited by a test stimulation (S1) of the same sural nerve. The experimental procedure was designed so as to allow an indirect measurement of the conduction velocity (c.v.) of the conditioning inputs. When the S2 parameters produced an activation of afferent fibers belonging only to the A alpha beta group, it produced a facilitation of the RIII reflex which was maximal when 40 m/s conducting fibers were recruited. In contrast, when the S2 parameters activated also the A delta and C groups, the facilitatory effects were maximal when 20 m/s and 1 m/s conducting fibers were activated.
In the rat cells antidromically activated by stimulation of the thalamic centrum medianum and centralis lateralis were searched for in the bulbopontine region which receives spinoreticular pathways. Antidromically activated cells were found in the nuclei gigantocellularis and pontis oralis and they possessed peripheral receptive fields that were large, bilateral and often responded to nociceptive stimuli. Injections of horseradish peroxidase or iron-dextran at the same thalamic level revealed retrogradely labelled cells in the same bulbopontine nuclei. Cells retrogradely labelled were also found in the mesencephalic reticular formation, the inferior colliculus and grisea centralis.
Medial thalamic cells responded to stimulation of the striatum in either lightly anaesthetized or chronically implanted awake rats. Orthodromic and antidromic short-latency excitatory responses were associated with a pause in spontaneous activity followed by bursting activity. The thalamic distribution of the different types of response is given; the main nuclei involved were parafascicularis, centrum medianum, centralis lateralis, habenula and lateralis posterior. When observed with intracellular electrodes the pause in spontaneous activity was accompanied by a long hyperpolarisation. The possibility that this effect could be due either to inhibition or to disfacilitation is examined. Electrophysiological evidence is given to show that a direct striatothalamic pathway does not exist. Different relayed pathways which could be responsible for the observed responses are proposed and their possible role is discussed on the basis of anatomical and electrophysiological findings obtained in cats and rats. A role for a pathway making a cortical detour is suggested.
Neurophysiological exploration of the trigeminal sensory complex was done on 42 cats under ketamine anaesthesia, paying special attention to units receiving a periodontal input. Among 492 cells recorded in the trigeminal sensory complex, 73 responded to mechanical stimulation of the periodontium and were precisely localized histologically. Thalamic stimulation was also delivered to the ipsi and contralateral ventro-posterior nucleus to test for antidromic responses. Results of this systematic study were plotted on reference drawings of the full extent of the trigeminal sensory complex.
The effects exerted by the cortex on thalamic neuronal activity were studied using the technique of cortical spreading depression. Glass micropipette recordings were made simultaneously in the thalamus and cortex and we found that the activity of a portion of the thalamic neurons was suppressed when the cortical spreading depression arrived at a particular and localised cortical area, which was different for different thalamic nuclei. The suppression of spontaneous activity was longer and more frequently observed for cells of the intralaminar thalamic nuclei. To determine if the action of the cortex on the intralaminar thalamic nuclei, demonstrated by these experiments, involved a monosynaptic pathway we used both electrophysiological and anatomical methods. When recording in the cortical area which we had found to control intralaminar thalamic activity we observed that, antidromic activation and also a pause of cortical cells was produced by intralaminar stimulation. When HRP was injected into the intralaminar nuclei we found retrogradely labelled cells in the same cortical area. To determine if a reciprocal connection exists we injected HRP into the same cortical area; retrogradely labelled cells were subsequently found in the intralaminar nuclei. A reciprocal cortico-thalamic connection thus appears to exist between the controlling cortical area and the intralaminar thalamic region under this control. The possibility that this loop is involved in the facilitatory descending influence exerted on intralaminar nuclei is discussed.
The following points emerge from a systematic investigation of the 4 divisions of the cat trigeminal sensory complex. (1) The subnucleus oralis receives a large representation from the oral cavity, a region also represented in the 3 other divisions of the trigeminal sensory complex. (2) Nucleus principalis cells project heavily to the contralateral and to the ipsilateral ventroposterior thalamus. Ipsilateral projections are only from the oral cavity representation. (3) Units responding to noxious mechanical stimulation have been found at two different loci: the subnucleus caudalis for the entire trigeminal area, and subnucleus oralis for the oral cavity alone. (4) The dental pulp projects to the 4 divisions of the trigeminal sensory complex, but the heaviest projection was found in the rostral part (nucleus principalis and subnucleus oralis). (5) Three distinct types of post-synaptic responses were found to be evoked by dental pulp stimulation: (a) short latency, consistent and synaptically secure, (b) strongly variable latency, inconstant and easily fatigued and (c) a class showing progressive enhancement by progressive increase in stimulus intensity and repetition.
Explore the source record for details and available documents.
High frequency (100 Hz) low intensity (2 mA) peripheral conditioning stimulation of either segmental or heterosegmental cutaneous nerves induced non-naloxone-reversible depression of the nociceptive component of the human blink reflex. Electrophysiological studies suggest that this depression is due to a local synaptic inhibitory mechanism involving convergence interactions between several cutaneous afferents onto a same internuncial pool in the trigemino-facial path.
Experiments using the same glass microelectrode (6--8 M omega) for recording and stimulating were performed on 12 rats in which 379 cortical cells were studied in 65 penetrations through the motor and somatosensory cortical zones. To avoid anaesthetic effects the rats were chronically implanted with a head system derived from the one developed by Noda et al. (1971). These animals well accepted head fixation and the peripheral receptive fields could thus be easily investigated. In a preliminary experiment the number of pyramidal cells activated by a given stimulus intensity was evaluated. The lowest threshold intensities were always observed in the Vth pyramidal layer, as well as correspondence between cell input and output. The same type of organization, with identical thresholds, existed in the so-called "Motor" and "Somatosensory" cortical zones. Movements could be obtained when stimulating near non-PT cells (600--700 micron below the cortical surface). However, thresholds were higher at this level and it is thought that the movements were due to a spread of the stimulating current to the pyramidal tract cell layer.