Reciprocal interactions between intralaminar and lateral thalamic nuclei in rats.

Reciprocal interactions between intralaminar thalamic nuclei (ncl. centralis lateralis, CL, and ncl. parafascicularis, Pf), the pretectal area (Pt) and lateral thalamic nuclei (ventrobasal complex, VB, ncl. anterior ventralis, AV, and ncl. ventralis anterior, VA) have been observed in ketamine-anaesthetized rats. Extracellular single unit activity has been recorded after single electrical stimuli. Electrical stimulation of the VB evoked a short latency orthodromic response followed by a pause in spontaneous activity in neurones of medial thalamic nuclei. Lateral thalamic neurones responded to electrical stimulation of the intralaminar nuclei or the pretectal area with the same pattern of response. Striatal, sensorimotor cortical or peripheral electrical stimulation also evoked similar responses. The pauses in spontaneous activity were shown to be the result of inhibition since the responsiveness of the intralaminar nuclei or the lateral thalamic neurones to all inputs was abolished or reduced after a conditioning electrical single-shock stimulation in the VB or in the intralaminar nuclei, respectively. The two components of the response were of a different origin, since most of the short latency responses disappeared after medullary, upper cervical sections or large decortications, while the inhibitions persisted. These inhibitions were shown to be of thalamic origin since their duration was decreased after extensive decortications increased after medullary section. It is concluded that the neuroneal properties studied in this report are probably broadly represented throughout the thalamus and that thalamic neurones are under inhibitory control elicited by afferent volleys. This inhibitory control includes a relay in the nucleus reticularis thalami (nRT). The mechanisms of sensory interaction can be purely thalamic, but they can be modulated by suprathalamic and/or mesencephalic loops.

Abnormal neuroneal activities in intralaminar thalamic nuclei following chronic lesions of nucleus reticularis thalami in rats.

Extracellular single unit activity in the intralaminar thalamic nuclei (ncl. centralis lateralis, CL, n = 77 and ncl. parafascicularis, Pf, n = 163) and in the pretectal area (Pt, n = 75) was examined following chronic electrolytic lesions of the nucleus reticularis thalami (nRT) in ketamine-anaesthetized rats after single electrical stimuli to the ventrobasal complex (VB). Extensive alterations of either the ongoing ("spontaneous") activity or the pattern of VB evoked responses were observed. Four major changes were observed in the activity of these intralaminar or pretectal neurones: 1) many neurones were silent, two times more frequently than in a parallel study with control intact rats; 2) the firing pattern of all the other neurones was in the form of tonic (stationary-like) discharge, without burst discharges as previously described in intact animals. They were ranked into classes according to their spontaneous discharge: class I, silent (no resting discharge) 12%, class II (1-15 Hz), 54 % and class III (> 16 Hz), 34%. Class III neurones were never found in intact rats; 3) electrical stimulation of the VB evoked a short latency orthodromic excitatory response in these neurones but this response was not followed by any slowing or depression of the spontaneous activity in more than 40% of recorded cells. When it occurred, this pause was shorter than that always observed in intact rats by more than 35% and longer in 7% of the responsive cells. All these changes were correlated with the extent of damage to the ipsilateral nRT; 4) VB stimulation evoked prolonged excitatory responses lasting more than 150 ms in 13% of the responsive cells, and nRT stimulation led to a short latency response followed by a pause of activity. These findings suggest that the nRT is involved in sensory integration and modulation.

[Cerebrospinal fluid beta-endorphin in chronic pain in man]. / Bêta-endorphine du liquide céphalo-rachidien et douleurs chroniques chez l'homme.

Concentrations of beta-endorphin in the cerebrospinal fluid were measured in 21 painless subjects and 37 patients with chronic pain. Statistical analysis of the results showed no significant difference between the two groups. This lack of correlation between beta-endorphin concentrations in the CSF and the presence of chronic pain highlights the difficulties and limitations encountered when trying to determine the role of endogenous opioid systems with this method.

[Cerebrospinal fluid beta-endorphin in congenital insensitivity to pain]. / Béta-endorphine du liquide céphalo-rachidien au cours de l'insensibilité congénitale à la douleur.

Spontaneously elevated nociceptive threshold levels were markedly diminished after Naloxone injections in 4 patients with congenital insensitivity to pain. This finding suggested the hypothesis of a relation between congenital insensitivity to pain and permanent hyperfunction of an endomorphinic system. Radio-immunoassay of CSF beta-endorphin was performed in all 4 cases. The normal or only slightly elevated levels cannot explain electrophysiologic findings, but as a function of the multiplicity of endogenous opioid systems, hyperactivity of another endomorphinic system cannot be excluded. Other hypotheses may also be proposed.

[Organization of the median and intralaminar nuclei of the thalamus: hypotheses on their role in the onset of certain central pain]. / Organisation des noyaux médians et intralaminaires du thalamus: hypothèses sur leur rôle dans la survenue de certaines douleurs centrales.

Afferent neurons from thalamic median and intralaminar (IL) nuclei arise in the spinal cord, brain stem synapses, substantia nigra, internal pallidum and cerebral cortex, directly and through the intermediary of the reticular nucleus of the thalamus (RT). Efferent neurons terminate in the anterior thalamic nuclei, RT, striatum and cerebral cortex. Tracking methods in the rat have demonstrated that some RT neurons which project towards the IL are surrounded by endings from the posterior ventral nucleus (VP). Electrical stimulation of multiple prosencephalic structures (mainly VP) and of sensory pathways induce responses in IL of brief latency followed by inhibition. Whereas the responses appear to be related to activation of excitatory projections (under the tonic facilitating control of cerebral cortex) the inhibition phases could be related to activation of RT, since they disappear after lesion of the RT. This nucleus could act as a common final pathway of inhibitions exerted on IL in the rat. Studies in this species have demonstrated that a lateral lesion of the thalamus that includes the RT provokes the appearance in IL of abnormal neuronal hyperactivity of a tonic nature and yet still exaggerated by stimuli normally capable of inducing responses of brief duration followed by inhibition. Human studies using a tomoscintigraphic method to determine regional blood flow have shown "hyperactivity" of the thalamic region in patients with pain of central origin during a natural stimulus provoking hyperpathia. This was not observed during painful states without hyperpathia. The working hypothesis proposed is that of a central lesion inducing a hyperpathia provoking pathologic hyperactivity in certain thalamic nuclei.(ABSTRACT TRUNCATED AT 250 WORDS)