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Biomedical subjects

J M Besson

Publications and source records attributed to J M Besson.

At least 127 records · Page 7Linked to original sources
PubMed1988

Absence of long-term changes in biochemical markers of monoaminergic systems afferent to the excitotoxically neuron-depleted somatosensory thalamus.

In a previous study, it was shown that, one month after kainic acid (KA) injection into the thalamus, afferents deprived of postsynaptic target neurons exhibit structural alteration, including the loss of synaptic vesicles. The present study was undertaken to determine whether these long-term morphological changes were associated with changes in biochemical markers of monoaminergic pathways. In situ injection of KA was performed into the right ventrobasal complex of the rat thalamus (VB). Protein content and total amount of norepinephrine, dopamine, 5-hydroxytryptamine and 5-hydroxyindolacetic acid were analyzed in the lesioned area one, two, three and four months after injection using high-performance liquid chromatography and electrochemical detection. The results were compared to those obtained in an equal volume of tissue dissected out from the opposite (intact) VB. Protein content per unit volume decreased progressively to 50% of control in the neuron-depleted area. In contrast, whatever the amine considered, its total amount remained unaltered up to 4 months after the excitotoxic lesion. 5-hydroxyindolacetic acid was also unchanged 4 months after lesion. This study suggests that (i) the quantity of monoamines in afferents to the rat VB does not depend upon the presence of postsynaptic target neurons, (ii) a non-vesicular storage compartment may compensate the loss of synaptic vesicles in afferent fibers to the lesioned area.

Afferent Pathways↗
PubMed1988

[Convergence of nociceptive information on the parabrachio-amygdala neurons in the rat].

Neurones were recorded with extracellular micropipettes, in the parabrachial area located in the dorsolateral region of the pons of anaesthetized rats. All the neurones were identified by antidromic stimulation from the nucleus centralis of the amygdala. Numerous parabrachio-amygdala neurones (70%) were exclusively affected by noxious stimuli applied to several areas of the body. The rest of the neurones (30%) were not activated by any of these stimuli. The "nociceptive" neurones were classified in two groups: the neurones in the first group ("specific nociceptive", 55% of the whole population), responded to mechanical nociceptive and thermal nociceptive stimulation (threshold greater than 44 degrees C), with a strong and sustained activation. The neurones in the second group (15% of the whole population) responded by a strong inhibition to the nociceptive stimulation. Transcutaneous electrical stimulation demonstrated that the specific nociceptive parabrachial neurones received messages from A delta and C fibres. These results demonstrate that a spino-(trigemino)-ponto-amygdala nociceptive pathway exists which could be implicated in the emotional responses to noxious events.

Amygdala↗
PubMed1987

Postsynaptic receptors for cholecystokinin in the thalamic reticular nucleus: a possible modulatory system for sensory transmission.

Cholecystokinin (CCK) binding sites have been described in several areas of the brain with a particularly rich localization being found in the thalamic reticular nucleus (TRN). We have studied the distribution of CCK binding sites in the TRN using a high resolution autoradiographic technique and observed that the CCK receptors were dense throughout the whole nucleus. Using kainic acid excitotoxic lesions, it was demonstrated that CCK receptors were attached to postsynaptic elements and not to afferent fibers. These results are discussed in view of the known functional role of the thalamic reticular nucleus as an inhibitory control, gating all thalamic sensory transmission systems.

Animals↗
PubMed1987

In vivo electrochemical detection of 5-hydroxyindoles in the dorsal horn of the spinal cord: the contribution of uric acid to the voltammograms.

Treated carbon fiber electrodes were used with differential normal pulse voltammetry (DNPV) for in vivo determination of the relative participation of uric acid (UA) to peak 3 derived between 250-300 mV in the dorsal horn of the spinal cord of anesthetized rats. In vitro, treated carbon fiber electrodes respond linearly over a large range of concentrations of UA (oxidation potential around 250 mV) and 5-hydroxyindoleacetic acid (5-HIAA, oxidation potential around 280-290 mV), but are 3 to 4 times more sensitive to 5-HIAA than to UA. In vivo the question remains as to the exact nature of peak 3 because the difference between oxidation potentials of UA and 5-HIAA is not great enough to permit a separate monitoring of the two compounds. In normal rats, administration of the xanthine oxidase inhibitor allopurinol, produced a progressive decrease of the signal, which reached 64.3% of controls at 120 min (35.6% diminution) after injection, and then plateaued around this value for up to 2 h. The administration of the monoamine oxidase inhibitor (MAOI) clorgyline, produced a classical decay in the voltammograms due to a diminution of endogenous 5-HIAA; however, allopurinol injected 3 h after MAOI gave an additional decrease of peak 3 of about 28%. Finally, in rats pretreated with parachlorophenylalanine (pCPA), the residual peak (32.48% as compared to peak 3 of normal rats taken as 100%), the potential of which is shifted to near that of UA, could be decreased by allopurinol to a level of 9.6% of the peak in control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1987

Paradoxical hyperalgesic effect of exceedingly low doses of systemic morphine in an animal model of persistent pain (Freund's adjuvant-induced arthritic rats).

The effects of exceedingly low doses of morphine (3-50 micrograms/kg i.v.) were studied upon the vocalization threshold induced by paw pressure in rats with Freund's adjuvant-induced arthritis. The highest dose used (50 micrograms/kg i.v.) clearly induced an analgesic effect. No significant modification of the vocalization threshold was observed with 30 micrograms/kg. By contrast, a significant hyperalgesic effect resulted with doses of 10 down to 3 micrograms/kg. Maximum hyperalgesia was observed with 6 micrograms/kg.

Animals↗
PubMed1987

Structural alteration and possible growth of afferents after kainate lesion in the adult rat thalamus.

Afferents to the thalamic ventrobasal complex (VB) originating from the spinal cord, the dorsal column nuclei, and the somatosensory cortex were anterogradely labeled by WGA-HRP 30 days after an injection of kainic acid (KA), which produced a complete unilateral neuronal loss in the VB, the opposite side being used as a control. At the light microscopic level, there was no obvious rerouting of spinal afferents away from the lesioned areas towards unlesioned parts of VB. There was an apparent decrease in the number of lemniscal afferents to the lesioned side, which may indicate a progressive retrograde degeneration. At higher magnification, all three afferent systems studied demonstrated morphological changes, predominantly manifested by terminal swellings that reached up to 25 micron in diameter. Control experiments suggested that these morphological alterations were related neither to a direct action of the excitotoxin nor to the absence of a different afferent system but to the loss of neuronal postsynaptic targets. At the electron microscopic level, the normal ultrastructural features of VB were not observed after a KA lesion. No neuronal somata, dendrites, or normal presynaptic elements were observed. Neural elements, some of which were labeled from the somatosensory cortex or the dorsal column nuclei, were essentially of two types: varicosities and unmyelinated axonal profiles. Varicosities could be separated into two broad classes: The majority were large structures derived from large, sometimes myelinated, axons and containing a wealth of organelles. Since they were not completely surrounded by glial elements, we have denoted them unensheathed varicosities. Among the organelles, the most obvious features were vesicles and tubules of smooth endoplasmic reticulum, microtubules, mitochondria, and various lysosome-like inclusions. These unensheathed varicosities gave rise to large, mound-like protrusions containing large vacuoles and thin long protrusions either filled with neurofilaments or resembling unmyelinated axonal profiles. Others were completely surrounded by a glial sheet and were therefore called ensheathed varicosities. These ensheathed varicosities presented several characteristics typical of degenerating profiles, including neurofilamentous proliferation and morphological alterations of the mitochondria. Unmyelinated axonal profiles occupied a substantial territory in the lesioned area. They were most often grouped in bundles sometimes wrapped by glial processes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Is there a serotonergic tonic descending inhibition on the responses of dorsal horn convergent neurons to C-fibre inputs?

In the anaesthetized rat the intravenous injection of 5-HT antagonists, cinanserin and methysergide, induces in two-thirds of neurones studied, an increase in the responsiveness of dorsal horn convergent neurones to C-fibre stimulation. These results are in favour of the existence of serotonergic tonic descending inhibitory effects on the spinal transmission of noxious messages.

Animals↗
PubMed1986

Opioid receptor types and antinociceptive activity in chronic inflammation: both kappa- and mu-opiate agonistic effects are enhanced in arthritic rats.

The antinociceptive effects obtained in arthritic rats with morphine, the opioid mu-agonist DAGO [D-Ala2,MePhe4,Gly-ol5]enkephalin, the delta-selective agonist DTLET [D-Thr2, Leu5]enkephalyl-Thr, and the kappa-agonist U-50,488H were compared to their corresponding effects in normal animals and morphine-pretreated arthritic rats, respectively, using a paw pressure test. The effects of the mu- and kappa-agonists were increased in arthritic rats. While morphine-treated rats were cross-tolerant to the mu- and kappa-agonists, no tolerance to the delta-selective agonist was found. The possibility that the potent action of morphine in this model for chronic inflammatory pain is mediated partly through kappa-mechanisms is discussed.

Analgesics↗
PubMed1986

Behavioral evidence for a crossed ascending pathway for pain transmission in the anterolateral quadrant of the rat spinal cord.

Thresholds of two behavioral responses to noxious pressure of the hindpaws (withdrawal, vocalization) were analyzed before and 3 weeks after a lesion of various quadrants of the spinal cord at the cervical level. The threshold of the spinal reflex could not be modified. Threshold of vocalization elicited by the pressure of one hindpaw was significantly increased when, and only when, the opposite ventrolateral quadrant was cut. These results emphasize the role of the lateral spinothalamic tract in the transmission of noxious messages.

Afferent Pathways↗
PubMed1986

Slow and fast axonal transport of acetylcholinesterase molecular forms in polyarthritic rats.

Acetylcholinesterase (AChE) activity and its distribution among different molecular forms were studied in the sciatic nerve of normal and polyarthritic rats. Axonal transport of each form was investigated on the basis of its accumulation on both sides of a transection. Although an increase in total AChE activity could be detected in the sciatic nerves of polyarthritic animals, both anterograde and retrograde axonal transport of all the molecular forms investigated were similar in normal and polyarthritic rats. This suggests that neither slow nor fast axonal transport is impaired in polyarthritic rats. Hence, the neurophysiological modifications observed at the spinal, thalamic and cortical levels of the CNS are presumably not a consequence of peripheral axonal disability.

Acetylcholinesterase↗