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M J Besson

Publications and source records attributed to M J Besson.

At least 73 records · Page 4Linked to original sources
PubMed1985

Local cerebral metabolic effects induced by nigral stimulation following ventromedial thalamic lesions. II: Sensory motor, reticular and limbic systems.

The involvement of the ventromedial thalamic nucleus (VM) in mediating the local cerebral metabolic effects induced by unilateral substantia nigra (SN) electrical stimulation was investigated in the awake rat. Local cerebral glucose utilization (LCGU) was measured during ipsilateral SN-stimulation in VM-intact rats as well as in animals bearing 8 or 30 days old electrolytic VM-lesions, using the 14C-deoxyglucose quantitative autoradiographic method. In VM-intact rats, SN-stimulation enhanced LCGU in several bilateral components of the sensory motor, reticular, and limbic systems despite the lack of direct anatomical connections. Almost all these metabolic activations were no longer apparent one week following VM-lesion. In contrast, one month after the VM-injury, the above activations reappeared even more dramatically than in VM-intact animals especially on the contralateral side. It is concluded that SN-stimulation activates several brain regions of both hemispheres beyond the traditional motor areas, the role of the VM in mediating these activations is crucial, and the plasticity of the adult CNS allows for recovery of metabolic responsiveness in a disturbed system.

Afferent Pathways↗
PubMed1984

In vivo release of [3H]GABA in cat caudate nucleus and substantia nigra. II. Involvement of different thalamic nuclei in the bilateral changes induced by a nigral application of muscimol.

The contribution of motor and intralaminar thalamic nuclei to the changes of [3H]GABA release evoked in both caudate nuclei (CN) and both substantia nigra (SN) by a unilateral nigral application of muscimol (10(-6) M) was investigated on halothane-anaesthetized cats. Acute lesions were performed on one side of the thalamus at the level of either the ventralis medialis and ventralis lateralis (motor nuclei) or the centralis lateralis and paralamellar zone of the medialis dorsalis (intralaminar nuclei). The release of [3H]GABA neosynthesized from [3H]glutamine was measured by perfusing continuously a [3H]glutamine-enriched physiological medium through a push-pull cannula implanted in the 4 structures under investigation. After two hours of superfusion, muscimol (10(-6) M) was delivered for 60 min through the nigral push-pull cannula implanted ipsilaterally to the thalamic lesion. Evoked changes of [3H]GABA release were analyzed either in motor or intralaminar nuclei lesioned cats and compared to those observed in intact animals. Whatever the localization of the thalamic lesions was, an increased release of [3H]GABA was elicited locally in the SN and distally in the ipsilateral CN as in intact animals, suggesting that the responses induced ipsilaterally did not require nigro-thalamic pathways. On the contrary, in the contralateral CN changes of [3H]GABA release evoked by the nigral muscimol application were reversed by both types of thalamic lesion. Instead of a decreased release of [3H]GABA observed in intact cats, an increased release of [3H]GABA was detected in lesioned animals. In the contralateral SN, the response was reversed only after the intralaminar nuclei lesion. In this situation nigral muscimol application induced a decreased release of [3H]GABA in contrast to the enhanced release observed in intact and motor thalamic lesioned cats. The parallel increased release of [3H]GABA observed in the contralateral CN and SN in motor thalamic nuclei lesioned cats suggests an activation of the striatonigral cells by the nigral muscimol treatment. The asymmetrical changes of [3H]GABA release measured in the contralateral CN and SN in intact and intralaminar nuclei lesioned cats could indicate a presynaptic modulation of the [3H]GABA release acting either at the CN or the SN levels. The possible pathways involved in the interhemispheric transfer of information originating from one SN to the contralateral basal ganglia components are also discussed.

Animals↗
PubMed1984

Adaptive reaction of nigral neurons following lesion of their ventromedial-thalamic projection field.

The response of reticulata-nigral neurons to injury of their ventromedial-thalamic (VM) projection was studied in the rat, by the autoradiographic [14C]deoxyglucose method. Electrolytic lesion of the VM induced reversible: reticulata hypoexcitability; and hyporesponsiveness of areas receiving reticulata efferents, to nigral electrical stimulus. The results suggest that distal axonal injury (in the VM) induces reversible rearrangement of functional properties in the nigral parent cells and their uninjured collaterals, as a retrograde reaction.

Afferent Pathways↗
PubMed1984

Role of the thalamus in the bilateral regulation of dopaminergic and GABAergic neurons in the basal ganglia.

In halothane-anaesthetized cats implanted with several push-pull cannulae the release of dopamine from nerve terminals and dendrites of the two nigrostriatal dopaminergic pathways is shown to be asymmetrically or symmetrically regulated bilaterally when dopaminergic or GABAergic drugs are infused into one side of the nigra. Nigrothalamic GABAergic neurons may intervene in the asymmetrical regulation, as sagittal section of the thalamic massa intermedia blocks the contralateral effects induced by dopaminergic drugs. The role of thalamic nuclei in the bilateral regulation of dopamine and GABA release in the caudate nucleus and substantia nigra is further demonstrated by studies showing that (1) electrical stimulation of thalamic motor nuclei induces bilateral asymmetrical changes in dopamine release resembling the changes evoked by unilateral sensory stimuli or stimulation of cerebellar nuclei; (2) electrical stimulation of intralaminar or some midline thalamic nuclei leads to bilateral (or contralateral) symmetrical changes in dopamine release, some of these effects being comparable to those induced by unilateral stimulation of the motor cortex; (3) unilateral lesions of motor or intralaminar thalamic nuclei reverse the changes in GABA release in the contralateral caudate nucleus or substantia nigra induced by unilateral infusion of muscimol into the nigra; and (4) unilateral infusion of GABA into thalamic motor nuclei induces bilateral symmetrical regulation of dopamine release in caudate nuclei by means of presynaptic facilitatory influences.

Animals↗
PubMed1984

Local cerebral metabolic effects induced by nigral stimulation following ventromedial thalamic lesions. I: Basal ganglia and related motor structures.

The effects of unilateral electrical stimulation of the substantia nigra (SN) were mapped in the extrapyramidal system of conscious rats bearing ventromedial thalamic (VM) lesions, using the quantitative autoradiographic 14C-deoxyglucose method. SN-stimulation in VM-intact rats resulted in metabolic activation within the deep layer of superior colliculus, subthalamic nucleus, ventrolateral thalamus and sensory-motor cortex ipsilaterally, and bilaterally in the reticulata, compacta, centrolateral and ventromedial thalamus, striatum, globus pallidus and entopeduncular nucleus. SN-stimulation 8 days following ipsilateral VM-lesion, induced activation only within the ipsilateral compacta, subthalamic and entopeduncular nuclei and the globus pallidus and in addition, the reticulata bilaterally. However, SN-stimulation 30 days following VM-injury elicited bilateral metabolic activation in all the examined structures. It is concluded that the VM-thalamic nucleus mediates information from one SN to the ipsilateral motor cortex and striatum, as well as to the extrapyramidal components of the contralateral hemisphere. Moreover, due to the plasticity of the central nervous system, one month following the VM-lesion transmission of information from the SN to all the bilateral components of this network is reestablished.

Animals↗
PubMed1983

In vivo release of [3H]GABA in cat caudate nucleus and substantia nigra. I. Bilateral changes induced by a unilateral nigral application of muscimol.

Push-pull cannulae were implanted in both caudate nuclei and both substantiae nigrae (SN) of halothane-anesthetized cats and the release of [3H]GABA, continuously synthesized from [3H]glutamine, was measured in these structures during 4 h of superfusion. In some experiments, multi-unit neuronal activity was recorded at the tip of the nigral push-pull cannulae, using a bipolar electrode. Two hours after the onset of superfusion with [3H]glutamine, 10(-6)M of muscimol was added (for 1 h) in the superfusion medium delivered to one SN. This treatment increased locally the release of [3H]GABA and enhanced the neuronal activity of the nigral cells in the zona reticulata. An increased release of [3H]GABA was also observed in the contralateral SN, in association with an inhibition of the activity of the zona reticulata cells. The unilateral nigral application of muscimol also induced asymmetric changes in the release of [3H]GABA in both caudate nuclei, since [3H]GABA release was increased ipsilaterally and reduced on the contralateral side. The present findings are considered in relation to possible GABAergic neuronal populations affected by this local pharmacological treatment.

Animals↗
PubMed1983

Local cerebral glucose consumption in the rat. I. Effects of halothane anesthesia.

Rates of cerebral glucose utilization were measured by means of the autoradiographic 2-deoxy-D-(1-14C)glucose technique in normal rats under light halothane-anesthesia. Three types of region-specific metabolic alterations were elicited by inhalation of 0.5% halothane. The most striking effect observed was a significant increase of glucose consumption within the locus coeruleus, substantia nigra compacta and reticulata, interpeduncular nucleus, hippocampus, and fornix of the anesthetized animals in comparison to the corresponding brain areas of the conscious control rats. Halothane-anesthesia was also associated with significant metabolic depression in 21 (out of the 74 examined) discrete regions of the rat brain, distributed within the pons, cerebellum, diencephalon, and cortex, and was more prevalent in thalamus and neocortex. However, halothane failed to alter consistently the rates of glucose utilization in the rest of the rat brain areas investigated. The present findings suggest that halothane specifically alters the regional cerebral glucose utilization, with some limbic system components and the basal ganglia displaying increased metabolism, in contrast to the sensorimotor system which demonstrates significantly decreased metabolic activity.

Anesthesia, General↗
PubMed1983

Local cerebral glucose consumption in the rat. II. Effects of unilateral substantia nigra stimulation in conscious and in halothane-anesthetized animals.

The energy metabolism of 74 anatomically discrete central nervous structures was investigated by means of the autoradiographic 2-deoxy-D-(1-14C)glucose method (14C-DG) in conscious awake, as well as in halothane-anesthetized rats, following unilateral substantia nigra (SN) electrical stimulation. All the basal ganglia structures displayed bilateral metabolic activation in conscious animals, with only the contralateral subthalamic nucleus being unaffected. In anesthetized rats only the SN reticulata, globus pallidus, and subthalamic nucleus were affected ipsilaterally whereas anesthesia masked the effects of SN stimulation in SN compacta and striatum ipsilaterally, as well as within all the above structures contralaterally. The entopeduncular nucleus was bilaterally activated no matter the state of consciousness. Unilateral SN stimulation also increased glucose utilization within several thalamic regions (ventromedial, ventrolateral, ventroanterior, intralaminar, ventrobasal, and mediodorsal nuclei), the habenular complex, a few mesencephalic, brainstem (locus coeruleus and dorsal raphe) and cerebellar structures, mostly bilaterally and independently of the state of consciousness. Some of the factors suggested to be responsible for the masking effects of halothane-anesthesia on the metabolic activations elicited by unilateral SN stimulation are the following: (1) absence of movements in anesthetized rats, (2) halothane-induced depression of polysynaptic pathways mostly mediated through the thalamus, and (3) the stimulatory effect of halothane-anesthesia itself on metabolic activity in both parts of the SN.

Anesthesia, General↗
PubMed1983

Damage to the epithelial basement membrane in the corneas of diabetic rabbits.

Epithelial healing problems and basement membrane abnormalities have been observed in the corneas of patients with diabetes mellitus. In this study the rates of corneal epithelial wound healing following transcorneal freezing (with a 6-mm-diameter probe cooled in liquid nitrogen) were compared in diabetic (alloxan-induced) and nondiabetic rabbits. Also compared was the extent of injury to the epithelial basement membrane between the two groups. The overall rate of wound healing was faster in the diabetic animals; the wounds closed at 40 hours after freezing in diabetic animals and at 45 hours after in the nondiabetic controls. The lamina densa of the basement membrane was removed by the freezing procedure in two thirds of the diabetic animals but not in any of the controls. The results of this study indicate that epithelial healing problems in diabetes may be related to damage to the basement membrane, with resulting poor adhesion of regenerating epithelial cells.

Animals↗
PubMed1983

Effects of nigral application of muscimol on release of [3H] gamma-aminobutyrate and on multiunit activity in various cat thalamic nuclei.

The release of [3H] gamma-aminobutyrate (GABA) neosynthesized from [3H]glutamine was estimated in one substantia nigra and in the ipsilateral thalamus of halothane-anesthetized cats by perfusing a [3H]glutamine-enriched physiological medium through a push-pull cannula implanted in the two structures under investigation. After two hours of superfusion, muscimol (10(-6)M) was delivered through the nigral push-pull cannula for 50-60 min and local- and distal-evoked changes of [3H]GABA release were analyzed. In some experiments, changes of global neuronal activity induced by muscimol application were recorded in different thalamic nuclei, using a bipolar electrode. In a few of the above experiments, biochemical and electrophysiological determinations were simultaneously performed in the substantia nigra and the thalamus. The nigral application of muscimol (10(-6)M) induced locally an activation of the substantia nigra reticulata cells, as well as an increase in release of [3H]GABA. Distally, in the thalamus, two types of biochemical and electrophysiological responses were observed according to the localization of the tip of the push-pull cannula or the electrode. (1) An increased release of [3H]GABA and a depression of the global multi-unit cellular activity were obtained in the ventralis medialis-ventralis lateralis, the centralis lateralis and the paracentralis nuclei. These effects could reflect an activation of the GABAergic nigrothalamic neurons projecting to these different thalamic nuclei. (2) In contrast, in the medialis dorsalis paralamellar zone adjacent to the intralaminar nuclei of the thalamus, a decrease of [3H]GABA release and an activation of the multi-unit activity were obtained. These latter results may suggest either a polysynaptic response or the non-GABAergic nature of the nigrothalamic neurons afferent to the medialis dorsalis paralamellar zone.

Animals↗
PubMed1982

Bilateral asymmetrical changes in the nigral release of [3H]GABA induced by unilateral application of acetylcholine in the cat caudate nucleus.

In halothane anaesthetized cats, a push-pull cannula was implanted into the right caudate nucleus (CN) and in each substantia nigra (SN). The release of [3H]GABA continuously formed from [3H]glutamine was estimated in each structure. Acetylcholine (ACh, 5 x 10(-5) M) added in presence of eserine (5 x 10(-5) M) for 50 min in the right caudate nucleus 2 h after the onset of superfusion with [3H]glutamine, stimulated the [3H]GABA release locally. The effect was biphasic when ACh application was made in the median two-thirds of the structure and it was monophasic and transient when the ACh application was restricted to the lateral part. ACh application in the right caudate nucleus also induced changes in [3H]GABA released in the anterior (pars reticulata) and posterior (pars compacta) parts of both SN. While [3H]GABA release was enhanced in the ipsilateral anterior SN, it was reduced in the contralateral anterior SN. Respective opposite effects were observed in the posterior parts of the ipsi- and contralateral SN. These bilateral asymmetrical changes in [3H]GABA release were not dependent on the site of ACh application in the right caudate nucleus. These results indicate that the facilitation of cholinergic transmission in one caudate nucleus influences in an opposite way the striato-nigral GABA neurones on both sides of the brain.

Acetylcholine↗
PubMed1982

[Pharmacology of central noradrenergic receptors (author's transl)].

The pharmacological characteristics of adrenergic receptors in the central nervous system (CNS) can be studied using micro-iontophoretic electrophysiological approaches and binding of radiolabeled specific adrenergic receptors ligands. These approaches allowed the identification of different sub-classes of adrenergic receptors (alpha 1, alpha 2; beta 1, beta 2) in the CNS. Some of these receptors have a noradrenergic transmission dependent regulation. At the level of cerebral cortex, regulation mechanisms were particularly well studied. Interruption of noradrenergic transmission induces an hypersensitivity of alpha and beta adrenergic receptors. The hypersensitivity is linked to an increase of receptor density, and this has been shown for alpha 1, alpha 2 and beta 1 adrenergic receptors. After repeated injections of antidepressant drugs an hyposensitivity of beta receptors was observed. More precisely these treatments induced a reduction of beta 1 binding sites, without modification of beta 2 binding sites. On the other hand, the alpha 2 binding sites were increased. These regulation processes of alpha 2 receptors appear earlier than those of beta receptors, and this phenomenon could contribute to the late appearance of beta receptors hyposensitivity. In favor of this hypothesis, the reduction of beta binding sites is induced more rapidly after coadministration of alpha 2 receptor antagonist (such as yohimbine) and antidepressant drugs. The regulation mechanisms of these different types of adrenergic receptors could contribute to the delayed action of antidepressant drugs.

Animals↗
PubMed1981

Inhibitory effects of GABA, L-glutamic acid and nicotine on the potassium-evoked release of substance P in substantia nigra slices of the rat.

Rat substantia nigra slices were superfused with a physiological medium containing a diluted substance P (SP) antiserum, bacitracin and serum albumin to measure SP released in superfusates. As shown by measuring the degradation of a SP-labelled derivative incubated with cerebellar slices, this medium prevented the enzymatic inactivation of SP. Potassium (K+, 50 mM) and veratridine (5 X 10(-5) M) stimulated SP release and these effects were respectively prevented in absence of calcium and in presence of tetrodotoxin (5 X 10(-7) M). GABA (5 X 10(-5) M), nicotine (10(-6) M) and L-glutamic acid (5 X 10(-5) M) reduced the K+ (50 mM)-evoked release of SP. In contrast, glycine (5 X 10(-5) M), oxotremorine (5 X 10(-5) M), D-glutamic acid (5 X 10(-5) M) and serotonin (5 X 10(-5) M) were without effect. Pempidine (10(-5) M) prevented the inhibitory effect of nicotine (10(-6) M) on the K+-evoked release of SP. Glutamic acid diethyl ester (10(-4) M) completely abolished the L-glutamic acid-induced inhibition of the K+-evoked release of SP. Picrotoxin (5 X 10(-5) M) did not influence the L-glutamic acid inhibitory effect excluding the intervention of GABAergic mechanisms.

Animals↗
PubMed1980

In vivo release of endogenously synthesized [3H]GABA from the cat substantia nigra and the pallido-entopeduncular nuclei.

Halothane anesthetized cats were implanted with push--pull cannulae to study the release of [3H]GABA continuously formed from [3H]glutamine in the substantia nigra (SN) and in the pallido-entopeduncular nuclei (PEP). A spontaneous release of [3H]GABA was observed from both structures and it reached a steady state level 1 h after the beginning of the superfusion with [3H]glutamine. In cats implanted with two push--pull cannulae, the local application of potassium (47 mM) in the PEP stimulated the release of [3H]GABA from the ipsilateral SN. In cats implanted with 4 push--pull cannulae, the unilateral 10 min electrical stimulation of the caudate nucleus evoked the release of [3H]GABA not only from the ipsilateral SN, but also in most cases from the contralateral structure. This stimulus also enhanced the release of [3H]GABA from PEP but the effects were mainly observed in the medio-caudal part of the ipsilateral PEP and in the latero-rostral part of the contralateral structure. In all cases, the changes in [3H]GABA release were observed during and after the electrical stimulation. The ipsilateral effects can be attributed to the direct activation of the caudato-PEP or caudato-SN GABAergic neurons. A polysynaptic neuronal loop must be involved in the symmetric contralateral effects.

Animals↗