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M J Besson

Publications and source records attributed to M J Besson.

At least 55 records · Page 3Linked to original sources
PubMed1990

Co-expression of neuropeptides in the cat's striatum: an immunohistochemical study of substance P, dynorphin B and enkephalin.

The expression of tachykinin-like and opioid-like peptides was studied in medium-sized neurons of the caudate nucleus in tissue from adult cats pretreated with colchicine. Two methods, a serial thin-section peroxidase-antiperoxidase technique and a two-fluorochrome single-section technique, were applied. Quantitative estimates were made mainly with the peroxidase-antiperoxidase method. The numbers of neurons expressing substance P-like, dynorphin B-like, and enkephalin-like immunoreactivity were recorded in regions identified, respectively, as striosomes and extrastriosomal matrix. Striosomes were defined by the presence of clustered substance P-positive and dynorphin B-positive neurons and neuropil. Tests for the co-existence of enkephalin-like peptide and glutamate decarboxylase-like immunoreactivity were also made with the peroxidase-antiperoxidase method. Co-expression of substance P-like and dynorphin B-like immunoreactivities was the rule both in striosomes and in the matrix. In striosomes, substance P-like immunoreactivity was found in 96% of dynorphin B-immunoreactive neurons, and in the matrix 89% of dynorphin B-positive cells contained substance P-like immunoreactivity. Substance P/dynorphin B-positive neurons corresponded to over half (57%) of the neurons in striosomes but only 39% of the neurons in the matrix. Both in the matrix and in striosomes, about two-thirds of all neurons (63% and 65%, respectively) were identified as enkephalin-positive. Among all substance P/dynorphin B-positive medium-sized neurons, 76% also contained enkephalin-like antigen. The enkephalin-positive neurons characterized by triple peptide co-existence (enkephalin/substance P/dynorphin B) represented a mean of 63% of striosomal enkephalin-positive neurons (41% of all striosomal neurons) and 35% of matrical enkephalin-positive neurons (26% of all matrical neurons). Finally, nearly all enkephalin-positive neurons were immunoreactive for glutamate decarboxylase, and therefore probably GABAergic, but only about half the glutamate decarboxylase-positive population was enkephalin-immunoreactive. These findings suggest that neuropeptides from three distinct precursors may be co-localized in single medium-sized neurons in the striatum, and that the differential patterns of co-expression of substance P-like, dynorphin B-like, and enkephalin-like peptides may confer functional specializations upon subpopulations of GABAergic neurons giving rise to the efferent projections of the striatum. The linked expression of substance P-like and dynorphin B-like peptides in single neurons both in striosomes and matrix suggests that some regulatory mechanisms controlling peptide expression apply regardless of compartment.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

[D2 dopaminergic receptor activation enhances the spontaneous release of 3H-GABA in the prefrontal cortex of rats, in vitro. The facilitating role of D1 dopaminergic receptors].

The effects of three D2 dopaminergic agonists on the spontaneous release of 3H-GABA have been studied on rat prefrontal cortical slices. LY171555 (10(-9) M), RU24926 (3 x 10(-8) M) and lisuride (10(-7) M) respectively enhanced the spontaneous release by 25, 20.5 and 23%. These effects were totally reversed by the D2 antagonist sulpiride (10(-5) M). Furthermore, subliminar concentration of RU24926 (10(-9) M) and of the D1 agonist SKF38393 (10(-6) M) induced a clear enhancement of the spontaneous release of 3H-GABA when they were superfused simultaneously. Our results suggest that in the prefrontal cortex, the spontaneous release of 3H-GABA is under an activatory D2 dopaminergic control. The activation of D1 receptors seems to have an enabling effect on this regulation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Three-dimensional organization of the striosomal compartment and patchy distribution of striatonigral projections in the matrix of the cat caudate nucleus.

Acetylcholinesterase staining on successive frontal or sagittal sections was used to determine the three-dimensional organization of the striosomal and matrix compartments in the adult cat caudate nucleus. Reconstruction drawings of the acetylcholinesterase-poor zones (striosomes) indicated that the striosomal compartment is a labyrinthine network organized in the rostrocaudal and mediolateral axis which is reproducible from one animal to another. Four main anteroposterior channels converging in the mediorostral pole of the caudate nucleus were distinguished. Seven to eight diagonally oriented channels crossing the previous ones were seen also in the mediolateral axis on the central core of the caudate nucleus. The pattern of organization of the numerous and tortuous striosomal channels was more complicated medially, while the lateral part of the caudate nucleus was represented mainly by the matrix compartment. In addition, a sub-compartmentation of the matrix was demonstrated by retrograde tracing studies made by injecting either horseradish peroxidase-wheat germ agglutinin, [14C]amino acids or a mixture of horseradish peroxidase-wheat germ agglutinin and [14C]amino acids in several areas of the substantia nigra pars reticulata. Labelled patches were seen with both tracers, their topographical localization depended on the nigral injection site but reconstruction analysis indicated that the populations of cells which innervate the substantia nigra pars reticulata originate in the two third lateral parts of the caudate nucleus all along its rostrocaudal extension. Examination of horseradish peroxidase-wheat germ agglutinin labelled cells indicated that not all cells were labelled in patches suggesting a further sub-compartmentation of these patches. Finally, a comparison of the topographical distributions of labelled patches and of striosomes revealed that most patches were located in the extrastriosomal matrix.

Acetylcholinesterase↗
PubMed1989

Postnatal evolution of the gamma-aminobutyric acid/benzodiazepine receptor complex in a model of inherited epilepsy: the quaking mouse.

Binding assays of [3H]muscimol and [3H]-flunitrazepam have been performed on brain homogenates of brainstem, cerebellum, and forebrain of genetically epileptic quaking (qk) mutant mice 20, 40, 70, and 90 days old and their corresponding controls of the same strain (C57BL/6J). The endogenous gamma-aminobutyric acid (GABA) content has been determined in various brain regions of 70-day-old qk and control mice. Finally, the behavioral effects of diazepam, of the mixed GABAA/GABAB receptor agonist progabide, and of the selective GABAB receptor agonist baclofen have been assessed in adult qk mutants. Our results strongly suggest a lack of involvement of GABAergic neurotransmission in the inherited epilepsy of the qk mutant mouse.

Aging↗
PubMed1989

Neuroleptic-sensitive binding sites in the nigrostriatal system: evidence for differential distribution of sigma sites in the substantia nigra, pars compacta of the cat.

The sigma site is a recently described binding site to which dextrorotary isomers of certain psychotomimetic benzomorphans bind specifically. Classical and nonclassical neuroleptics also have high affinity for the sigma site, including neuroleptics known to bind to the D2 dopamine receptor. The affinity of some D2-binding neuroleptics for the sigma site has raised the possibility that certain important effects of antipsychotic drugs may relate to the sigma site. Left unresolved has been the question of how these actions could relate to dopaminergic systems. To explore this issue we carried out an autoradiographic binding study of the distribution of the sigma-selective ligand 3H-DTG in the nigrostriatal system. We report here that haloperidol-displaceable 3H-DTG binding sites are densely concentrated in an anatomically discrete subdivision of the cat's substantia nigra pars compacta. This zone, identifiable as the striosome-projecting densocellular zone of the pars compacta, also shows heightened D2-related ligand binding but has reduced D1-related ligand binding relative to other parts of the nigral complex. This evidence suggests that sigma-mediated interactions with dopaminergic systems may occur in the substantia nigra pars compacta and that the functional effects of these interactions may influence the nigrostriatal projection to striosomes differentially.

Animals↗
PubMed1988

Topographical organization of efferent projections from the cat substantia nigra pars reticulata.

The topographical organization of the efferent projections from the cat substantia nigra (SN) to the thalamus and the superior colliculus was examined using the anterograde transport of horseradish peroxidase-wheat germ agglutinin (HRP-WGA) and of labelled proteins. HRP-WGA or a mixture of [14C]amino acids was injected into various areas of the SN and the transported material visualized on coronal brain sections by histochemistry or autoradiography, respectively. The retrograde transport of [14C]gamma-aminobutyric acid ([14C]GABA) injected into thalamic nuclei was used also to determine the identity of the nigrothalamic projections. Identical results were found using either the anterograde transport of HRP-WGA or of labelled proteins. In the thalamus, dense nigral projections were observed in the nucleus ventralis medialis (VM) and in the rostromedioventral part of the nucleus ventralis lateralis (VL) whilst more limited projections were seen in the nuclei centralis lateralis (CL) and paracentralis (PC) as well as in the paralamellar zone of the nucleus medialis dorsalis (MD-Il). In addition, a patchy distribution of HRP-WGA or of radioactivity was found in the intermediate layer of the superior colliculus. More precisely, labelling of the VM was dense following injection of [14C]amino acids into the intermediate part of the SN pars reticulata (SNR) regardless of the depth of the injection site, whilst the intralaminar nuclei were labelled preferentially following injections made into the dorsal part of the intermediate SNR. Nigral projections to the intermediate layer of the superior colliculus were visualized over the whole mediocaudal and laterorostral extent when [14C]amino acids were injected into the rostral part of the SNR. Labelling of the superior colliculus was also seen following injection of [14C]amino acids into the intermediate part of the SNR but, in this case, ventral injections led to a more intense labelling than dorsal ones. Both the SNR and the SN pars compacta (SNC) were labelled when [14C]GABA was injected into the VM nucleus of the thalamus, confirming that the nigro VM projection is GABAergic and showing that recurrent collaterals of these GABAergic cells innervating the SNC also contained the transported radioactive material. In this condition ([14C]GABA injection into the VM), the thalamic reticularis nucleus also exhibited a dense labelling.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗
PubMed1988

[3H]SCH 23390 binding to D1 dopamine receptors in the basal ganglia of the cat and primate: delineation of striosomal compartments and pallidal and nigral subdivisions.

The distribution of D1 dopamine receptors was studied autoradiographically in the basal ganglia of the cat, monkey and human. These receptor binding sites were labeled directly with the D1-selective antagonist [3H]SCH 23390, and ligand-binding assays were performed concurrently. Serial- or same-action analysis permitted comparisons among D1 binding distributions, acetylcholinesterase staining and tyrosine hydroxylase immunoreactivity. In all species studied, the dorsal striatum exhibited patches of particularly dense D1 binding in correspondence with acetylcholinesterase-poor striosomes. Highly patterned binding was present in the ventral striatum. Distinctions in binding density were observed among the subdivisions of the globus pallidus and of the substantia nigra. The external segment of the pallidum was extremely sparse in D1 binding, whereas the internal segment (or entopeduncular nucleus in the cat) was a site of high D1 binding density. The binding density was greatest in the core of the internal segment, and tyrosine hydroxylase-positive fibers surrounded and weakly dispersed themselves through this core. Weak binding was present in the ventral pallidum. In the substantia nigra, the pars reticulata demonstrated the densest binding, particularly medially. The pars compacta showed much sparser binding, though some of its tyrosine hydroxylase-positive neurons had dendrites extending ventrally into the zone of dense D1 binding in the pars reticulata. We conclude that [3H]SCH 23390-defined D1 binding is compartmentalized in the dorsal striatum and that, particularly in relation to the reported distributions of striatal D2 dopamine receptors, this is likely to be of functional significance in the dopaminergic modulation of intrastriatal neurotransmission as well as of afferent and efferent neurotransmission. The segregated localizations of D1 receptors in the substantia nigra suggest predominant activation of the pars reticulata, including ventral and medial regions adjacent to the densocellular zone. Specific pathways from compartments in the striatum to subdivisions of the pallidum may also be differentially modulated by dopamine acting via distinct receptor subtypes. At the level of the pallidum, such D1 modulation appears to be restricted to the internal segment, which projects to the thalamus, rather than to the external pallidum, which projects to the subthalamic nucleus.

Acetylcholinesterase↗
PubMed1987

The role of dopamine released from distal and proximal dendrites of nigrostriatal dopaminergic neurons in the control of GABA transmission in the thalamic nucleus ventralis medialis in the cat.

Halothane-anaesthetized cats implanted with push-pull cannulae were used in this study. Amphetamine was applied in the pars reticulata or pars compacta of the substantia nigra in order to determine the role of dopamine released from distal or proximal dendrites of dopaminergic cells in the control of GABAergic transmission in the nucleus ventralis medialis of the thalamus. When applied for 30 min in either the pars reticulata or the pars compacta, amphetamine (10(-6) M) enhanced to a similar extent the local release of [3H]dopamine synthesized from [3H]tyrosine, these effects being seen mainly during the drug application. The amphetamine-evoked release of dopamine in the pars reticulata produced a long lasting reduction in the release of [3H]GABA synthesized from [3H]glutamine in the nucleus ventralis medialis as well as in the paralamellar zone of the nucleus ventralis lateralis. Opposite effects were observed when amphetamine (10(-6) M) was applied in the pars compacta. In complementary experiments, single unit recordings were made in the intermediate part of the pars reticulata, some of the cells being identified by antidromic activation from the nucleus ventralis medialis. Whether applied in the pars reticulata or pars compacta, amphetamine (10(-6) M, 10 min) evoked a reversible decrease in the firing rate of most recorded cells whether or not they were identified as projecting to the nucleus ventralis medialis. Therefore, the decreased release of [3H]GABA in the nucleus ventralis medialis seen following application of amphetamine in the pars reticulata of the substantia nigra could result from an inhibition of nigrothalamic GABAergic neurons. Since the nucleus ventralis medialis is also innervated by GABAergic neurons originating in the entopeduncular nucleus, single unit recordings were made from cells in this nucleus during the application of amphetamine (10(-6) M, 10 min) into the pars compacta of the substantia nigra, some of which were identified antidromically as projecting to the nucleus ventralis medialis. Most cells identified or not were found to be activated during this treatment. These results suggested that the increased release of [3H]GABA seen in the nucleus ventralis medialis following application of amphetamine in the pars compacta of the substantia nigra might be linked to the enhanced firing rate of entopeduncular-thalamic GABAergic neurons.

Action Potentials↗
PubMed1986

Enhancement of glutamate release in the rat striatum following electrical stimulation of the nigrothalamic pathway.

The release of unlabelled amino acids and newly synthesized [3H]dopamine was estimated in the striatum of halothane-anaesthetized rats superfused using a push-pull cannula. Electrical stimulation of the substantia nigra pars reticulata (SNR), enhanced the release of glutamate (maximal effect +51%) in the ipsilateral striatum. The outflow of [3H]dopamine, aspartate, serine and glutamine was unchanged. Seven-12 days after electrolytic lesion of the ipsilateral ventromedial nucleus of the thalamus SNR, stimulation no longer increased the striatal release of glutamate. It is suggested that electrical stimulation of the SNR enhances the striatal release of glutamate, presumably originating from corticostriatal fibres, by activating a nigrothalamocortical polysynaptic pathway.

Animals↗
PubMed1986

Supernumerary locus coeruleus neurons as a determinant of inherited epilepsy in the convulsive mutant mouse quaking.

In quaking mice (a genetic model of epilepsy with an increased number of noradrenergic neurons) bilateral electrolytic coagulation of locus coeruleus (LC) in adult mice inhibited the convulsions elicited by somatic stimulations while neonatal 6-hydroxydopamine (6-OHDA) treatment remained ineffective upon the convulsions. Biochemical effects of the two treatments differed only in the brainstem where electrolytic lesion decreased while 6-OHDA treatment increased noradrenaline (NA) and 3-methoxy 4-hydroxyphenylethyleneglycol (MHPG) levels. Our results suggest that supernumerary LC neurons mediate the convulsions of the mutants through an action presumably restricted to the brainstem.

Animals↗
PubMed1986

In vivo release of [3H]gamma-aminobutyric acid in the rat neostriatum--I. Characterization and topographical heterogeneity of the effects of dopaminergic and cholinergic agents.

The release of [3H]gamma-aminobutyric acid continuously synthesized from [3H]glutamine was studied in the striatum of halothane-anaesthetized rats superfused with a push-pull cannula. The levels of spontaneously released [3H]GABA were identical in all striatal regions examined, but were found to be higher at the junction between the striatum and the globus pallidus. Superfusion with a medium enriched in K+ ions induced a concentration-dependent increase in [3H]GABA release. Superfusion with a Ca2+-free medium did not affect the spontaneous outflow of [3H]GABA but sharply reduced the release of [3H]GABA evoked by 30 mM K+. Locally applied tetrodotoxin (50 microM) decreased slightly the spontaneous release of [3H]GABA (-22%). When acetylcholine (50 or 500 microM) was added to a superfusion medium containing eserine (50 microM), the spontaneous release of [3H]GABA was enhanced in the ventral but not in the dorsal region of the striatum. The local application of 2,3,4,5-tetrahydro, 7,8,-dihydroxy, 1-phenyl, 1-H, 3-benzazepine (10 microM), a dopaminergic agonist acting preferentially on D1 receptors increased the release of [3H]GABA in the dorsal striatum (+32%) but decreased it slightly (-19%) in the ventral striatum. 3-(2-(N-3 hydroxyphenylethyl)N-propylamino)ethyl-phenol (50 microM), a preferential D2 receptor agonist, decreased [3H]GABA release when it was applied dorsally (-23%) but not ventrally in the striatum. It is concluded that the regulation of the release of [3H]GABA by acetylcholine and dopaminergic drugs is different in the dorsal and ventral regions of the striatum. These differences may be related to the existence of subpopulations of GABA neurons and may well have functional implications as suggested by behavioural studies.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1986

In vivo release of [3H]gamma-aminobutyric acid in the rat neostriatum--II. Opposing effects of D1 and D2 dopamine receptor stimulation in the dorsal caudate putamen.

The effects of several dopaminergic agonists and antagonists on the spontaneous release of [3H]gamma-aminobutyric acid were investigated in the dorsal striatum of halothane-anaesthetized rats. A push-pull cannula was implanted and the tissue was superfused continuously with a physiological medium containing [3H]glutamine, the precursor of [3H]GABA. Drugs were added to the superfusion medium. 2-Amino,6,7-dihydroxy,1,2,3,4-tetrahydro-naphtalene (ADTN, a mixed D1 and D2 receptor agonist) and D-amphetamine (a drug that enhances the release of endogenous dopamine) increased the release of 3H-GABA. The effect of ADTN was blocked by a D1 antagonist [R-(+),8-chloro, 7-hydroxy,2,3,4,5-tetrahydro,3-methyl,5-phenyl,1-H,3-benzazepine (SCH 23390)] but not by a D2 antagonist (S-sulpiride). Furthermore the stimulation of D1 receptors either by 2,3,4,5-tetrahydro,7,8-dihydroxy,1-phenyl,1-H,3-benzazepine or by D-amphetamine in the presence of S-sulpiride also enhanced the release of [3H]GABA. On the other hand, a selective D2 receptor agonist (3-(2-(N-3-hydroxy-phenylethyl)N-propylamino)ethyl-phenol) decreased the release of [3H]GABA. This effect was blocked in the presence of S-sulpiride. By itself the D1 receptor antagonist (SCH 23390) decreased the release of [3H]GABA whereas the D2 receptor antagonist (S-sulpiride) had no effect. It was concluded that stimulation of D1 and D2 receptors produces opposing effects on the spontaneous release of [3H]GABA in the dorsal striatum. Stimulation of D1 receptors facilitates the release of [3H]GABA whilst stimulation of D2 receptors inhibits it. The effect of D1 receptor stimulation appears to be predominant, and endogenous dopamine may activate tonically the release of GABA through these receptors in our experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Release of newly synthesized 3H-dopamine in the striatum: an adaptation of the push-pull cannula method to awake restrained and anesthetized rats.

The release of newly synthesized 3H-dopamine (3H-DA) was measured in the rat striatum superfused, through a push-pull cannula, with a physiological medium enriched in 3H-tyrosine. The level of spontaneous 3H-DA release was dependent on the topographical localisation of the cannula in the striatum (anterior parts displayed higher levels than posterior ones) and on the anesthetic state (halothane anesthetized rats demonstrated higher levels than awake ones). Inhibition of DA inactivation processes by local application of benztropine (a DA reuptake inhibitor, 10(-6) M) or by IV administration of pargyline (a MAO inhibitor, 100 mg/kg) enhanced the detectable outflow of 3H-DA from the striatum in both halothane anesthetized and awake rats. Local application of D-amphetamine (10(-5) M) or acetylcholine (5 X 10(-5) M) in the presence of eserine (5 X 10(-5) M) evoked respectively a fivefold and a 30% increase in spontaneous 3H-DA release in halothane anesthetized rats. Inhibition of the firing of dopaminergic neurons by IV injection of gamma-hydroxybutyrate (400 mg/kg) produced a 30% decrease in striatal 3H-DA release. The present results demonstrate that the push-pull cannula method is suitable for the study of DA release in both the anesthetized and the awake rat.

Acetylcholine↗
PubMed1986

Apomorphine and haloperidol effects on striatal 3H-dopamine release in anesthetized, awake restrained and freely moving rats.

The ability of apomorphine (APO) and haloperidol (HAL) to affect the spontaneous release of newly synthesized 3H-DA in the striatum was studied in halothane anesthetized, gallamine paralyzed, awake restrained and freely moving rats. The striatum was continuously superfused through a push-pull cannula with a physiological medium enriched in 3H-tyrosine. Basal levels of 3H-DA release were different in the four experimental models: highest in halothane anesthetized rats, intermediate in awake restrained and gallamine treated rats and lowest in freely moving rats. In all experimental models IV or SC injection of APO (1 mg/kg) inhibited the release of 3H-DA (30-50%) from 15 to 90 min following its administration. In awake restrained and freely moving rats, stereotyped behaviour was observed for one hour following the APO injection. In halothane anesthetized rats the inhibitory effect of APO on 3H-DA release was prevented by pretreatment with HAL (2 mg/kg IV). Injection of HAL (2 mg/kg IV or SC) failed to enhance the release of 3H-DA in anesthetized and awake restrained rats, whilst a long-lasting increase in 3H-DA release was observed in gallamine treated and freely moving animals (55% and 120% respectively). However, catalepsy was observed in both restrained and freely moving rats. It is concluded that the modifications of 3H-DA release produced by HAL but not those produced by APO are dependent on the experimental model used, a fact possibly related to the different sites of action of these two drugs.

Anesthesia, General↗
PubMed1986

In vivo release of endogenous amino acids from the rat striatum: further evidence for a role of glutamate and aspartate in corticostriatal neurotransmission.

By means of the push-pull cannula method, the outflow of endogenous amino acids was studied in the striatum of halothane-anesthetized rats. Addition of K+ ions (30 mM for 4 min) to the superfusion fluid increased the release of aspartate (+116%), glutamate (+217%), taurine (+109%), and gamma-aminobutyric acid (GABA) (+429%) whereas a prolonged decrease in the outflow of glutamine (-28%) and a delayed reduction in the efflux of tyrosine (-25%) were observed. In the absence of Ca2+, the K+-induced release of aspartate, glutamate, and GABA was blocked whereas the K+-induced release of taurine was still present. Under these conditions, the decrease in glutamine efflux was reduced and that of tyrosine was abolished. Local application of tetrodotoxin (5 microM) decreased only the outflow of glutamate (-25%). One week following lesion of the ipsilateral sensorimotor cortex the spontaneous outflow of glutamine and of tyrosine was enhanced. Despite the lack of change in their spontaneous outflow, the K+-evoked release of aspartate and glutamate was less pronounced in lesioned than in control animals, whereas the K+-evoked changes in GABA and glutamine efflux were not modified. Our data indicate that the push-pull cannula method is a reliable approach for the study of the in vivo release of endogenous amino acids. In addition, they provide further evidence for a role for glutamate and aspartate as neurotransmitters of corticostriatal neurons.

Amino Acids↗
PubMed1986

[Effect of lesions of the ventromedial nucleus of the thalamus on cerebral metabolism: experimental study in the rat using the 14C-deoxyglucose method].

Local cerebral glucose utilization (LCGU) was studied quantitatively in awake rats one week and one month following unilateral electrolytic lesion of the ventromedial thalamic nucleus (VM). Significant decrease in LCGU were observed in the ipsilateral cortex as well as in some contralateral cortical areas and bilateral subcortical structures. The modifications by the VM lesion, of the metabolic activations induced by electrical stimulation of substantia nigra pars reticulata (SNR, main afference of the VM) were investigated also. Results suggest that VM is an important relay nucleus on the pathways directed from one SNR towards ipsilateral corticostriatal system and contralateral thalamus and basal ganglia. Finally, one month following the VM lesion a recovery of metabolic activations induced by SNR stimulation was observed whereas basal glucose consumption remained decreased.

Animals↗
PubMed1985

Bilateral cerebral metabolic alterations following lesion of the ventromedial thalamic nucleus: mapping by the 14C-deoxyglucose method in conscious rats.

The functional role of the ventromedial thalamic nucleus (VM) was investigated by means of the quantitative autoradiographic 14C-deoxyglucose method. Local cerebral glucose utilization (LCGU) was measured bilaterally in 53 discrete brain areas of conscious rats 1 week and 1 month following electrolytic lesion of the VM. There was no difference observed in the LCGU values between the two groups of lesioned animals. In the VM-lesioned rats glucose consumption was decreased in several ipsilateral (pre-frontal, frontal, cingulate, sensorimotor, visual) and in some contralateral (cingulate, sensorimotor, visual) cortical areas. Furthermore, LCGU values were depressed bilaterally in the striatum, hippocampus, dentate gyrus, substantia nigra compacta, superficial layers of the superior colliculus, oculomotor complex, and cerebellar dentate nuclei. Glucose utilization was diminished also in the deep layers of the superior colliculus and in the fastigial nucleus ipsilateral to the lesion. Within the thalamus, glucose metabolism was decreased in several nuclei either bilaterally (reticular, intralaminar, paralamellar mediodorsal) or ipsilaterally (lateroposterior, ventrobasal, ventrolateral, ventroanterior, and medioventral) to the lesion. A significant correlation between the percentage of injured VM and the regional metabolic depression was demonstrated in the areas displaying the most pronounced decrease in LCGU. These results support a widespread influence of the VM on brain function extending beyond the limits of purely motor systems and reveal the consequences of a unilateral lesion of the thalamus on metabolic activity in several contralateral structures.

Animals↗