Biomedical subjects

G Li Volsi

Publications and source records attributed to G Li Volsi.

At least 19 recordsLinked to original sources

PubMed2006

Aminergic control of neuronal firing rate in thalamic motor nuclei of the rat.

The effects induced on neuronal firing by microiontophoretic application of the biological amines noradrenaline (NA) and 5-hydroxytryptamine (5-HT) were studied "in vivo" in ventral-anterior (VA) and ventrolateral (VL) thalamic motor nuclei of anaesthetized rats. In both nuclei the amines had a mostly depressive action on neuronal firing rate, the percentage of units responsive to NA application (88%) being higher than to 5-HT (72%). Short-lasting (less than 2 min) and long lasting (up to 20 min) inhibitory responses were recorded, the former mostly evoked by NA and the latter by 5-HT ejection. In some cases 5-HT application had no effect on the firing rate but modified the firing pattern. NA-evoked responses were significantly more intense in VL than in VA neurons. Short-lasting inhibitory responses similar to NA-induced effects were evoked by the alpha2 adrenergic receptor agonist clonidine and to a lesser extent by the beta adrenergic receptor agonist isoproterenol. Inhibitory responses to 5-HT were partially mimicked by application of the 5-HT(1A) receptor agonist 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT) and of the 5-HT2 receptor agonist alpha-methyl-5-hydroxytryptamine (ALPHA-MET-5-HT). The latter evoked excitatory responses in some cases. Both 5-HT agonists were more effective on VA than on VL neurons. The effects evoked by agonists were at least partially blocked by respective antagonists. These results suggest that although both 5-HT and NA depress neuronal firing rate, their effects differ in time course and in the amount of inhibition; besides aminergic modulation is differently exerted on VA and VL.

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PubMed2005

Effects of 5-hydroxytryptamine on the neuronal firing rate of bulbar reticular neurons.

The effects of 5-hydroxytryptamine (5-HT) on neuronal firing rate were studied in the reticular gigantocellular nucleus (GRN) and, for a comparison, in the interstitial (IRN), the parvicellular (PRN) and the lateral (LRN) nuclei, sharing some of GRN functional characteristics. Unitary extracellular recordings performed in anesthetized rats demonstrated that microiontophoretic application of 5-HT modulated the background firing rate in 92% of GRN, in 100% of IRN and LRN, and in 77% of PRN tested neurons. In GRN, 5-HT application induced excitatory responses in 49% of the neurons tested and inhibitions in 43% of them. Both types of effects were dose dependent and appeared scattered throughout the nucleus. Enhancements and decreases of firing rate in response to 5-HT application were also recorded in IRN (58% and 42% respectively), LRN (43% and 57%) and PRN (36% and 41%). The 5-HT(1A) receptor agonist 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT) mimicked 5-HT evoked inhibitions in all the nuclei tested and induced weak inhibitory responses also in neurons excited by 5-HT. The 5-HT2A receptor agonist alphamethyl-5-hydroxytryptamine (alpha-me-5-HT) mimicked excitatory as well as inhibitory responses to 5-HT, the former prevailing in GRN and the latter in the remaining reticular nuclei. Both excitatory and inhibitory responses to 5-HT were partially or totally blocked by the application of 5-HT2 receptor antagonist ketanserin. It is concluded that an extended, strong and differentiated control is exerted by 5-HT on the electrical activity of bulbar reticular neurons. Both 5-HT(1A) and 5-HT(2A) receptors mediate these effects, but the involvement of other receptors appears probable.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2004

Alpha 2- and beta-adrenoceptors differentially modulate GABAA- and GABAB-mediated inhibition of red nucleus neuronal firing.

In mesencephalic red nucleus (RN), GABA-induced inhibition of neuronal firing is modulated by noradrenaline acting on alpha2- and beta-adrenoceptors. Since both GABAA and GABAB receptors are present in the rat RN, we have recorded the firing activity of RN neurons in vivo from anaesthetized rats to study how GABAA- and GABAB-mediated effects are modulated by either alpha2- or beta-adrenoceptor activation. Both the GABAA agonist isoguvacine and the GABAB agonist baclofen depressed the firing of RN neurons. During simultaneous application of clonidine, an alpha2-adrenoceptor agonist, half of the isoguvacine- and baclofen-mediated responses were modified: isoguvacine-mediated inhibition was enhanced by 97% without any change in effect duration, whereas baclofen responses were either increased or slightly reduced in the same number of cases. Application of isoprenaline, a beta-adrenoceptor agonist, increased isoguvacine effect in 66% of neurons without modifying effect duration; the amount of increase (43%) was significantly lower than that induced by clonidine. On the other hand, in the presence of isoprenaline, baclofen response was reduced in 72% of neurons with respect to both the amount (52%) and the duration (34%) of effect. Taken together, these results indicate that alpha2-adrenoceptors mainly enhance GABAA-induced inhibition and induce mixed effects on GABAB response; on the other side, beta-adrenoceptors exert an opposite modulation on GABA effects, respectively, enhancing and depressing GABAA- and GABAB-mediated responses.

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PubMed2001

Serotonin modifies the neuronal inhibitory responses to gamma-aminobutyric acid in the red nucleus: a microiontophoretic study in the rat.

The effects of 5-hydroxytryptamine (5-HT) on the inhibitory responses evoked by gamma-aminobutyric acid (GABA) in neurons of the red nucleus (RN) were studied using a microiontophoretic technique. Extracellular unitary recordings performed in anesthetized rats demonstrated that 5-HT ejection influenced GABA-evoked inhibition in 94% of RN neurons, enhancing them in 52% and depressing them in 46% of cases. Both effects were specific and dose-dependent,although enhancements or depressions of the GABA responses were respectively inversely and directly related to the doses of 5-HT applied. The type of modulation exerted by 5-HT on the GABA responses was independent of the action of the amine on background firing. In fact, 5-HT induced an enhancement of the GABA responses in neurons mostly located in the rostral RN and a depression in those in the caudal RN. The application of 8-hydroxy-2(di-n-propylamino)tetralin, a specific 5-HT(1A) receptor agonist, enhanced GABA responses, whereas alpha-methyl-5-hydroxytryptamine, a 5-HT(2A) receptor agonist, depressed them. Both the 5-HT(2) antagonist methysergide and the 5-HT(2A) selective antagonist ketanserin were able to block partially or totally the depressive action of 5-HT on GABA responses. In contrast, the same 5-HT antagonists mimicked the enhancing action of 5-HT on the GABA responses or were ineffective. Application of bicuculline, a GABA(A) receptor antagonist, enhanced the excitatory action of 5-HT on the background firing and slightly reduced the inhibitory action. It is concluded that 5-HT is able to modulate GABA-evoked responses in RN neurons by acting on both 5-HT(1A) and 5-HT(2A) receptors. The functional significance of a serotonergic control on GABAergic inhibitory effects in RN is discussed.

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PubMed2001

Influence of serotonin on the glutamate-induced excitations of secondary vestibular neurons in the rat.

The excitatory responses evoked by glutamate and its agonists in secondary vestibular neurons of the rat were studied during microiontophoretic application of 5-hydroxytryptamine (5-HT). Ejection of 5-HT modified neuronal responsiveness to glutamate in 86% of the studied units, the effect being a depression of the excitatory responses in two-thirds of cases and an enhancement in the remaining third. 5-HT was also effective in modifying 94% of the responses evoked by N-methyl-d-aspartate (NMDA), inducing a depressive effect in 76% of cases and an enhancement in the remaining ones. Quisqualate-evoked effects were depressed and enhanced by 5-HT in about the same number of cases; in contrast, kainate-evoked responses were enhanced. The depressive action of 5-HT was mimicked by application of alpha-methyl-5-hydroxytryptamine (alpha-Me-5-HT), a 5-HT(2) receptor agonist, whereas the enhancing effect could be evoked by application of 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT), a selective 5-HT(1A) receptor agonist. The 5-HT(2) receptor antagonist ketanserin was able to reduce, but not to block totally, the depressive action of 5-HT on glutamate- or NMDA-evoked responses. No significant difference was detected between neuronal responses in the lateral and the superior vestibular nucleus. These results indicate that 5-HT is able to modulate the responsiveness of secondary vestibular neurons to excitatory amino acids. Its action is mostly depressive, involves 5-HT(2) receptors, and is exerted on NMDA receptors. A minor involvement of other 5-HT receptors (at least 5-HT(1A)) and other glutamate receptors (for quisqualate and kainate) in the modulatory action of 5-HT is plausible.

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PubMed2000

Neurotransmitter-mediated control of neuronal firing in the red nucleus of the rat: reciprocal modulation between noradrenaline and GABA.

The electrical activity of neurons from the red nucleus, a mesencephalic structure involved in motor control, is under the influence of several neurotransmitters released from afferent fibers and/or from local interneurons. We have investigated the combined effects of gamma-aminobutyric acid (GABA) and noradrenaline (NA), both present at high levels in the red nucleus, on the firing activity of single rubral neurons recorded extracellularly in vivo on anesthetized adult rats. NA inhibited the firing activity of a large part of rubral neurons and induced excitatory or biphasic inhibitory/excitatory effects in a smaller group of cells. Neuronal firing was also inhibited by GABA in all the cells studied. When the effect of GABA was tested during continuous applications of NA, the magnitude of GABA response was modified in 58% of the cells: the effect of GABA was potentiated by NA in half of the responding neurons and was decreased in the remaining half. NA-induced potentiation of GABA response was mimicked by the alpha(2)-adrenoceptor agonist clonidine and was abolished by the alpha(2)-adrenoceptor antagonist yohimbine. On the other side, the decrease of GABA response was reproduced by the beta-adrenoceptor agonist isoprenaline and was blocked by timolol, an antagonist of beta-adrenoceptors. Neuronal firing activity was reduced by nipecotic acid, an inhibitor of GABA reuptake mechanism, and was instead increased during application of the GABA(A) receptor antagonist bicuculline, suggesting that rubral neurons in vivo were under tonic control by endogenous GABA. Both the inhibitory and the excitatory effects of NA were reduced in the presence of nipecotic acid and were instead potentiated during application of bicuculline, suggesting that NA responses were modified by endogenous GABA. Taken together, our results indicate a reciprocal modulation between the effects of GABA and NA on neuronal firing activity in the red nucleus of the rat: GABA depresses the responsiveness of rubral neurons to NA, whereas NA is able either to potentiate or to decrease the effects of GABA by activation of alpha(2)- and beta-adrenoceptors, respectively. The functional significance of such interaction, as well as the possible implication in diseases affecting motor control, will be discussed.

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PubMed1998

Electromyographic effects of serotonin application into the lateral vestibular nucleus.

Electromyographic responses (EMGs) of limb muscles were studied during microiontophoretic application of 5-hydroxytryptamine (5-HT) into the lateral vestibular nucleus (LVN) or the spinal vestibular nucleus (SpVe) of anaesthetized rats. The aim was to ascertain whether the level of 5-HT in these nuclei was able to modulate muscle responsiveness. Increased levels of 5-HT in LVN (and to a weaker extent in SpVe) enhanced the EMGs of proximal extensor muscles and depressed those of flexors. The 5-HT2A receptor antagonist ketanserin, applied into the LVN, prevented 5-HT effects on EMG-evoked responses. It is concluded that 5-HT can modulate the motor output via the vestibulospinal pathway, exerting a differential control over flexor and extensor muscles.

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PubMed1998

5-Hydroxytryptamine modifies neuronal responses to glutamate in the red nucleus of the rat.

The effects of 5-hydroxytryptamine (5-HT) on the responses of red nucleus (RN) neurones to glutamate (glu) and its agonists were studied using a microiontophoretic technique in anaesthetised rats. Extracellular unitary recordings of RN neuronal activity showed that 5-HT application induced a significant and reversible depression of glu-evoked excitations in 85% of the RN units tested. This effect was independent of the action of the amine on background firing, which appeared enhanced in the majority of cases but was either depressed or uninfluenced in other cases. Microiontophoretic 5-HT also depressed the excitatory responses evoked in RN neurones by electrical stimulation of sensorimotor cortex. Methysergide application, which prevented the enhancing effects of 5-HT on the background firing, was scarcely effective in antagonising the depression of glu responses. In contrast, the serotonergic effects on the glu responses were reduced by the iontophoretically applied antagonist of 5-HT1A receptors, NAN-190. Microiontophoretic 5-HT was also able to influence the neuronal responses evoked by glu agonists quisqualate (quis) and N-methyl-D-aspartate (NMDA), acting on non-NMDA and NMDA receptors respectively. In fact 5-HT depressed quis-evoked excitations and induced mixed effects on NMDA responses, which were reduced in 45%, enhanced in 34% and unmodified in 21% of the units tested. These results suggest that 5-HT is able to modulate the motor glutamatergic input to RN by acting mostly on non-NMDA receptors. The modulation of non-NMDA and NMDA receptors by 5-HT in the RN appears significant and its functional meaning is discussed.

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PubMed1996

Noradrenaline modifies the spontaneous spiking activity of red nucleus neurons in the rat by activation of alpha 2- and beta-adrenoceptors.

We have investigated the effects of noradrenaline (NA) on the spontaneous firing activity of red nucleus (RN) neurons recorded extracellularly in anesthetized rats by using an in vivo electrophysiological technique. Microiontophoretic applications of NA (5-100 nA for 30 s) modified the background firing rate in 99 out of 124 neurons and three different patterns of response were observed in distinct cells. In 61% of the responding neurons NA decreased the mean firing rate, whereas 22% of the neurons responded to NA application with an increase of their spiking activity; in a smaller group of cells (17%) NA exerted a biphasic inhibitory/excitatory effect on the spontaneous firing rate. The effects of NA were reversible and dose-dependent. From histological examination, the neurons responding to NA with a purely inhibitory effect were scattered throughout the RN. On the other hand, the neurons responding to NA with an excitation were found to be more numerous in the dorso-medial part of the RN, whereas the neurons in which NA induced biphasic effects appeared to be segregated in the outer lateral portion of the RN. The alpha 2-adrenoceptor antagonist yohimbine completely blocked the inhibitory effect of NA but was unable to antagonize the excitatory response. In addition, the inhibitory effect of NA was mimicked by clonidine, a selective agonist of alpha 2-adrenoceptors; clonidine had no effect on those cells which responded to NA with an increase of the mean firing rate. The excitatory effect of NA was mimicked by the beta-receptor agonist isoprenaline and was antagonized by timolol, a selective antagonist of beta-adrenoceptors. Isoprenaline was ineffective in those cells in which NA exerted inhibitory responses. Taken together, our results indicate that the inhibitory effect of NA on the firing activity of rat RN neurons were mediated by alpha 2-adrenoceptors, whereas beta-adrenoceptors were responsible for the excitatory effects.

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PubMed1995

Neuronal responses to 5-hydroxytryptamine in the red nucleus of rats.

The effects of microiontophoretic 5-hydroxytryptamine (5-HT) on the firing rate of red nucleus (RN) neurons were studied in urethane-anesthetized rats. The background discharge rate of almost all the neurons tested (97%) was modified by 5-HT, and generally increased (89%). Responses were dose dependent. Twenty-three percent of the excitatory responses were preceded by a short inhibitory phase. No significant difference in the effect of 5-HT was found between those RN neurons that project to the spinal cord and those that do not The excitatory responses to 5-HT were blocked or greatly reduced by the 5-HT antagonists methysergide and ketanserin, and were even reversed in some cases. The 5-HT2/5-HT1A antagonist spiperone, in small doses, also blocked the transient inhibitory phases in addition to the excitatory effects. In RN neurons exhibiting a short-lasting inhibition in the response to 5-HT, the 5-HT1A agonist 8-hydroxy-2(di-n-propyl-amino)tetralin (8-OH-DPAT) induced inhibitory effects. These results support the hypothesis that 5-HT exerts control throughout the RN, mostly by acting on 5-HT2 receptors. Furthermore, an influence of this amine on the electrical activity of small groups of RN neurons by 5-HT1A receptors, and eventually by different mechanisms, appears probable. The functional significance of serotoninergic control of RN neuronal activity is discussed.

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PubMed1993

Excitatory and inhibitory effects of 5-hydroxytryptamine on the firing rate of medial vestibular nucleus neurons in the rat.

The effects of microiontophoretic application of 5-hydroxytryptamine (5-HT) on the neuronal firing rate of the medial vestibular nucleus (MVN) were studied in anaesthetized rats. Ninety-three % of the units modified their background activity following 5-HT iontophoresis, enhancements of the firing rate being recorded in 42%, decreases in 38% and biphasic effects in 13%. 5-HT antagonists methysergide and ketanserin blocked the excitatory but not the inhibitory responses to 5-HT. These latter were, however, mimicked by 5-HT agonists 5-methoxy-N,N-dimethyltryptamine (5MeODMT) and 8-hydroxy-2(di-n-propyl-amino)tetralin (8-OH-DPAT). It is concluded that 5-HT can variously influence the background activity of MVN neurons and that 5-HT2 and probably 5-HT1A receptors are involved in the responses.

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PubMed1993

Effects of noradrenaline on the firing rate of vestibular neurons.

The effects of microiontophoretic noradrenaline on the firing rate of neurons located in the vestibular complex have been studied in anaesthetized rats. Eighty-five per cent of the neurons tested in all the vestibular nuclei modified their background firing rate upon noradrenaline application, generally by reducing it (86% of them). In few cases inhibitions were followed by a rebound. Responses were dose-dependent. No significant difference was found between vestibular neurons projecting to the spinal cord and those delivering their fibres to the oculomotor complex. Phentolamine, an alpha-adrenergic antagonist, blocked the noradrenaline-evoked inhibitions, whereas beta-adrenergic antagonist timolol was ineffective or enhanced them. Furthermore, responses were blocked by yohimbine, an alpha 2-adrenergic antagonist, and mimicked by clonidine, an alpha 2-adrenergic agonist, in the majority of neurons. In few cases prazosin, an alpha 1-adrenergic antagonist, was able to antagonize weak inhibitions and phenylephrine, an alpha 1-adrenergic agonist, to evoke an inhibitory effect blocked by prazosin. Isoproterenol, a beta-adrenergic agonist was totally ineffective on the neuronal firing rate. It is concluded that noradrenaline can modify the level of neuronal activity in the vestibular complex by acting mostly, but not exclusively, through alpha 2-adrenergic receptors. An influence of noradrenergic systems on the vestibular function by a direct action of noradrenaline inside the vestibular nuclei is proposed.

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PubMed1993

Serotonin-evoked modifications of the neuronal firing rate in the superior vestibular nucleus: a microiontophoretic study in the rat.

Microiontophoretic ejection (10-100 nA) of serotonin (5-hydroxytryptamine) into the superior vestibular nucleus induced modifications of the mean firing rate in 87% of the neurons examined. The responses to 5-hydroxytryptamine application were excitatory in 48% of the cells, inhibitory in 29%, and biphasic (inhibitory/excitatory) in the remaining 10%. The excited neurons were scattered throughout the nucleus; the units inhibited or characterized by biphasic responses were distinctly more numerous in the ventrolateral sector of the nucleus. The magnitude of both excitatory and inhibitory effects was dose-dependent. The excitatory responses to 5-hydroxytryptamine were blocked or greatly reduced by two 5-hydroxytryptamine antagonists, methysergide and ketanserin, or even reversed in many cases. Inhibitory responses were enhanced by simultaneous application of 5-hydroxytryptamine antagonists in half of the units studied. In the remaining units, ketanserin left the response unmodified, whereas methysergide reduced but never quite blocked it. The application of 5-methoxy-N,N- dimethyltryptamine, a 5-hydroxytryptamine agonist more effective on 5-hydroxytryptamine1 than on 5-hydroxytryptamine2 receptors, and of 8-hydroxy-2(di-n-propyl-amino) tetralin, a 5-hydroxytryptamine1A-specific agonist, induced a decrease in the firing rate which was unaffected by methysergide. These results support the hypothesis that 5-hydroxytryptamine exerts various functions throughout the superior vestibular nucleus by various receptors and that the inhibitory action is limited to an area of it.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1993

Glutamate immunocytochemistry in the dorsal horn after injury or stimulation of the sciatic nerve of rats.

Glutamate is a major neurotransmitter of fine afferent fibers to the spinal cord. Neuropeptides are also released by the same fibers. We explored, by quantitative immunocytochemistry, the effects of two experimental manipulations of peripheral nerves on the levels of these two classes of mediators. Glutamate levels in the superficial dorsal horn of rats increased after chronic loose ligature of the sciatic nerve, a model for hyperpathic peripheral neuropathy. A similar increase was observed acutely, after stimulation of C fibers, but not A fibers, in the sciatic nerve. In contrast, immunostaining for substance P and calcitonin gene-related peptide decreased in the same region with both manipulations. The decrease in immunocytochemical levels of peptides is in agreement with previous observations and can result from activity-related depletion. We propose that the increase in glutamate levels reflects differences in the regulation and kinetics of amino acid versus peptide neuromediators.

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PubMed1992

Computerized topographical analysis of functionally homogeneous neuronal sets.

A computer-assisted analysis of the spatial distribution of neurons having homogeneous characteristics is described in this paper. The camera lucida drawings of sections of a brain nucleus and the points representing the neurons labeled on the basis of a specific behavior of discharge rates were digitized on a personal computer Amiga 2000 or IBM compatible. Our software provided: a) the computerized, stereotaxically oriented reconstruction of the stored sections and of the plotted neurons; b) the identification within each section of the mass center (MC) of the units sharing a given behavior and of the area where the density of such neurons was maximal (MDA). The routine was tested on the spatial distribution of neuronal responses to serotonin in the lateral vestibular nucleus.

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PubMed1990

Effects of 5-hydroxytryptamine on the firing rates of neurons of the lateral vestibular nucleus in the rat.

5-hydroxytryptamine (5-HT) was delivered microiontophoretically (20-80 nA) to cells of the lateral vestibular nucleus of anaesthetized rats to test its influence on the spontaneous activity of single neurons. 5-HT increased the rate of firing of 94% of the units tested. The enhancement persisted for up to 700 s after the end of the 5-HT ejection and the maximum magnitude of the excitation (10-3400%) showed a hyperbolic correlation (rho = 0.86) with background firing. In 43% of units the enhancement was preceded by a short-lasting (less than 105 s) depression of the neuronal firing rate, the magnitude of which was unrelated to the background mean firing rate. Both components of the 5-HT response were dose-dependent. Only the excitatory responses were antagonized by metergoline, methysergide and ketanserin. The putative 5-HT agonist, 5-methoxy-N,N-dimethyltryptamine, applied microiontophoretically, depressed the background firing rate and was not antagonized by methysergide. These results demonstrate that 5-HT modifies the responsiveness of vestibular neurons and suggest that at least two mechanisms and maybe two types of receptors are activated by 5-HT in this nucleus.

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PubMed1990

Effects of motor cortex and single muscle stimulation on neurons of the lateral vestibular nucleus in the rat.

The neuronal responses to stimulation of motor cortical sites and of forelimb single muscles were studied in the lateral vestibular nucleus of anaesthetized rats. Of the 228 neurons tested for response to stimulation of contralateral motor cortex, 63% responded to cortical sites controlling extensor muscles and 30% to those controlling flexors. The corresponding figures for responders to ipsilateral stimulation were 34 and 21%. Vestibulospinal units responded to cortical sites controlling extensor and flexor muscles whereas the remaining lateral vestibular nucleus neurons, very reactive to cortical sites controlling extensor muscles, responded little to contralateral and not at all to ipsilateral cortical sites controlling flexor muscles. The effects evoked by contralateral cortical sites controlling extensors varied, those induced by cortical sites controlling flexors were inhibitory in 77% of cases. The responses to ipsilateral motor cortex stimulation differed not so much by cortical sites controlling extensor or flexor muscles as by whether the neuron was in the dorsal or ventral zone of the lateral vestibular nucleus: mixed in the former, all inhibitory in the latter. Of the lateral vestibular nucleus units tested for response to stimulation of ipsilateral or contralateral forelimb distal muscles, only 11% responded. All the vestibulospinal units responsive to muscle stimulation lay in the dorsal zone of the nucleus. The remainder, dorsal or ventral, were not responsive to contralateral muscles. Single lateral vestibular nucleus cells influenced both by ipsilateral muscle and by contralateral motor cortex made up 24% of the pool, vestibulospinal and non-vestibulospinal. They fell into three groups: responsive to one or both structures but responding more strongly to combined stimulation; responsive to each of the two structures but showing a response to combined stimulation not significantly different from that evoked by the cortex alone; responsive only to combined stimulation. The lateral vestibular nucleus units included in these three groups accounted for 29% of those tested for response to extensor muscles and cortical sites controlling extensors and 15% of those tested for response to flexor muscles and cortical sites controlling flexors. Twenty-five per cent of the vestibulospinal neurons responded both to contralateral muscles and to ipsilateral motor cortex stimulation but none of the non-vestibulospinal neurons responded to both. All the responders to both were in the dorsal zone of the lateral vestibular nucleus and responded to extensor stimuli, always in the same way. These results indicate that motor cortex output exerts a major influence on lateral vestibular nucleus discharges, while the muscle afferents have a modulatory influence on the lateral vestibular nucleus responses to cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed1990

Effects of glutamate on the serotonin-induced responses of vestibular neurons.

The aim of this work was to verify whether and how spontaneous or glutamate(GLU)-induced enhancements of the neuronal firing rate modified the responsiveness of the vestibular neurons to microiontophoretic application of serotonin (5-HT). During experiments performed on anaesthetized Wistar rats the responses to 5-HT applications were studied in neurons of the lateral vestibular nucleus identified by the antidromic activation upon stimulation of the vestibulospinal tract. The magnitude (in percent) of the 5-HT induced excitatory responses decreased (hyperbolic correlation, r = 0.91) when the background mean firing rate was enhanced spontaneously or by long-lasting application of GLU. Even in high-discharging units, the response never changed its sign. The trend to a depression of the response to 5-HT in function of the background discharge was observed when either the enhancement of firing occurred spontaneously and it was induced by an application of GLU, no significant difference (F-test) being found between the two cases. It is concluded that serotoninergic afferents can exert a strong control upon the vestibular neurons when the background activity is depressed, and only a weak influence when the neuronal firing is enhanced by other excitatory afferents. It remains to verify whether the type of interference observed between GLU and 5-HT is specific or can be also detected between 5-HT and other excitatory neuromediators.

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