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Biomedical subjects

C de Montigny

Publications and source records attributed to C de Montigny.

At least 109 records · Page 6Linked to original sources
PubMed1989

Apparent absence of serotonin1B receptors in biopsied and post-mortem human brain.

In order to determine if post-mortem delays could account for the apparent absence of 5-HT1B sites reported in human brain, 5-HT1B binding parameters were determined in fresh and fresh-frozen cortical biopsies and compared to results obtained in post-mortem tissues. Binding parameters and in vitro receptor autoradiography were performed by using two different ligands which have been shown to label 5-HT1B sites, namely [3H]5-HT, in presence of 100 nM 8-OH-DPAT, and [125I]cyanopindolol, in presence of 10 microM (-)isoproterenol. No specific binding was detected with [125I] cyanopindolol in either fresh cortical biopsies or post-mortem tissues, suggesting that the apparent absence of 5-HT1B receptor sites reported earlier was not related to long post-mortem delays. Some specific labelling was seen with [3H]5-HT, in presence of 8-OH-DPAT. This binding, which is unlikely to be to the 5-HT1B type, could represent labelling to the 5-HT1D or 5-HT1E sites.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1989

Domoic acid, the alleged "mussel toxin," might produce its neurotoxic effect through kainate receptor activation: an electrophysiological study in the dorsal hippocampus.

Domoic acid, an excitatory amino acid structurally related to kainate, was recently identified as being presumably responsible for the recent severe intoxication presented by more than 100 people having eaten mussels grown in Prince Edward Island (Canada). The amino acid kainate has been shown to be highly neurotoxic to the hippocampus, which is the most sensitive structure in the central nervous system. The present in vivo electrophysiological studies were undertaken to determine if domoic acid exerts its neurotoxic effect via kainate receptor activation. Unitary extracellular recordings were obtained from pyramidal neurons of the CA1 and the CA3 regions of the rat dorsal hippocampus. The excitatory effect of domoic acid applied by microiontophoresis was compared with that of agonists of the three subtypes of glutamatergic receptors: kainate, quisqualate, and N-methyl-D-aspartate. In CA1, the activation induced by domoic acid was about threefold greater than that induced by kainate; identical concentrations and similar currents were used. In CA3, domoic acid was also three times more potent than kainate. However, the most striking finding was that domoic acid, similar to kainate, was more than 20-fold more potent in the CA3 than in the CA1 region, whereas no such regional difference could be detected with quisqualate and N-methyl-D-aspartate. As the differential regional response of CA1 and CA3 pyramidal neurons to kainate is attributable to the extremely high density of kainate receptors in the CA3 region, these results provide the first electrophysiological evidence that domoic acid may produce its neurotoxic effects through kainate receptor activation.

Action Potentials↗
PubMed1989

Electrophysiological assessment of putative antagonists of 5-hydroxytryptamine receptors: a single-cell study in the rat dorsal raphe nucleus.

The intravenous administration of low doses of lysergic acid diethylamide (LSD) or of the selective 5-hydroxytryptamine1A (5-HT1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) depresses the firing activity of dorsal raphe 5-HT-containing neurons, presumably via the activation of 5-HT1A receptors. The present studies were undertaken to determine the effect of different types of 5-HT receptor antagonists on this effect of LSD and 8-OH-DPAT. (-)-Propranolol (2 mg/kg i.v.), methiothepin (2 mg/kg i.p., twice daily for 4 days followed by an additional dose of 2 mg/kg i.p., prior to the experiment), pelanserine (0.5 mg/kg i.v.), and indorenate (125 micrograms/kg i.v.) failed to block the effects of either LSD or 8-OH-DPAT on the firing activity of 5-HT neurons of the dorsal raphe nucleus. However, spiperone (1 mg/kg i.v.) significantly reduced the effect of both LSD and 8-OH-DPAT. These results indicate that, among the five putative 5-HT receptor antagonists tested, only spiperone can antagonize the suppressant effect of 5-HT receptor agonists on the firing of dorsal raphe 5-HT neurons.

5-Methoxytryptamine↗
PubMed1989

Reduced neuroexcitatory effect of domoic acid following mossy fiber denervation of the rat dorsal hippocampus: further evidence that toxicity of domoic acid involves kainate receptor activation.

Domoic acid, an excitatory amino acid structurally related to kainic acid, has been shown to be responsible for the severe intoxication presented, in 1987, by more than one hundred and fifty people having eaten mussels grown in Prince Edward Island (Canada). Unitary extracellular recordings were obtained from pyramidal neurons of the CA3 region of the rat dorsal hippocampus. The excitatory effects of microiontophoretic applications of domoic acid and of the agonists of the two other subtypes of glutamatergic receptors, quisqualate and N-methyl-D-aspartate, were compared on intact and colchicine-lesioned sides. Similar to what has been previously found for kainate, the colchicine lesion of the mossy fiber projections induced a 95% decrease of the neuronal responsiveness to domoic acid, whereas the effect of quisqualate was unchanged and that of N-methyl-D-aspartate was only slightly decreased. These results provide further electrophysiological evidence that domoic acid is a potent agonist of kainate receptors and that it may produce its neuroexcitatory and neurotoxic effects, in the hippocampal CA3 region, through activation of kainate receptors located on the mossy fiber terminals.

Animals↗
PubMed1988

Electrophysiological characterization of adrenoceptors in the rat dorsal hippocampus. I. Receptors mediating the effect of microiontophoretically applied norepinephrine.

The rat hippocampus receives a dense noradrenergic innervation originating exclusively from the locus coeruleus. The present electrophysiological study was undertaken to characterize the adrenoceptor mediating the suppressant effect of microiontophoretically applied norepinephrine (NE) on CA1 and CA3 dorsal hippocampus pyramidal neurons of the rat. The rank order of potency of microiontophoretically applied agonists, in suppressing the firing rate of hippocampus pyramidal neurons was: oxymetazoline greater than NE greater than phenylephrine greater than isoproterenol greater than clonidine. In the hippocampus, oxymetazoline was more potent than NE, whereas it was ineffective in the lateral geniculate nucleus where the effect of NE is mediated by an alpha 1-adrenoceptor. Low currents of clonidine antagonized the effect of NE suggesting that clonidine may exert a partial agonistic effect. The rank order of potency of i.v. administered adrenergic antagonists in blocking the suppressant effect of microiontophoretically applied NE was: idazoxan much greater than prazosin much greater than propranolol. Idazoxan also blocked the effect of oxymetazoline, phenylephrine, and isoproterenol but did not modify the effect of microiontophoretically applied gamma-aminobutyric acid (GABA). In addition, idazoxan, applied by microiontophoresis, readily blocked the suppressant effect of NE without affecting that of GABA. These results suggest that the suppressant effect of microiontophoretically applied NE on rat dorsal hippocampus pyramidal neurons is primarily mediated by alpha 2-adrenoceptors.

Action Potentials↗
PubMed1988

Electrophysiological characterization of adrenoceptors in the rat dorsal hippocampus. II. Receptors mediating the effect of synaptically released norepinephrine.

The present studies were undertaken to determine the nature of the receptors mediating the effects of endogenous norepinephrine (NE) released by stimulation of the locus coeruleus (LC) on the firing activity of dorsal hippocampus pyramidal neurons in the rat. Unitary activity of CA3 pyramidal neurons was recorded extracellularly. In most neurons, the LC stimulation produced a period of suppression, followed by a period of activation. The suppression was selectively blocked by prazosin, an alpha 1-adrenoceptor antagonist, whereas the activation was selectively blocked by propranolol, a beta-adrenoceptor antagonist. Idazoxan, an alpha 2-adrenoceptor antagonist, increased the period of suppression without affecting the period of activation. The effectiveness of microiontophoretic applications of NE on the same neurons was reduced by idazoxan, but was modified neither by propranolol nor prazosin. Lesion of the central noradrenergic system by intracerebroventricular 6-hydroxydopamine markedly decreased the NE content in the hippocampus in all rats but the effectiveness of the LC stimulation was reduced only in rats with a depletion greater than 90%. These results demonstrate that the suppressant effect of endogenous NE released by LC stimulation on hippocampus pyramidal neurons is mediated by an alpha 1-adrenoceptor and suggest that its late excitatory effect might involve beta-adrenoceptors. Since the effect of microiontophoretically applied NE on the same neurons is mediated by alpha 2-adrenoceptors, these data provide evidence that, in the rat hippocampus, postsynaptic alpha 1-adrenoceptors are intrasynaptic, whereas postsynaptic alpha 2-adrenoceptors are extrasynaptic.

Action Potentials↗
PubMed1988

Increased neuronal responsiveness to cholecystokinin and dopamine induced by lesioning mesolimbic dopaminergic neurons: an electrophysiological study in the rat.

In the rat, cholecystokinin (CCK) and dopamine (DA) coexist in a subpopulation of neurons of the ventral tegmental area (VTA) projecting to the nucleus accumbens. However, in the dorsal hippocampus, dopaminergic projections from the VTA do not contain CCK, the latter neurotransmitter being mainly localized in intrinsic hippocampal neurons. The present experiments were undertaken in order to compare the interactions of CCK and DA and the effects of lesioning VTA dopaminergic neurons in a region where these neurotransmitters coexist and in one where they do not. The effects of microiontophoretic applications of CCK, kainate (KA), glutamate (GLU) and DA were determined in control rats and in rats pretreated with a local injection of 6-hydroxydopamine (6-OHDA) in the VTA. In the nucleus accumbens and in the hippocampus of intact rats, DA exerted a similar depressant effect whether applied during CCK-, KA- or GLU-induced activations. The 6-OHDA lesion enhanced responsiveness of accumbens neurons to KA, GLU and CCK (the responsiveness to this latter peptide being increased by more than 15-fold) and the depressant effect of DA when applied during neuronal activation by KA or GLU but not when the same neurons were activated with CCK. In the dorsal hippocampus, the 6-OHDA lesion enhanced neuronal responsiveness to KA and DA in the CA1, but not in the CA3 region, whereas the responsiveness to CCK remained unchanged in both regions. These results suggest a physiological role for the coexistence of CCK and DA in the nucleus accumbens. The induction of a supersensitivity to DA in the CA1, but not in the CA3, region of the dorsal hippocampus following a VTA lesion is consistent with the regional distribution of the dopaminergic innervation in this structure.

Action Potentials↗
PubMed1988

Long-term 5-HT reuptake blockade, but not monoamine oxidase inhibition, decreases the function of terminal 5-HT autoreceptors: an electrophysiological study in the rat brain.

5-HT-containing terminals possess autoreceptors which modulate the release of 5-HT into the synaptic cleft. Tritiated imipramine ([3H]IMI), and more specifically [3H]citalopram and [3H]paroxetine, bind to a site associated with the 5-HT reuptake carrier on the 5-HT terminals. The function of terminal 5-HT autoreceptors is decreased following long-term treatment with the 5-HT reuptake blocker citalopram. The present study was undertaken to determine whether an increased synaptic availability of 5-HT or, the occupation of the [3H]IMI site, were responsible for this modification. Unitary extracellular recordings were obtained from CA3 dorsal hippocampus pyramidal neurons under chloral hydrate anesthesia in rats treated daily with fluoxetine (10 mg/kg/day X 14 days), a selective 5-HT reuptake blocker, or clorgyline (1 mg/kg/day X 21 days), an inhibitor of type A monoamine oxidase. The function of the terminal 5-HT autoreceptors was assessed by comparing the effectiveness of the electrical stimulation of the ascending 5-HT pathway on the firing activity of hippocampus pyramidal neurons prior to, and following, the administration of methiothepin, an antagonist of the terminal 5-HT autoreceptor, and, by determining the ratio of effectiveness of 0.8 Hz (S1) and 5 Hz (S2) stimulations. Long-term administration of fluoxetine or clorgyline both increased the efficacy of the stimulation of the 5-HT pathway. However, the enhancing effect of methiothepin on the efficacy of the stimulation was attenuated by the fluoxetine, but not by the clorgyline, treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Validation of the I.T50 method for assessing neuronal responsiveness to microiontophoretic applications: a single-cell recording study.

The I.T50 method consists of determining the charge required to obtain a 50% depression of firing activity of neurons recorded extracellularly with microiontophoretic applications of inhibitory agents. This method has been used successfully to detect modification of neuronal responsiveness, but the limits of its validity had never been determined. In the present study, it was found that the use of microiontophoretic currents greater than 3 nA yielded consistent I.T50 values when serotonin (5-HT) was applied to rat hippocampal pyramidal neurons. The departure from linearity of I.T50 values measured from applications carried out with a very low current (0.5 nA) of 5-HT is probably due to the relatively important contribution of the leak when a minimal ejecting current is used. The responsiveness to 5-HT was not altered by the activation of the recorded neuron produced by acetylcholine.

Animals↗
PubMed1988

Effects of the 5-hydroxytryptamine receptor antagonist, BMY 7378, on 5-hydroxytryptamine neurotransmission: electrophysiological studies in the rat central nervous system.

In the present electrophysiological studies, the effects of the putative 5-hydroxytryptamine (5-HT) receptor antagonist, BMY 7378, on the response of dorsal raphe nucleus 5-HT neurons and of CA3 dorsal hippocampus pyramidal neurons to 5-HT and 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) were investigated in chloral hydrate-anesthetized rats. The effectiveness of microiontophoretically applied 5-HT and 8-OH-DPAT in suppressing the firing activity of both neuronal populations was assessed before and during the microiontophoretic application of BMY 7378. BMY 7378 reduced the effectiveness of 8-OH-DPAT, but not that of 5-HT, in depressing 5-HT neuron firing rate, whereas that of both agonists was reduced by concurrent application of BMY 7378 in the hippocampus. To assess whether endogenous 5-HT also could be antagonized, the response of pyramidal neurons to electrical activation of the 5-HT pathway was determined before and after i.v. BMY 7378. Low doses enhanced the efficacy of the stimulation, whereas higher doses decreased it. The latter finding suggests that BMY 7378 antagonizes the effect of endogenous 5-HT. Three procedures were used to investigate the enhancing effect of BMY 7378 on 5-HT synaptic transmission: 1) administration of BMY 7378 after terminal 5-HT autoreceptor blockade by methiothepin: methiothepin abolished the enhancing effect of BMY 7378; 2) blockade of the effect of RU 24969, a terminal 5-HT autoreceptor agonist: pretreatment with methiothepin, but not with BMY 7378, blocked the effect of RU 24969 on 5-HT synaptic transmission; and 3) administration of BMY 7378 during a reduced level of activation of terminal 5-HT autoreceptors, obtained by lowering the stimulation frequency from 1 to 0.5 Hz: the enhancing effect of BMY 7378 was reduced when the stimulation was delivered at 0.5 Hz. It is concluded that BMY 7378 is an effective antagonist of 5-HT1A receptors in vivo and that the mechanism of its enhancing effect on 5-HT transmission at low doses, although still undetermined, is not due to a competitive interaction at the terminal 5-HT autoreceptor.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1988

Electrophysiological assessment of the effects of antidepressant treatments on the efficacy of 5-HT neurotransmission.

The efficacy of serotoninergic (5-HT) neurotransmission was assessed in the rat brain following different types of antidepressant treatments. First, the firing rate of 5-HT neurons was assessed. Second, the responsiveness of postsynaptic neurons to 5-HT was evaluated by applying directly onto these neurons the neurotransmitter by microiontophoresis. Finally, the effect of the electrical stimulation of the 5-HT pathway on the firing activity of the same postsynaptic neurons was studied in order to determine the efficacy of synaptic transmission. Long-term administration of tricyclic antidepressant drugs induces a sensitization of rat forebrain neurons to 5-HT without altering 5-HT neuron properties. This sensitization results in an enhancement of the effect of the stimulation of the 5-HT pathway on the firing activity of postsynaptic neurons. Long-term administration of antidepressant monoamine oxidase inhibitors also results in an enhancement of the effectiveness of the stimulation of the 5-HT pathway. This is not due to a modification of postsynaptic neuron properties, since there is no enhancement of their responsiveness to 5-HT. Furthermore, the function of the terminal 5-HT autoreceptor is not altered by long-term treatment with a monoamine oxidase inhibitor. Therefore, the enhancement of 5-HT neurotransmission produced by this type of drugs is due to an increased availability of releasable 5-HT. The acute administration of 5-HT reuptake blockers does not enhance the efficacy of the stimulation of the 5-HT pathway. However, their long-term administration produces such an enhancement without altering the responsiveness of postsynaptic neurons to 5-HT. This modification of 5-HT transmission is attributable to a desensitization of the terminal 5-HT autoreceptor, thereby allowing a greater amount of 5-HT to be released per impulse in the synaptic cleft. The electrophysiological assessment of the effects of these different types of antidepressant treatments on the 5-HT system therefore revealed as a common effect an enhancement of 5-HT neurotransmission, albeit each one achieving this via a different mechanism.

Animals↗
PubMed1987

Long-term antidepressant treatment reduces neuronal responsiveness to flurazepam: an electrophysiological study in the rat.

Long-term administration of various types of antidepressant drugs has been recently reported to reduce the density of benzodiazepine receptors in the rat CNS. In the present study, using the microiontophoretic technique, the effect of flurazepam application on cholecystokinin-induced activation of hippocampal pyramidal neurons was assessed in rats treated with the antidepressants desipramine, trimipramine and citalopram, and the antipsychotic chlorpromazine, for 3 weeks. All 3 antidepressant drugs, but not chlorpromazine, reduced the efficacy of flurazepam. A two-week treatment with desipramine produced a similar effect, whereas a one-week treatment with this drug failed to alter the effect of flurazepam. These results constitute further evidence that long-term antidepressant treatment down-regulates benzodiazepine receptors.

Acetylcholine↗
PubMed1987

Short-term lithium treatment enhances responsiveness of postsynaptic 5-HT1A receptors without altering 5-HT autoreceptor sensitivity: an electrophysiological study in the rat brain.

Short-term lithium administration to rats has previously been shown to enhance 5-HT neurotransmission through a modification of 5-HT neuron properties. In the first part of the present study, the effect of lithium on the function of terminal 5-HT autoreceptors was assessed by comparing in controls and lithium-treated rats the differential effect of two frequencies of stimulation (0.8 and 5 Hz) and that of methiothepin, a terminal 5-HT autoreceptor antagonist, on the effectiveness of the electrical activation of the ascending 5-HT pathway in suppressing dorsal hippocampus pyramidal neuron firing activity. Both procedures produced similar effects in controls and lithium-treated rats. In the second part of the study, the function of somatodendritic 5-HT autoreceptors was studied. The effect of intravenous LSD, an agonist of the somatodendritic 5-HT autoreceptor, on the firing activity of 5-HT neurons was not modified by the lithium treatment, whereas that of intravenous 8-OH-DPAT, a 5-HT1A receptor agonist, was increased two-fold. However, lithium did not alter the responsiveness of 5-HT neurons to direct microiontophoretic applications of 8-OH-DPAT as well as of LSD and 5-HT. It is concluded that short-term lithium treatment does not alter the function of terminal and somatodendritic 5-HT autoreceptors and that it enhances the sensitivity of a subset of postsynaptic 5-HT1A receptors involved in controlling 5-HT neuron firing activity, presumably through a feedback loop.

Acetylcholine↗
PubMed1987

Noradrenergic denervation prevents sensitization of rat forebrain neurons to serotonin by tricyclic antidepressant treatment.

The effect of prior lesioning of noradrenergic neurons with 6-hydroxydopamine (6-OHDA) on the ability of amitriptyline to enhance the responsiveness of hippocampal pyramidal neurons to serotonin (5-HT) was examined in Sprague-Dawley rats. In control rats, amitriptyline (5 mg/kg/day for 14 days), administered either by daily injection or by an osmotic minipump, enhanced the responsiveness of these neurons to microiontophoretically applied 5-HT, leaving their responsiveness to norepinephrine (NE) and to acetylcholine unaltered. However, in 6-OHDA-pretreated rats, amitriptyline failed to enhance the responsiveness of hippocampal pyramidal neurons to 5-HT. The effect of NE and, to a lesser extent, that of 5-HT were prolonged in 6-OHDA-pretreated rats, presumably because NE and 5-HT released by microiontophoresis are taken up by NE terminals in the intact rat. The present results provide additional evidence that the integrity of the NE system is required for antidepressant treatments to modify 5-HT neurotransmission.

Acetylcholine↗
PubMed1987

Modification of 5-HT neuron properties by sustained administration of the 5-HT1A agonist gepirone: electrophysiological studies in the rat brain.

The sustained administration of the 5-HT1A agonist gepirone (15 mg/kg/day, s.c.) in the rat produced an initial decrease of the firing activity of dorsal raphe 5-HT neurons which was followed by a progressive recovery to normal after 14 days of treatment. At this point in time, the effect of intravenous lysergic acid diethylamide (LSD) on the firing activity of 5-HT neurons was markedly reduced, whereas those of 8-hydroxy-2-N,N-propylamino-tetralin (8-OH-DPAT) and of gepirone were unchanged; however, the responsiveness of 5-HT neurons to direct microiontophoretic application of 5-HT, LSD, 8-OH-DPAT, and gepirone, but not of GABA, was reduced. The responsiveness of postsynaptic dorsal hippocampus pyramidal neurons to 5-HT, 8-OH-DPAT, and gepirone was not altered by the 14-day gepirone treatment. The effectiveness of the electrical stimulation of the ascending 5-HT pathway in reducing pyramidal neuron firing activity was not significantly modified in rats treated with gepirone for 14 days. Furthermore, this treatment did not alter the function of the terminal 5-HT autoreceptor. It is concluded that the progressive restoration of the firing activity of 5-HT neurons, due to a desensitization of the somatodendritic 5-HT autoreceptor, combined with the direct activation of normosensitive postsynaptic 5-HT1A receptor by gepirone, should result in an augmented tonic activation of postsynaptic 5-HT1A receptors. The progressive appearance of this phenomenon would be consistent with the time course of the clinical anxiolytic, and possibly antidepressant, effects of gepirone.

Animals↗
PubMed1987

Reduced excitatory effect of kainic acid on rat CA3 hippocampal pyramidal neurons following destruction of the mossy projection with colchicine.

Rats were injected unilaterally with colchicine in the dentate gyrus of the dorsal hippocampus. Two weeks later, under urethane anesthesia, extracellular recordings were obtained on both sides from pyramidal neurons of the CA1 and of the CA3 regions of the dorsal hippocampus. Microiontophoresis was used to assess the responsiveness of these neurons to kainate, glutamate and ibotenate. The colchicine injection produced a nearly complete destruction of the granule cells of the ipsilateral dentate gyrus and of their mossy fiber projections to CA3 without apparently affecting other hippocampal neurons. On the lesioned side, the potency of kainate in activating CA3 pyramidal neurons was reduced by 94% compared to the same neurons on the intact side. However, the excitatory effect of glutamate was unchanged and that of ibotenate only slightly reduced. Kainate was 80 times more potent in activating CA3 than CA1 pyramidal neurons on the intact side, whereas this ratio had dropped to 2.6 on the lesioned side. The selective decrease of the effectiveness of kainate in activating CA3 pyramidal neurons following the colchicine lesion suggests that this amino acid, but not glutamate and ibotenate, produces most of its excitatory effect in the intact CA3 region by releasing (an) excitatory neurotransmitter(s) from mossy fibers terminals, the nature of which remains to be identified.

Animals↗
PubMed1987

Pipequaline acts as a partial agonist of benzodiazepine receptors: an electrophysiological study in the hippocampus of the rat.

Pipequaline (PK 8165), a quinoline derivative and a ligand of the benzodiazepine binding site, is a clinically-effective anxiolytic, which is devoid of sedative and anticonvulsant properties. Several biochemical and behavioral studies have indicated that this molecule shares some properties with both agonists and antagonists of benzodiazepine receptors. The present in vivo electrophysiological studies were undertaken to determine the effects of microiontophoretic applications and of intravenous injections of pipequaline on hippocampal pyramidal neurons, activated by kainate, glutamate or acetylcholine and to characterize the effects of pipequaline on the action of benzodiazepines. Intravenously administered pipequaline exerted a partial suppression of activations by kainate, glutamate and acetylcholine. Microiontophoretic applications of pipequaline reduced the neuronal activation by kainate. This effect was blocked by RO 15-1788. In small intravenous doses, pipequaline potentiated the effect of microiontophoretically-applied flurazepam whereas, in larger doses, it suppressed the effects of microiontophoretically-applied flurazepam and of intravenously administered lorazepam on kainate-induced activation. Similarly, microiontophoretic applications of pipequaline blocked the suppressant effect of microiontophoretically-applied flurazepam on kainate-induced activation. These results constitute further evidence that the selective anxiolytic activity of pipequaline might be ascribed to its partial agonistic action on benzodiazepine receptors.

Animals↗