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Klaus G. Reymann - One of the best experts on this subject based on the ideXlab platform.
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ACPD-mediated slow-onset potentiation is associated with cell death in the rat CA1 region in vivo.
Neuropharmacology, 1999Co-Authors: Denise Manahan-vaughan, Thomas Behnisch, Klaus G. ReymannAbstract:Slow-onset potentiation of synaptic transmission in the hippocampus in vitro and in vivo is induced by application of the metabotropic glutamate receptor (mGluR) agonist, 1S,3R-amino cyclopentane 2,3-dicarboxylic acid (ACPD). This study investigated the cellular response in the CA1 region of freely moving rats to ACPD application. Drugs were applied via the lateral cerebral ventricle, and measurements were obtained from the CA1 region via permanently implanted electrodes. ACPD (20 nmol/5 μl) produced a dose-dependent slow-onset potentiation in the CA1 region which lasted over 4 h. Histological evaluation at either 4 h or 7 days following ACPD-injection indicated that slow-onset potentiation was associated with gradual but marked cell death in the CA1 region. Whereas 20 nmol ACPD produced significant CA1 neurotoxicity, concentrations which did not induce potentiation had little or no neurotoxic effect. Both the general mGluR antagonist R,S-α-methyl-carboxyphenylglycine (1 μmol/5 μl), and the group 1 mGluR antagonist (S)-4-carboxyphenylglycine (4CPG, 100 nmol/5 μl) significantly inhibited ACPD-induced neuropathology. In addition, 4CPG inhibited the expression of ACPD-mediated slow-onset potentiation. These results confirm previous findings that in the CA1 region in vivo, slow-onset potentiation is mediated group 1 mGluRs, and indicate that slow-onset potentiation may involve pathological processes.
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1S,3R-ACPD dose dependently induces a slow onset potentiation in the dentate gyrus in vivo
European journal of pharmacology, 1995Co-Authors: Denise Manahan-vaughan, Klaus G. ReymannAbstract:It has been demonstrated by others in vitro that application of 1S,3R-aminocyclopentane-2,3-dicarboxylic acid (ACPD) facilitates long-term potentiation and triggers a slow-onset potentiation in the hippocampus. This study examined the effect of ACPD in the dentate gyrus when applied in vivo. Weak tetanisation produced a short-term potentiation of field excitatory post-synaptic potential (EPSP) and population spike. A similar response was seen upon application of ACPD (40 μM in 5 μl vehicle) via the lateral cerebral ventricle 30 min prior to tetanus, whereas ACPD (80 μM/5 μl) facilitated short-term potentiation into long-term potentiation. (R,S)-α-Methyl-4-carboxyphenyl-glycine (MCPG 200 mM/5 μl), completely inhibited this effect. ACPD had no effect on baseline recordings at 40 and 80 μM/5 μl, however 4 mM/5 μl ACPD induced a slow-onset potentiation of field EPSP and population spike which was maintained for over 4 h. MCPG or d-2-amino-5-phosphonopentanoate (AP5 20 mM/5 μl) applied prior to ACPD completely inhibited this effect. These results suggest that previously reported in vitro effects of ACPD in the CA1 region, also occur in the dentate gyrus in vivo. Furthermore, they confirm that activation of mGlu receptors by ACPD in vivo facilitates long-term potentiation, and indicate that in the dentate gyrus, ACPD-induced slow-onset potentiation is NMDA receptor-dependent.
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1S,3R-ACPD dose-dependently induces a slow-onset potentiation in the rat hippocampal CA1 region in vivo
Neuropharmacology, 1995Co-Authors: Denise Manahan-vaughan, Klaus G. ReymannAbstract:Abstract It has been reported that application of 1S,3R-1-aminocyclopentane 1,3-dicarboxylic acid (ACPD) in vitro triggers a slow-onset potentiation in the hippocampal CA1 region. This study examined the effect of ACPD in the CA1 of freely moving rats. No effect on fEPSP baseline recordings occurred at 40 and 400 μM/5 μ1, however at 4 mM/5 μ1 ACPD induced a slow-onset potentiation. MCPG (200 mM/5 μ1) completely inhibited this ACPD effect. These results indicate that slow-onset potentiation in the CA1 region, also occurs in vivo.
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(1S, 3R)-ACPD protects synaptic transmission from hypoxia in hippocampal slices.
Neuropharmacology, 1993Co-Authors: Thoralf Opitz, Klaus G. ReymannAbstract:The influence of (1S, 3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S, 3R)-ACPD], an agonist of the metabotropic glutamate receptor (mGluR), on recovery from in vitro hypoxia was investigated. Transverse hippocampal slices were exposed to a severe hypoxia, and the recovery of field excitatory postsynaptic potentials (fEPSPs) of CA1 neurons was monitored 1 hr after reoxygenation. If 20 μM (1S, 3R)-ACPD was present during hypoxia, the recovery of the fEPSPs was significantly higher compared to controls. This protective effect was not observed, when the mGLuR-antagonist L-2-amino-3-phosphonopropionate (L-AP3, 300 μM) was coapplied with (1S, 3R)-ACPD.
Denise Manahan-vaughan - One of the best experts on this subject based on the ideXlab platform.
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ACPD-mediated slow-onset potentiation is associated with cell death in the rat CA1 region in vivo.
Neuropharmacology, 1999Co-Authors: Denise Manahan-vaughan, Thomas Behnisch, Klaus G. ReymannAbstract:Slow-onset potentiation of synaptic transmission in the hippocampus in vitro and in vivo is induced by application of the metabotropic glutamate receptor (mGluR) agonist, 1S,3R-amino cyclopentane 2,3-dicarboxylic acid (ACPD). This study investigated the cellular response in the CA1 region of freely moving rats to ACPD application. Drugs were applied via the lateral cerebral ventricle, and measurements were obtained from the CA1 region via permanently implanted electrodes. ACPD (20 nmol/5 μl) produced a dose-dependent slow-onset potentiation in the CA1 region which lasted over 4 h. Histological evaluation at either 4 h or 7 days following ACPD-injection indicated that slow-onset potentiation was associated with gradual but marked cell death in the CA1 region. Whereas 20 nmol ACPD produced significant CA1 neurotoxicity, concentrations which did not induce potentiation had little or no neurotoxic effect. Both the general mGluR antagonist R,S-α-methyl-carboxyphenylglycine (1 μmol/5 μl), and the group 1 mGluR antagonist (S)-4-carboxyphenylglycine (4CPG, 100 nmol/5 μl) significantly inhibited ACPD-induced neuropathology. In addition, 4CPG inhibited the expression of ACPD-mediated slow-onset potentiation. These results confirm previous findings that in the CA1 region in vivo, slow-onset potentiation is mediated group 1 mGluRs, and indicate that slow-onset potentiation may involve pathological processes.
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1S,3R-ACPD dose dependently induces a slow onset potentiation in the dentate gyrus in vivo
European journal of pharmacology, 1995Co-Authors: Denise Manahan-vaughan, Klaus G. ReymannAbstract:It has been demonstrated by others in vitro that application of 1S,3R-aminocyclopentane-2,3-dicarboxylic acid (ACPD) facilitates long-term potentiation and triggers a slow-onset potentiation in the hippocampus. This study examined the effect of ACPD in the dentate gyrus when applied in vivo. Weak tetanisation produced a short-term potentiation of field excitatory post-synaptic potential (EPSP) and population spike. A similar response was seen upon application of ACPD (40 μM in 5 μl vehicle) via the lateral cerebral ventricle 30 min prior to tetanus, whereas ACPD (80 μM/5 μl) facilitated short-term potentiation into long-term potentiation. (R,S)-α-Methyl-4-carboxyphenyl-glycine (MCPG 200 mM/5 μl), completely inhibited this effect. ACPD had no effect on baseline recordings at 40 and 80 μM/5 μl, however 4 mM/5 μl ACPD induced a slow-onset potentiation of field EPSP and population spike which was maintained for over 4 h. MCPG or d-2-amino-5-phosphonopentanoate (AP5 20 mM/5 μl) applied prior to ACPD completely inhibited this effect. These results suggest that previously reported in vitro effects of ACPD in the CA1 region, also occur in the dentate gyrus in vivo. Furthermore, they confirm that activation of mGlu receptors by ACPD in vivo facilitates long-term potentiation, and indicate that in the dentate gyrus, ACPD-induced slow-onset potentiation is NMDA receptor-dependent.
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1S,3R-ACPD dose-dependently induces a slow-onset potentiation in the rat hippocampal CA1 region in vivo
Neuropharmacology, 1995Co-Authors: Denise Manahan-vaughan, Klaus G. ReymannAbstract:Abstract It has been reported that application of 1S,3R-1-aminocyclopentane 1,3-dicarboxylic acid (ACPD) in vitro triggers a slow-onset potentiation in the hippocampal CA1 region. This study examined the effect of ACPD in the CA1 of freely moving rats. No effect on fEPSP baseline recordings occurred at 40 and 400 μM/5 μ1, however at 4 mM/5 μ1 ACPD induced a slow-onset potentiation. MCPG (200 mM/5 μ1) completely inhibited this ACPD effect. These results indicate that slow-onset potentiation in the CA1 region, also occurs in vivo.
S A Eaton - One of the best experts on this subject based on the ideXlab platform.
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Mediation of Thalamic Sensory Responses In Vivo by ACPD‐activated Excitatory Amino Acid Receptors
The European journal of neuroscience, 1993Co-Authors: S A Eaton, David C. Sunter, Peter M. Udvarhelyi, Jeffrey C. Watkins, E. F. Birse, B. Wharton, Thomas E. SaltAbstract:The existence of the so-called metabotropic excitatory amino acid receptor has been known for some years. Various functions have been suggested for this receptor, but the lack of selective antagonists for (IS, 3R)-aminocyclopentane dicarboxylic acid (ACPD) has precluded the direct demonstration of a functional role for this receptor in synaptic processes. We describe here a specific antagonism of the excitatory responses of thalamic neurons to ACPD by two novel antagonists, and a parallel antagonism by these compounds of sensory synaptic responses to noxious stimuli of the same neurons. This provides the first direct pharmacological evidence for a functional role of ACPD-sensitive receptors in central neurotransmission, and indicates that these receptors may play an important part in central sensory processes.
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mediation of thalamic sensory responses in vivo by ACPD activated excitatory amino acid receptors
European Journal of Neuroscience, 1993Co-Authors: S A Eaton, David C. Sunter, Peter M. Udvarhelyi, E. F. Birse, B. Wharton, J C Watkins, T E SaltAbstract:The existence of the so-called metabotropic excitatory amino acid receptor has been known for some years. Various functions have been suggested for this receptor, but the lack of selective antagonists for (IS, 3R)-aminocyclopentane dicarboxylic acid (ACPD) has precluded the direct demonstration of a functional role for this receptor in synaptic processes. We describe here a specific antagonism of the excitatory responses of thalamic neurons to ACPD by two novel antagonists, and a parallel antagonism by these compounds of sensory synaptic responses to noxious stimuli of the same neurons. This provides the first direct pharmacological evidence for a functional role of ACPD-sensitive receptors in central neurotransmission, and indicates that these receptors may play an important part in central sensory processes.
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excitatory actions of the metabotropic excitatory amino acid receptor agonist trans 1 amino cyclopentane 1 3 dicarboxylate t ACPD on rat thalamic neurons in vivo
European Journal of Neuroscience, 1991Co-Authors: T E Salt, S A EatonAbstract:The metabotropic excitatory amino acid receptor agonist trans-(+/-)-1-amino-cyclopentane-1,3-dicarboxylate (t-ACPD) was applied to rat ventrobasal thalamic neurons by iontophoresis. This agonist typically evoked an excitatory response which was slower in onset and of longer duration than responses to the other excitatory amino acid agonists, N-methyl-aspartate, kainate or (R,S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate. Responses to t-ACPD were resistant to the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3-dione, 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid and kynurenate. These results suggest that t-ACPD may exert its effects via the so-called 'metabotropic' excitatory amino acid receptor. The putative antagonists at this receptor, D-2-amino-4-phosphono-butyrate (D-AP4), L-2-amino-4-phosphono-butyrate (L-AP4) and L-2-amino-3-phosphono-propionate (L-AP3), were able to reduce responses to t-ACPD under certain circumstances. However, such antagonism was always accompanied by similar reductions in excitatory responses to other agonists. These non-selective effects would appear to limit the usefulness of AP4 and AP3 as antagonists of t-ACPD.
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Excitatory Actions of the Metabotropic Excitatory Amino Acid Receptor Agonist, trans‐(±)‐1‐amino‐cyclopentane‐1,3‐dicarboxylate (t‐ACPD), on Rat Thalamic Neurons In Vivo
The European journal of neuroscience, 1991Co-Authors: T E Salt, S A EatonAbstract:The metabotropic excitatory amino acid receptor agonist trans-(+/-)-1-amino-cyclopentane-1,3-dicarboxylate (t-ACPD) was applied to rat ventrobasal thalamic neurons by iontophoresis. This agonist typically evoked an excitatory response which was slower in onset and of longer duration than responses to the other excitatory amino acid agonists, N-methyl-aspartate, kainate or (R,S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate. Responses to t-ACPD were resistant to the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3-dione, 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid and kynurenate. These results suggest that t-ACPD may exert its effects via the so-called 'metabotropic' excitatory amino acid receptor. The putative antagonists at this receptor, D-2-amino-4-phosphono-butyrate (D-AP4), L-2-amino-4-phosphono-butyrate (L-AP4) and L-2-amino-3-phosphono-propionate (L-AP3), were able to reduce responses to t-ACPD under certain circumstances. However, such antagonism was always accompanied by similar reductions in excitatory responses to other agonists. These non-selective effects would appear to limit the usefulness of AP4 and AP3 as antagonists of t-ACPD.
T E Salt - One of the best experts on this subject based on the ideXlab platform.
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stereospecific antagonism by α methyl 4 carboxyphenylglycine mcpg of 1s 3r ACPD induced effects in neonatal rat motoneurones and rat thalamic neurones
Neuropharmacology, 1993Co-Authors: David E. Jane, T E Salt, David C. Sunter, P.l.st.j. Jones, P.c.-k. Poor, J C WatkinsAbstract:The (+)-enantiomer of α-methyl-4-carboxyphenylglycine (MCPG) stereoslectively antagonized the depolarization of neonatal rat motoneurones and the excitation of rat thalamic neurons induced by the specific metabotropic glutamate receptor agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylate (ACPD). (+)-MCPG preferentially reduced (1S,3R)-ACPD-induced responses relative to responses induced by (S)-α-amino-3-hydorxy-5-methylisoxazole-4-propionic acid (AMPA) and N-methyl-d-aspartate (NMDA).
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mediation of thalamic sensory responses in vivo by ACPD activated excitatory amino acid receptors
European Journal of Neuroscience, 1993Co-Authors: S A Eaton, David C. Sunter, Peter M. Udvarhelyi, E. F. Birse, B. Wharton, J C Watkins, T E SaltAbstract:The existence of the so-called metabotropic excitatory amino acid receptor has been known for some years. Various functions have been suggested for this receptor, but the lack of selective antagonists for (IS, 3R)-aminocyclopentane dicarboxylic acid (ACPD) has precluded the direct demonstration of a functional role for this receptor in synaptic processes. We describe here a specific antagonism of the excitatory responses of thalamic neurons to ACPD by two novel antagonists, and a parallel antagonism by these compounds of sensory synaptic responses to noxious stimuli of the same neurons. This provides the first direct pharmacological evidence for a functional role of ACPD-sensitive receptors in central neurotransmission, and indicates that these receptors may play an important part in central sensory processes.
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excitatory actions of the metabotropic excitatory amino acid receptor agonist trans 1 amino cyclopentane 1 3 dicarboxylate t ACPD on rat thalamic neurons in vivo
European Journal of Neuroscience, 1991Co-Authors: T E Salt, S A EatonAbstract:The metabotropic excitatory amino acid receptor agonist trans-(+/-)-1-amino-cyclopentane-1,3-dicarboxylate (t-ACPD) was applied to rat ventrobasal thalamic neurons by iontophoresis. This agonist typically evoked an excitatory response which was slower in onset and of longer duration than responses to the other excitatory amino acid agonists, N-methyl-aspartate, kainate or (R,S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate. Responses to t-ACPD were resistant to the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3-dione, 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid and kynurenate. These results suggest that t-ACPD may exert its effects via the so-called 'metabotropic' excitatory amino acid receptor. The putative antagonists at this receptor, D-2-amino-4-phosphono-butyrate (D-AP4), L-2-amino-4-phosphono-butyrate (L-AP4) and L-2-amino-3-phosphono-propionate (L-AP3), were able to reduce responses to t-ACPD under certain circumstances. However, such antagonism was always accompanied by similar reductions in excitatory responses to other agonists. These non-selective effects would appear to limit the usefulness of AP4 and AP3 as antagonists of t-ACPD.
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Excitatory Actions of the Metabotropic Excitatory Amino Acid Receptor Agonist, trans‐(±)‐1‐amino‐cyclopentane‐1,3‐dicarboxylate (t‐ACPD), on Rat Thalamic Neurons In Vivo
The European journal of neuroscience, 1991Co-Authors: T E Salt, S A EatonAbstract:The metabotropic excitatory amino acid receptor agonist trans-(+/-)-1-amino-cyclopentane-1,3-dicarboxylate (t-ACPD) was applied to rat ventrobasal thalamic neurons by iontophoresis. This agonist typically evoked an excitatory response which was slower in onset and of longer duration than responses to the other excitatory amino acid agonists, N-methyl-aspartate, kainate or (R,S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate. Responses to t-ACPD were resistant to the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3-dione, 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid and kynurenate. These results suggest that t-ACPD may exert its effects via the so-called 'metabotropic' excitatory amino acid receptor. The putative antagonists at this receptor, D-2-amino-4-phosphono-butyrate (D-AP4), L-2-amino-4-phosphono-butyrate (L-AP4) and L-2-amino-3-phosphono-propionate (L-AP3), were able to reduce responses to t-ACPD under certain circumstances. However, such antagonism was always accompanied by similar reductions in excitatory responses to other agonists. These non-selective effects would appear to limit the usefulness of AP4 and AP3 as antagonists of t-ACPD.
Joel P. Gallagher - One of the best experts on this subject based on the ideXlab platform.
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1S,3R-ACPD-preferring inward current in rat dorsolateral septal neurons is mediated by a novel excitatory amino acid receptor.
Neuropharmacology, 1995Co-Authors: Fang Zheng, Hiroshi Hasuo, Joel P. GallagherAbstract:Abstract Metabotropic glutamate receptors (mGluRs) form a receptor family that consists of diverse receptor subtypes; now, numbering 8—exclusive of splice variants. (1 S ,3 R )-1-aminocyclopentane-1,3-dicarboxylic acid (1 S ,3 R -ACPD) has been suggested to be a selective agonist for the mGluRs. We have recently reported that, in rat dorsolateral septal nucleus (DLSN) neurones, a 1 S ,3 R -ACPD-preferring inward current (ACPD i ) persists in pertussis toxin-treated rats. We now report that this ACPD i -current: (1) persists in DLSN neurones dialyzed with a stable analog of GTP, namely, GTPγS; (2) exhibits a negative slope region with inward rectification in its I – V relationship; (3) persists in neurones superfused with tetrodotoxin or low calcium solutions; (4) is dependent upon both sodium and calcium ions; and (5) is independent of a reduction in temperature. Furthermore, pharmacological data suggest that this current may be activated by a unique type of excitatory amino acid (EAA) receptor, i.e. a receptor which prefers “metabotropic” EAA agonists and is insensitive to AP5 or CNQX. Activation by ACPD of inward currents associated with a conductance increase have also been reported at cultured mouse cerebellar Purkinje neurones; in slices of rat hippocampal CA1 neurones and slice cultures of hippocampal CA3 neurones. We suggest that this ACPD i current may play an important role within the CNS in the induction of long-term potentiation and other neurological processes; processes attributed previously to currents associated with NMDA receptor activation.
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(1S,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) induces burst firing via an inositol-1,4,5-triphosphate-independent pathway at rat dorsolateral septal nucleus
Neuropharmacology, 1994Co-Authors: Fang Zheng, György Lonart, Kenneth M. Johnson, Joel P. GallagherAbstract:Abstract We have previously reported that a l -2-amino-3-phosphonopropionate (L-AP3)-sensitive metabotropic glutamate receptor was required for the induction of long-term potentiation (LTP) in rat dorsolateral septal nucleus neurons. (1S,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD), a selective agonist for metabotropic glutamate receptors, also causes burst firing of dorsolateral septal nucleus (DLSN) neurons. In this study, we investigated whether this response was mediated by a phospholipase C-(PLC) coupled metabotropic glutamate receptor. The threshold concentration of 1S,3R-ACPD for the induction of burst firing was about 5 μM, while 10 μM 1S,3R-ACPD produced a maximal effect. L-AP3 (50 μM) reduced the burst firing induced by 1S,3R-ACPD (5 μM). Although 1S,3R-ACPD stimulated the formation of inositol-1,4,5-triphosphate [Ins(1,4,5)P3] suggesting the presence of PLC-coupled metabotropic glutamate receptors, it was only effective in a higher (30–100 μM) concentration range. In addition, the 1S,3R-ACPD-stimulated formation of Ins(1,4,5)P3 level was not affected by L-AP3. These observations suggest that the 1S,3R-ACPD induced burst firing is not mediated by PLC-coupled metabotropic glutamate receptors.
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Trans-ACPD (trans-D,L-1-amino-1,3-cyclopentanedicarboxylic acid) elicited oscillation of membrane potentials in rat dorsolateral septal nucleus neurons recorded intracellularly in vitro.
Neuroscience letters, 1991Co-Authors: Fang Zheng, Joel P. GallagherAbstract:Abstract Glutamate receptors coupled to phosphoinositol turnover have been identified recently and named ‘metabotropic’ receptors. However, the exact functional roles of these receptors are still unknown. Trans-ACPD (trans- d,l -1-amino-1,3-cyclopentanedicarboxylic acid) is suggested to be the only selective agonist for metabotropic glutamate receptors. Here we report that trans-ACPD elicits membrane potential depolarization with oscillation of dorsolateral septal nucleus neurons recorded intracellularly in vitro. Our experiments also suggested that there may be multiple interactions between ionotropic quisqualate receptors and metabotropic glutamate receptors. The burst firing induced by high concentrations of trans-ACPD suggests that excessive activation of metabotropic glutamate receptors may lead to cellular toxicity or be associated with clinical disorders such as epilepsy.
