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Biomedical subjects

E X Albuquerque

Publications and source records attributed to E X Albuquerque.

At least 37 records · Page 2Linked to original sources
PubMed1999

Low concentrations of the organophosphate VX affect spontaneous and evoked transmitter release from hippocampal neurons: toxicological relevance of cholinesterase-independent actions.

In the present study, the patch-clamp technique was applied to cultured hippocampal neurons to evaluate the effects of the nerve agent VX on evoked and spontaneous postsynaptic currents mediated by gamma-aminobutyric acid (GABA) and glutamate. At 0.01 nM, VX reduced the amplitude of evoked GABAergic currents, and only at concentrations >1 nM did it decrease the amplitude of evoked glutamatergic currents. The effect of VX on GABAergic currents, which was partially reversible upon washing of the neurons with VX-free external solution, could be prevented by the muscarinic antagonist atropine. In contrast, the effect of VX on glutamatergic currents, which was not reversible upon washing, appears to be related to the VX-induced reduction of the amplitude and frequency of repetitively firing by action potentials. In the presence of the Na(+)-channel blocker tetrodotoxin (TTX), VX (>/=10 nM) increased the frequency of GABA- and glutamate-mediated miniature postsynaptic currents (MPSCs). This effect of VX was unrelated to cholinesterase inhibition and was Ca(2+) dependent. The lack of effect of VX on MPSC kinetics indicates that VX-induced alterations of evoked and spontaneous currents are exclusively due to alterations of the transmitter release processes. The ability of VX to affect transmitter release in the brain may underlie some of its neurotoxic effects and may provide the basis for the development of therapeutic countermeasures to treat and/or prevent VX-induced neurotoxicity.

Animals↗
PubMed1999

Lead increases tetrodotoxin-insensitive spontaneous release of glutamate and GABA from hippocampal neurons.

This study was aimed at investigating the effects of the environmental pollutant lead (Pb2+) on the tetrodotoxin (TTX)-insensitive release of neurotransmitters from hippocampal neurons. Evidence is provided that Pb2+ (>/=100 nM) increases the frequency of gamma-aminobutyric acid (GABA)- and glutamate-mediated miniature postsynaptic currents (MPSCs) recorded by means of the patch-clamp technique from cultured hippocampal neurons. Because Pb2+ changed neither the amplitude nor the decay-time constant of the MPSCs, Pb2+-induced changes in MPSC frequency are exclusively due to a presynaptic action of this heavy metal. Increase by Pb2+ of the action potential-independent release of GABA and glutamate was concentration dependent and was only partially reversible upon washing of the neurons with nominally Pb2+-free external solution. This effect was also Ca2+ independent and began approximately after 1-2-min exposure of the neurons to Pb2+. The latency for the onset of the Pb2+'s effect on the MPSC frequency and the inability of the chelator ethylenediaminetetraacetic acid (100 microM) to reverse the effect that remained after washing of the neurons with external solution suggested that Pb2+ acted via an intracellular mechanism. Of interest also was the finding that Pb2+ simultaneously increased the release of GABA and glutamate, overriding the ability of these neurotransmitters to decrease the release of one another. Given that synaptic activity is a key mechanism for the establishment of stable synaptic connections early in the development, it is possible that, by interfering with spontaneous transmitter release, Pb2+ has lasting effects on neuronal maturation and plasticity.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1999

Nanomolar concentrations of lead inhibit glutamatergic and GABAergic transmission in hippocampal neurons.

To investigate whether lead (Pb2+) affects the tetrodotoxin (TTX)-sensitive release of neurotransmitters, the whole-cell mode of the patch-clamp technique was applied to cultured hippocampal neurons. Pb2+ (>/=10 nM) reversibly blocked the TTX-sensitive release of glutamate and gamma-aminobutyric acid (GABA), as evidenced by the reduction of the amplitude and frequency of glutamate- and GABA-mediated postsynaptic currents (PSCs) evoked by spontaneous neuronal firing. This effect of Pb2+, which occurred 2-3 s after exposure of the neurons to Pb2+-containing external solution, was not related to changes in Na+-channel activity, and was quantified by measurements of changes in the amplitude of PSCs evoked when a 50-micros, 5-V stimulus was applied via a bipolar electrode to a neuron synaptically connected to the neuron under study. With an IC50 of approximately 68 nM, Pb2+ blocked the evoked release of glutamate and GABA. This effect was most likely mediated by Pb2+'s actions on extracellular targets, because there was a very short delay (<3 s) for its onset, and it could be completely reversed by the chelator ethylene diaminetetraacetic acid (EDTA). Given that Pb2+-induced blockade of evoked transmitter release could be reversed by 4-aminopyridine, it is suggested that the effect on release was mediated via the binding of Pb2+ to voltage-gated Ca2+ channels. Thus, it is most likely that the neurotoxic effects of Pb2+ in the mammalian brain involve a decrease of the TTX-sensitive, Ca2+-dependent release of neurotransmitters.

4-Aminopyridine↗
PubMed1999

Choline and selective antagonists identify two subtypes of nicotinic acetylcholine receptors that modulate GABA release from CA1 interneurons in rat hippocampal slices.

Neuronal nicotinic receptors (nAChR) are known to control transmitter release in the CNS. Thus, this study was aimed at exploring the diversity and localization of nAChRs present in CA1 interneurons in rat hippocampal slices. The use of a U-tube as the agonist delivery system was critical for the reliable detection of nicotinic responses induced by brief exposure of the neurons to ACh or to the alpha7 nAChR-selective agonist choline. The present study demonstrated that CA1 interneurons, in addition to expressing functional alpha7 nAChRs, also express functional alpha4beta2-like nAChRs and that activation of both receptors facilitates an action potential-dependent release of GABA. Depending on the experimental condition, one of the following nicotinic responses was recorded from the interneurons by means of the patch-clamp technique: a nicotinic whole-cell current, depolarization accompanied by action potentials, or GABA-mediated postsynaptic currents (PSCs). Responses mediated by alpha7 nAChRs were short-lasting, whereas those mediated by alpha4beta2 nAChRs were long-lasting. Thus, phasic or tonic inhibition of CA1 interneurons may be achieved by selective activation of alpha7 or alpha4beta2 nAChRs, respectively. It can also be suggested that synaptic levels of choline generated by hydrolysis of ACh in vivo may be sufficient to control the activity of the alpha7 nAChRs. The finding that methyllycaconitine and dihydro-beta-erythroidine (antagonists of alpha7 and alpha4beta2 nAChRs, respectively) increased the frequency and amplitude of GABAergic PSCs suggests that there is an intrinsic cholinergic activity that sustains a basal level of nAChR activity in these interneurons.

Action Potentials↗
PubMed1999

Expression of nicotinic acetylcholine receptor subunits in the cerebral cortex in Alzheimer's disease: histotopographical correlation with amyloid plaques and hyperphosphorylated-tau protein.

Impairment of cholinergic transmission and decreased numbers of nicotinic binding sites are well-known features accompanying the cognitive dysfunction seen in Alzheimer's disease (AD). In order to elucidate the underlying cause of this cholinoceptive dysfunction, the expression of two pharmacologically different nicotinic acetylcholine receptor (nAChR) subunits (alpha4, alpha7) was studied in the cerebral cortex of Alzheimer patients as compared to controls. Patch-clamp recordings of 14 dissociated neurons of control cortices showed responses suggesting the existence of alpha4- and alpha7-containing functional nAChRs in the human cortex. In cortices of Alzheimer patients and controls, the pattern of distribution and the number of alpha4 and alpha7 mRNA-expressing neurons were similar, whereas at the protein level a decrease in the density of alpha4- and alpha7-expressing neurons of approximately 30% was observed in Alzheimer patients. The histotopographical correlation of nAChR expression with accompanying pathological changes, e.g. accumulation of hyperphosphorylated-tau (HP-tau) protein and beta-amyloid showed that neurons in the vicinity of beta-amyloid plaques bore both nAChR transcripts. Neurons heavily labelled for HP-tau, however, expressed little or no alpha4 and alpha7 mRNA. These results point to an impaired synthesis of nAChRs on the protein level as a possible cause of the cholinoceptive deficit in AD. Further investigations need to elucidate whether interactions of HP-tau with nAChR mRNA, or alterations in the quality of alpha4 and alpha7 transcripts give rise to decreased protein expression at the level of individual neurons.

Aged↗
PubMed1999

Expression of functional alpha7 nicotinic acetylcholine receptor during mammalian muscle development and denervation.

We have studied, on the transcriptional, protein and functional level, the expression of alpha7 nicotinic acetylcholine receptors (nAChR) in the course of rat muscle development, denervation and renervation. At foetal day 13, alpha7 nAChR expression was observed in somites and developing muscles of the back, but not yet in migrating myoblasts. Two days later, concomitant with myoblast aggregation, the alpha7 isoform began to be expressed in isolated myoblasts, with the highest level of expression in the frontal zone of the migrating wave. On foetal day 18, a time when the myoblasts in the upper hindleg have fused, alpha7 nAChR expression was most prominent in the outer layer of muscle tissue. The highest level of expression was observed in the first postnatal week, when practically all muscle cells stained positively for alpha7 protein. During the following weeks, alpha7 nAChR expression slowly decreased and practically disappeared in adult hindleg muscle. Following chronic denervation of adult Soleus muscle fibres, expression of alpha7 nAChR returned within 2-4 weeks. Electrophysiological measurements showed that the alpha7 nAChR of chronically denervated soleus muscle fibres were functional and, in particular, that they could be activated by choline. The presence of the alpha7 nAChR in developing and denervated muscle suggests a role for this nicotinic receptor in neuronal pathfinding and/or endplate stabilization.

Animals↗
PubMed1999

The organophosphate sarin, at low concentrations, inhibits the evoked release of GABA in rat hippocampal slices.

In the present study, the whole-cell mode of the patch-clamp technique was applied to neurons of the CA1 pyramidal layer of rat hippocampal slices to investigate the effects of the organophosphate (OP) sarin on field stimulation-evoked and on tetrodotoxin (TTX)-insensitive postsynaptic currents (PSCs) mediated by activation of type A gamma-aminobutyric acid (GABA) receptors or AMPA-type glutamate receptors. At 0.3-1 nM, sarin reduced the amplitude of GABA-mediated PSCs and had no effect on the amplitude of glutamatergic PSCs evoked by field stimulation of neurons synaptically connected to the neuron under study. The effect of sarin on evoked GABAergic PSCs was unrelated to cholinesterase inhibition, was partially reversed upon washing of the neurons with sarin-free external solution, and was mediated by a direct interaction of the OP with muscarinic acetylcholine receptors present on presynaptic GABAergic neurons. Sarin had no effect on the amplitude or kinetics of GABA- or glutamate-mediated miniature postsynaptic currents (MPSCs) recorded in the presence of the Na+-channel blocker TTX (300 nM), indicating that the OP does not interact with GABA(A) or glutamate receptors. Further, sarin did not alter the frequency of GABAergic or glutamatergic MPSCs, a finding that led to the conclusion that this OP does not affect the TTX-insensitive release of neurotransmitters. A selective reduction by sarin of the action potential-dependent release of GABA in the hippocampus can account for the occurrence of seizures in intoxicated subjects.

Animals↗
PubMed1998

Neuronal nicotinic receptors modulate synaptic function in the hippocampus and are sensitive to blockade by the convulsant strychnine and by the anti-Parkinson drug amantadine.

Evidence is provided that rapid application of nicotinic agonists to CA1 interneurons in hippocampal slices can trigger responses with at least one of three components: (i) whole-cell currents due to activation of nicotinic receptors (nAChRs) on the neuron under study; (ii) fast current transients representing back-propagating action potentials; and (iii) post-synaptic currents mediated by gamma-aminobutyric acid (GABA) released from presynaptic neurons by activation of preterminal nAChRs. The use of the alpha7-nAChR-selective agonist choline and of nAChR-subtype-selective antagonists led to the conclusion that these responses can be mediated by alpha7 or alpha4beta2 nAChRs. Experiments carried out in cultured hippocampal neurons demonstrated that the evoked GABA release can also be reduced by activation of these receptors, and showed that the convulsant strychnine is a competitive antagonist of alpha7 nAChRs and a non-competitive antagonist of alpha4beta2 nAChRs, whereas the anti-Parkinson drug amantadine is a non-competitive antagonist of alpha7, alpha4beta2, and alpha3beta4 nAChRs.

Amantadine↗
PubMed1998

alpha-bungarotoxin- and methyllycaconitine-sensitive nicotinic receptors mediate fast synaptic transmission in interneurons of rat hippocampal slices.

This study demonstrates for the first time that alpha7 nicotinic receptors (nAChRs) mediate fast synaptic transmission in conventional hippocampal slices. In the presence of antagonists of muscarinic, AMPA, NMDA, GABAA, ATP, and 5-HT3 receptors, spontaneous and evoked postsynaptic currents (PSCs) recorded from CA1 interneurons were blocked by the alpha7 nAChR antagonists methyllycaconitine and alpha-bungarotoxin and by a desensitizing concentration of the alpha7 nAChR agonist choline. Spontaneous nicotinic PSCs were also accompanied by Na+ transients, indicating that alpha7 nAChR-mediated transmission serves as an excitatory signal to the CA1 interneurons in the hippocampus.

Aconitine↗
PubMed1998

Human and rodent bronchial epithelial cells express functional nicotinic acetylcholine receptors.

We demonstrated previously that human skin keratinocytes express acetylcholine receptors (AChRs) sensitive to acetylcholine and nicotine, which regulate cell adhesion and motility. We demonstrate here that human and rodent bronchial epithelial cells (BECs) express AChRs similar to those expressed by keratinocytes and by some neurons. Patch-clamp experiments demonstrated that the BEC AChRs are functional, and they are activated by acetylcholine and nicotine. They are blocked by kappa-bungarotoxin, a specific antagonist of the AChR isotypes expressed by neurons in ganglia. Their ion-gating properties are consistent with those of AChR isotypes expressed in ganglia, formed by alpha3, alpha5, and beta2 or beta4 subunits. Reverse transcription-polymerase chain reaction and in situ hybridization experiments demonstrated the presence in BECs of mRNA transcripts for all those AChR subunits, both in cell cultures and in tissue sections, whereas we could not detect transcripts for the alpha2, alpha4, alpha6, and beta3 AChR subunits. The expression of alpha3 and alpha5 proteins in BEC in vivo was verified by the binding of subunit-specific antibodies to sections of trachea. Mecamylamine and kappa-bungarotoxin, which are cholinergic antagonists able to block the ganglionic alpha3 AChRs, caused a reversible change of the cell shape of cultured, confluent human BECs. This resulted in a reduction of the area covered by the cell and in cell/cell detachment. The presence of AChRs sensitive to nicotine on the lining of the airways raises the possibility that the high concentrations of nicotine resulting from tobacco smoking will cause an abnormal activation, a desensitization, or both of the bronchial AChRs. This may mediate or facilitate some of the toxic effects of cigarette smoking in the respiratory system.

Animals↗
PubMed1998

An analysis of low level doses of cholinesterase inhibitors in cultured neurons and hippocampal slices of rats.

Recent data indicate that the neurotoxic effects of organophosphate compounds, including those of the nerve agents VX and sarin, are not solely due to irreversible cholinesterase inhibition. In this study we applied the patch clamp technique to hippocampal neurons in culture and slices to investigate the effects of VX, sarin and huperzine A on transmitter release and the mechanisms related with such effects. The nerve agents VX and sarin at very low concentrations significantly reduced the evoked release of GABA and glutamate. This effect was dependent of the activation of muscarinic receptors. In the presence or absence of the Na(+)-channel blocker tetrodotoxin (TTX), VX increased the frequency of spontaneous glutamate and GABA-induced postsynaptic currents. The effect of VX on TTX-insensitive spontaneous currents appears to be unrelated to cholinesterase inhibition, because it could be detected even after cholinesterase was blocked by high concentrations of the nerve agent soman. The ability of the nerve gases to decrease evoked release of GABA and increase spontaneous transmitter release may underlie some of the neurotoxic effects of the compounds. Huperzine A did not affect spontaneous or evoked release of GABA and glutamate, suggesting that this compound may be a pure cholinesterase inhibitor and had no effect on postsynaptic GABAA or AMPA receptors.

Alkaloids↗
PubMed1998

Strychnine: a potent competitive antagonist of alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors in rat hippocampal neurons.

In our study, evidence is provided that strychnine, a competitive antagonist at glycine-gated Cl- channels, is also a potent competitive antagonist at native alpha-7-containing, alpha-bungarotoxin-sensitive nicotinic acetylcholine receptor (nAChRs). To address the effects of strychnine on two types of nicotinic responses, the whole-cell mode of the patch-clamp technique was applied to rat hippocampal neurons in culture. Type IA and type II nicotinic currents evoked by acetylcholine (ACh) were inhibited by strychnine in a concentration-dependent manner with IC50S of 1.2 and 38 microM, respectively. Strychnine (2 microM) decreased the peak amplitude of the alpha-bungarotoxin-sensitive type IA current in a voltage-independent manner and prolonged the decay phase of this current. The concentration-response curve for ACh in evoking type IA current showed a parallel shift to the right in the presence of strychnine (2 microM); the EC50 for ACh was increased from 0.4 to 0.8 mM. These findings suggest that strychnine acts as a competitive antagonist of ACh at the alpha 7 nAChRs that subserve type IA current. In contrast, the inhibition by strychnine of type II current was strongly voltage dependent, and the decay phase of this current was markedly accelerated by the toxin, suggesting an open-channel blockade by strychnine of the alpha 4 beta 2 nAChRs subserving type II currents. Preexposure of the neurons to strychnine enhanced its ability to decrease the peak amplitude of type II currents, indicating that the toxin may also act on alpha 4 beta 2 nAChR channels that are not open. It is concluded that strychnine is a potent competitive antagonist of ACh at neuronal alpha 7 nAChRs and a noncompetitive antagonist at the alpha 4 beta 2 nAChR.

Acetylcholine↗
PubMed1998

Human vascular endothelial cells express functional nicotinic acetylcholine receptors.

ACh receptors sensitive to nicotine (nAChR) are present in human skin keratinocytes and in bronchial epithelial cells. They are stimulated by ACh secreted by the same cells that express them, and they modulate cell motility and shape. A variety of non-neuronal tissues, including endothelial cells, synthesize ACh, which raises the possibility that they are sensitive to nicotine. We demonstrate here that endothelial cells that line blood vessels express functional nAChRs. Their structure and ion-gating properties are similar to those of the nAChRs expressed by ganglionic neurons and by skin keratinocytes and bronchial epithelial cells. In situ hybridization experiments using primary cultures of endothelial cells from human aorta demonstrated the presence in these cells of the subunits believed to contribute to ganglionic ACh receptors (AChRs) of the alpha3 subtype: alpha3, alpha5, beta2 and beta4. Binding of radiolabeled epibatidine-a high-affinity specific ligand of certain neuronal AChRs, including the alpha3 subtypes-revealed the presence of approximately 900 specific binding sites per cell. We assessed the presence of functional AChRs by patch-clamp experiments. Cultured human endothelial cells express ion channels that are opened by (+)-anatoxin-a and are blocked by dihydro-beta-erythroidine. These are specific agonist and antagonist, respectively, of neuronal AChRs of the alpha3 subtype. The ion-gating properties of the endothelial AChRs were similar to those of neuronal ganglionic AChRs. The presence of AChRs sensitive to nicotine in endothelial cells may be related to the toxic effects of nicotine on the vascular system.

Animals↗
PubMed1997

Choline is a selective agonist of alpha7 nicotinic acetylcholine receptors in the rat brain neurons.

In the present study, we demonstrate that choline, a precursor of acetylcholine (ACh) and a product of acetylcholine hydrolysis by acetylcholinesterase (AChE), acts as an efficient and relatively selective agonist of alpha7-containing nicotinic acetylcholine receptors (nAChR) in neurons cultured from the rat hippocampus, olfactory bulb and thalamus as well as in PC12 cells. Choline was able to activate postsynaptic and presynaptic alpha7 nAChRs, with the latter action resulting in the release of other neurotransmitters. Although choline was approximately one order of magnitude less potent than ACh (EC50 of 1.6 mM for choline and 0.13 mM for ACh), it acted as a full agonist at alpha7 nAChRs. In contrast, choline did not activate alpha4beta2 agonist-bearing nAChRs on hippocampal neurons, and acted as a partial agonist at alpha3beta4-containing nAChRs on PC12 cells. The ethyl alcohol moiety of choline is required for the selective action on alpha7 nAChR. Exposure of cultured hippocampal neurons for 10 min to choline (10-100 microM) resulted in desensitization of the native alpha7 nAChRs. Moreover, chronic exposure (10 days) of the cultured hippocampal neurons to a desensitizing concentration of choline (approximately 30 microM) decreased their responsiveness to ACh. The selective action of choline on native alpha7 nAChRs suggests that this naturally occurring compound may act in vivo as an endogenous ligand for these receptors. Putative physiological actions of choline include retrograde messenger activity during the development of the mammalian central nervous system and during periods of elevated synaptic activity that leads to long-term potentiation.

Acetylcholine↗
PubMed1997

Amantadine inhibits nicotinic acetylcholine receptor function in hippocampal neurons.

The effects of amantadine on nicotinic acetylcholine receptors (nAChRs) of hippocampal neurons were studied by recording three types of acetylcholine (ACh)-evoked currents, using the whole-cell patch-clamp technique. The rapidly desensitizing type IA nicotinic current, which is alpha-bungarotoxin-sensitive and is mediated by nAChRs bearing alpha 7 subunits, was inhibited by application of amantadine to neurons for 10 min (IC50 = 6.5 microM), but the potency of ACh (EC50 = 0.27 mM) was not affected by the drug. Amantadine (30-50 microM) attenuated the peak current amplitude in a voltage-dependent manner, with greater effect at negative than at positive membrane potentials. In contrast, the decay phase of the currents was shortened in a voltage-independent manner. When amantadine was coapplied briefly with ACh, the drug was markedly less potent (IC50 = 130 microM). Thus, the noncompetitive effects of amantadine on the type IA nicotinic current are complex, involving actions on the closed and desensitized states of the alpha 7 nAChR. The slowly desensitizing, alpha-bungarotoxin-insensitive nicotinic currents of type II, which is inhibited by dihydro-beta-erythroidine and is mediated by alpha 4 beta 2 nAChRs, and of type III, which is inhibited by mecamylamine and is mediated by alpha 3 beta 4 nAChRs, were also sensitive to inhibition by amantadine. The peak amplitude of type II current was reduced only slightly by 10 microM amantadine coapplied with ACh, but the decay-time constant and amplitude of the sustained current were markedly reduced. Type III current was also inhibited when amantadine was briefly coapplied with ACh. In contrast to its effects on nicotinic currents, amantadine at 10 microM did not affect currents evoked by N-methyl-D-aspartate plus glycine, gamma-aminobutyric acid, glycine or kainate. Thus, on cultured hippocampal neurons, amantadine preferentially inhibits nicotinic currents.

Amantadine↗
PubMed1997

Neuronal nicotinic acetylcholine receptor activation modulates gamma-aminobutyric acid release from CA1 neurons of rat hippocampal slices.

In the present study we investigated electrophysiologically the nicotinic responses of pyramidal neurons and interneurons visualized by infrared-assisted videomicroscopy and fluorescence in the CA1 field of hippocampal slices obtained from 8- to 24-day-old rats. Application of nicotinic agonists to CA1 neurons evoked at least four types of nicotinic responses. Of major interest was the ability of these agonists to induce the release of gamma-aminobutyric acid (GABA) from interneurons. Slowly decaying ACh whole-cell currents and GABA-mediated postsynaptic currents could be recorded from pyramidal neurons and interneurons, whereas fast-decaying nicotinic currents and fast current transients were recorded only from interneurons. Nicotinic responses were sensitive to blockade by d-tubocurarine (10 microM), which indicated that they were mediated by nicotinic acetylcholine receptors (nAChRs). The slowly decaying currents, the postsynaptic currents and the fast current transients were insensitive to blockade by the alpha-7 nAChR-specific antagonist methyllycaconitine (up to 1 microM) or alpha-bungarotoxin (100 nM). On the other hand, the slowly decaying nicotinic currents recorded from the interneurons were blocked by the alpha4beta2 nAChR-specific antagonist dihydro-beta-erythroidine, and the fast-desensitizing nicotinic currents were evoked by the alpha-7 nAChR-specific agonist choline. In experimental conditions similar to those used to record nicotinic responses from neurons in slice (i. e., in the absence of tetrodotoxin), we observed that nicotinic agonists can also induce the release of GABA from hippocampal neurons in culture. In summary, these results provide direct evidence for more than one subtype of functional nAChR in CA1 neurons and suggest that activation of nAChRs present in GABAergic interneurons can evoke inhibitory activity in CA1 pyramidal neurons, thereby modulating processing of information in the hippocampus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗