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N Akaike

Publications and source records attributed to N Akaike.

At least 199 records · Page 11Linked to original sources
PubMed1993

Cellular mechanism of acetylcholine-induced response in dissociated outer hair cells of guinea-pig cochlea.

1. The acetylcholine (ACh)-induced currents (IACh) in dissociated outer hair cells (OHCs) of guinea-pig cochlea were investigated using the whole-cell patch-clamp technique, in both conventional and nystatin perforated-patch configurations. 2. ACh and carbamylcholine (CCh) induced outward currents at a holding potential (VH) of -60 mV in the perforated-patch configuration. The IACh increased in a sigmoidal fashion over the concentration range between 3 x 10(-6) and 10(-3) M. The dissociation constant (KD) was 1.7 x 10(-5) M and the Hill coefficient (n) was 2.7. The KD and n for CCh were 8.7 x 10(-5) M and 2.2, respectively. Neither nicotine nor muscarine induced any detectable current up to a concentration of 10(-3) M. 3. Various muscarinic agonists such as oxotremorine-M, McN-A-343 and oxotremorine could also induce the outward currents, although these current amplitudes were about one-third that of ACh, indicating that they were partial agonists. 4. The muscarinic antagonists atropine, 4-DAMP, AF-DX 116 and pirenzepine inhibited the IACh in a concentration-dependent manner. The half-inhibitory concentrations (IC50) for atropine, 4-DAMP, AF-DX 116 and pirenzepine were 4.8 x 10(-6), 6.2 x 10(-6), 2.1 x 10(-5) and 2.9 x 10(-4) M, respectively. 5. When the extracellular Ca2+ concentration ([Ca2+])o) was reduced to lower than 1 mM, the amplitude of IACh, abruptly decreased. In a nominally Ca(2+)-free external solution ACh did not induce any current. The increase of [Ca2+]o beyond 1 mM did not change the IACh. 6. When OHCs were perfused intracellularly with a pipette solution containing 10 mM BAPTA in the conventional whole-cell mode, ACh could not induce outward K+ currents. The Ca2+ ionophore A23187 induced an outward current. These results indicate that intracellular Ca2+ is involved in the ACh response. 7. Calmodulin inhibitors such as chlorpromazine, W-7 and trifluoperazine inhibited the IACh in a concentration-dependent manner. 8. When OHCs were dialysed with either 100 microM GDP beta S or 1 micrograms/ml pertussis toxin (PTX) through the patch pipette at a VH of -60 mV, the IACh diminished within 10 min, whereas the IACh of the control remained steady for over 20 min, suggesting that a PTX-sensitive G-protein is involved in the ACh response.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1993

Hyperpolarizing muscarinic responses of freshly dissociated rat hippocampal CA1 neurones.

1. Intracellular mechanisms of the muscarinic acetylcholine (ACh) response were investigated in pyramidal neurones freshly dissociated from the rat hippocampal CA1 region. Current recordings were made in the whole-cell mode using the nystatin 'perforated'-patch technique, by which the muscarinic ACh response can be continuously recorded without so-called 'run-down' phenomenon. The amount of intracellular free Ca2+ ([Ca2+]i) was fluorometrically measured using fura-2. 2. In current clamp conditions, ACh induced a transient hyperpolarization accompanied by a decrease in membrane input resistance. 3. Under voltage clamp conditions at a holding potential (Vh) of -40 mV, ACh induced two types of muscarinic currents observed either alone or together: a transient outward current and a slowly activating sustained inward current. 4. The ACh-induced transient outward current reversed the direction at K+ equilibrium potential (EK), and the reversal potential (EACh) shifted 56.7 mV for a tenfold change of extracellular K+ concentration ([K+]o). 5. The ACh-induced transient outward current increased in a sigmoidal fashion with increase in ACh concentration, where the half-maximal concentration (EC50) and the Hill coefficient (n) were 8 x 10(-7) M and 1.9, respectively. Both muscarine and carbamylcholine mimicked the ACh response, but neither McN-A-343 (M1 agonist) nor oxotremorine (cardiac M2 agonist) induced any current. 6. Muscarinic antagonists reversibly blocked the ACh response in a concentration-dependent manner. The inhibitory potency was in the order of atropine > pirenzepine > AF-DX-116. 7. The ACh-induced transient outward current was never recorded when [Ca2+]i was chelated by the acetoxymethyl ester form of 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA AM). On the other hand, in Ca(2+)-free external solution containing 2 mM EGTA and 10 mM Mg2+, the ACh response was elicited by the first application and successive ACh applications did not induce any response. Fura-2 imaging showed that [Ca2+]i was increased when ACh was added to the external medium with or without Ca2+, though in Ca(2+)-free medium only the first application of ACh increased the [Ca2+]i. 8. The ACh response was not affected by pretreatment with pertussis toxin (PTX) but the inhibitory effect of ACh on the high-threshold Ca2+ channel was abolished completely. 9. Pretreatment with Li+ enhanced the amplitude of the transient outward current and the increase in [Ca2+]i induced by ACh. 10. The calmodulin antagonists W-7, chlorpromazine and trifluoperazine reversibly inhibited the ACh response in a concentration-dependent manner.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1993

Cytoplasmic Ca2+ oscillation in rat megakaryocytes evoked by a novel type of purinoceptor.

1. The responses of megakaryocytes isolated from rat bone marrow to externally applied adenosine triphosphate (ATP) were investigated in the whole-cell mode by the use of nystatin perforated patch-clamp technique. 2. ATP at 1-100 microM evoked periodic outward currents at a holding potential of -40 mV. The reversal potential of the currents was close to K+ equilibrium potential (EK) and the K+ channel blockers such as quinine and quinidine suppressed the currents, indicating that the outward currents are predominantly carried by K+. 3. Since it has been reported that adenosine diphosphate (ADP) evoked monophasic K+ current using a conventional whole-cell recording, we compared the results obtained by perforated and conventional patch-clamp techniques. The crucial difference between our results and previous results was due to the intracellular perfusion with internal solution containing a high concentration of EGTA by which both current shape and concentration response were modified. 4. The membrane permeable Ca2+ chelator, 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (acetoxy methyl ester; BAPTA AM), inhibited the K+ current concentration dependently, suggesting that ATP-induced oscillatory K+ currents are caused by changes in cytoplasmic free Ca2+ concentration ([Ca2+]i). 5. With increasing ATP concentration, the frequency and the maximum amplitude of K+ current oscillation increased and the latency of current, which is the period required to activate the first K+ current after ATP application, decreased. 6. ADP, 2-methylthio-ATP and ATP-gamma-S could also evoke the periodic K+ currents, but adenosine, uridine triphosphate (UTP) and alpha-beta-methylene adenosine 5'-triphosphate (AMP-CPP) failed. 2-Methylthio-ATP was the most potent agonist; next was ADP which showed a 10-30 times stronger effect than ATP. Cross-desensitization was observed between ATP and ADP, but not between ATP or ADP and thrombin. 7. Extracellular Ca2+ was not required for the ATP-induced K+ current activation, indicating that Ca2+ released from intracellular pools induced the oscillatory response. In addition, the agonist potency increased when extracellular Ca2+ concentration ([Ca2+]o) decreased, suggesting that the principal agonists might be ATP4- and ADP3-. 8. The results suggest the presence of a novel subtype of purinoceptor in the megakaryocyte plasma membrane which induces cytoplasmic Ca2+ oscillation and evokes periodic K+ current flux.

Adenosine Diphosphate↗
PubMed1993

Theophylline affects three different potassium currents in dissociated rat cortical neurones.

1. The effects of theophylline in pyramidal neurones acutely dissociated from the rat frontal cortex were investigated in the whole-cell configuration, using the nystatin-perforated patch-clamp technique. 2. Ten millimolar theophylline evoked triphasic responses: a small slow outward current (Iso), then a large transient outward current (Ito) and finally a slow sustained inward current (Isi). The reversal potentials of the three current components shifted 56-58 mV for a 10-fold change in extracellular K+ concentration, thereby indicating that all these current components were predominantly carried by K+. 3. Iso had no voltage dependence, whereas Ito showed a steep outward rectification. Iso was relatively resistant to tetraethylammonium (TEA) with an IC50 of 10 mM. Ito was susceptible to submillimolar TEA with an IC50 of 0.8 mM. 4. Isi was a net inward current mainly resulting from suppression of the M-current (IM). 5. These three current components had a distinct concentration dependence; in particular, Isi was evoked at a relatively lower concentration range. 6. Ito was not observed when the intracellular Ca2+ was chelated by 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) of 10 mM, using the conventional whole-cell recording configuration, whereas both Iso and Isi were retained but gradually diminished. 7. In Ca(2+)-free external solution, these responses were fully elicited by the first application of theophylline. However, Ito disappeared during successive applications and Iso, but not Isi, also decreased. Similar results were obtained in the presence of ryanodine. 8. Theophylline apparently affects three different kinds of K+ currents in rat cortical neurones. Both Iso and Ito depend on internal calcium mobilized from an intracellular Ca2+ store by theophylline, while Isi was not primarily mediated by a change in [Ca2+]i.

Action Potentials↗
PubMed1993

Potassium currents operated by thyrotrophin-releasing hormone in dissociated CA1 pyramidal neurones of rat hippocampus.

1. Membrane currents activated by thyrotrophin-releasing hormone (TRH) were investigated in the dissociated rat hippocampal CA1 pyramidal neurone using the nystatin perforated patch recording configuration. 2. Under current-clamp condition, TRH caused a transient hyperpolarization accompanied by a decrease of firing activity and a successive long-lasting depolarization. The latter induced a blockade of firing. 3. When neurones were held at a holding potential (VH) of -40 mV under voltage clamp, TRH elicited a transient outward current with an increase in the membrane conductance, which was followed by a sustained inward current with a decrease in membrane conductance. The inactive TRH metabolite, TRH free acid, did not induce any currents. 4. The reversal potential of TRH-induced outward current (ETRH) was close to the K+ equilibrium potential (EK). The change in ETRH for a 10-fold change in extracellular K+ concentration was 56.4 mV, indicating that the membrane behaves like a K+ electrode in the presence of TRH. On the other hand, the TRH-induced inward current was due to suppression of a slow inward current relaxation during hyperpolarizing voltage commands to -50 mV from a VH of -40 mV, indicating the suppression of the voltage- and time-dependent component of the K+ current (M-current). 5. The TRH-induced outward current (ITRH) increased in a concentration-dependent manner over the concentration range 10(-8)-10(-6) M. The half-maximum concentration was 7.4 x 10(-8) M and the Hill coefficient was 1.5. 6. The TRH-induced outward current (ITRH) was antagonized by K+ channel blockers such as tetraethylammonium (TEA), 4-aminopyridine (4-AP) and Ba2+ in a concentration-dependent manner. ITRH was insensitive to both apamin and iberiotoxin. 7. The first application of TRH to neurones perfused with Ca(2+)-free external solution containing 2 mM EGTA could induce ITRH but the TRH response diminished dramatically with successive applications. Intracellular perfusion with a Ca2+ chelator, 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), also diminished the TRH response. 8. The depletion of Ca2+ from the intracellular Ca2+ store by thapsigargin blocked the TRH response without affecting the caffeine response. Pretreatment with Li+ significantly enhanced ITRH, suggesting that ITRH is involved in the elevation of intracellular free Ca2+ released from the inositol 1,4,5-trisphosphate (IP3)-sensitive Ca2+ store site but not from the caffeine-sensitive one. 9. Staurosporine, a protein kinase C (PKC) inhibitor, suppressed ITRH in a concentration-dependent manner (the half-maximum inhibitory concentration (IC50), was 2.45 x 10(-8) M).(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1993

Serotonin-operated potassium current in CA1 neurons dissociated from rat hippocampus.

1. The intracellular mechanisms of serotonin (5-HT) response were investigated in dissociated rat hippocampal pyramidal neurons using the nystatin-perforated patch technique. 2. Under voltage-clamp conditions, 5-HT evoked outward currents (I5-HT) with an increase in membrane conductance at a holding potential of -40 mV. The outward current reversed at the K+ equilibrium potential, which shifted 59.4 mV with a 10-fold change in extracellular K+ concentration. 3. The first application of 5-HT on neurons perfused with Ca(2+)-free external solution induced outward currents of I5-HT but the amplitude was diminished dramatically with successive applications. Pretreatment with the membrane-permeant Ca2+ chelator 1,2-bis-(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, tetraacetoxymethyl ester (BAPTA-AM) also diminished the I5-HT amplitude. 4. Pretreatment with pertussis toxin (PTX) had no effect on I5-HT. 5. The I5-HT was not cross-desensitized with the caffeine-induced outward current but with outward current mediated by the muscarinic acetylcholine receptor. Pretreatment with Li+ significantly enhanced the I5-HT, indicating that I5-HT is involved in the elevation of intracellular free Ca2+ released from inositol triphosphate (IP3)-sensitive Ca2+ store sites but not from the caffeine-sensitive ones. 6. The calmodulin (CaM) antagonists, trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), inhibited I5-HT in a concentration-dependent manner. 7. The Ca2+/CaM-dependent protein kinase II inhibitor 1-[N,O-Bis (5-isoquinolinesulfonyl)-N-methyl-L-tyrosil]-4-phenylpiperazine depressed the I5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Muscarinic receptor activation of potassium channels in rat dentate gyrus neurons.

1. The effects of acetylcholine (ACh) on granule cells freshly dissociated from rat dentate gyrus (DG) were studied using the nystatin perforated patch technique. This method allowed us to study ACh-induced currents (IACh) under voltage clamp without "run-down" of the ACh response. In some experiments, we used the conventional whole-cell method for intracellular application of drugs not permeable to cell membrane. 2. At a holding potential of -40 mV, ACh induced an outward current. The amplitude of IACh increased in a sigmoidal fashion with increasing ACh concentration. The half-maximal response and the Hill coefficient determined from the relation between ACh concentration and response were 4.98 x 10(-7) M and 1.70, respectively. 3. The reversal potential of IACh was close to the K+ equilibrium potential. The IACh was accompanied by an enhancement of the K+ current. 4. Muscarine and McN-A-343 mimicked the ACh response, whereas oxotremorine induced no response. 5. Muscarinic antagonists reversibly suppressed the IACh (10(-5) M) in a concentration-dependent manner, where the values of half-inhibition concentration (IC50) were 1.03 x 10(-6) M for pirenzepine and 2.21 x 10(-5) M for AF-DX-116. 6. Intracellular perfusion with GDP-beta S suppressed the IACh greatly. The IACh persisted in the neurons pretreated with an external solution containing pertussis toxin (IAP) for 18 h. 7. In the neurons perfused with Ca(2+)-free external solution containing 2 mM ethylene glycol-O,O'-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid and 10 mM Mg2+, the first application of ACh induced the IACh with an amplitude similar to that in the standard solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Effects of Ca2+ antagonists and antiepileptics on tetrodotoxin-sensitive Ca(2+)-conducting channels in isolated rat hippocampal CA1 neurons.

All Ca2+ antagonists blocked tetrodotoxin-sensitive Ca2+ current (TTX-ICa) more potently than Na+ current (INa). Phenytoin and MK-801, at concentrations which had no effect on INa, could block TTX-ICa concentration-dependently. Valproic acid and phenobarbital had no effect on both TTX-ICa and INa. In particular, flunarizine and phenytoin have more potent inhibitory effects on TTX-ICa than other test drugs. These results suggest that the abnormal excess-excitation of TTX-sensitive Ca(2+)-conducting channels may be one of the trigger factors generating epilepsy.

Animals↗
PubMed1992

A new type of Ca2+ channel blocker, NC-1100, inhibits the low- and high-threshold Ca2+ currents in the rat CNS neurons.

The effect of a new type of organic Ca2+ channel blocker, NC-1100 [(+/-)-1-(3,4-dimethoxyphenyl)-2-(4-diphenylmethylpiperazinyl)etha nol dihydrochloride], on both low- and high-threshold Ca2+ currents was studied in the whole-cell mode of the pyramidal neurons freshly dissociated from rat hippocampal CA1 region under voltage-clamp condition. The NC-1100 reversibly reduced the high-threshold Ca2+ current (HVA ICa) in a concentration-dependent manner without affecting the current-voltage relationship. The values of half-inhibition (IC50) were 1.3 x 10(-5) and 9.1 x 10(-6) M in external solution containing 10 and 2.5 mM Ca2+, respectively. The NC-1100 also decreased the low-threshold Ca2+ current (LVA ICa) in a concentration-dependent manner. The inhibitory potency was augmented by increasing the stimulation frequency and/or decreasing the extracellular Ca2+ concentration to a physiological range (2.5 mM). The IC50 value decreased to 7.7 x 10(-7) M in external solution containing 2.5 mM Ca2+ at a stimulation frequency of 1 Hz. The NC-1100 delayed the reactivation of LVA Ca2+ channel and enhanced voltage-dependently the steady-state inactivation, suggesting that this drug bound not only the resting LVA Ca2+ channel but also the inactivated one.

Animals↗
PubMed1992

Perforated-patch method reveals extracellular ATP-induced K+ conductance in dissociated rat nucleus solitarii neurons.

Extracellular adenosine 5'-triphosphate (ATP)-induced responses were investigated in acutely dissociated rat nucleus tractus solitarii (NTS) neurons, using nystatin perforated-patch and conventional whole-cell patch-clamp recordings. Extracellular application of ATP could evoke the inward currents with both methods. An additional outward current was observed only with the perforated patch method. The outward current resulted in an increase of K+ conductance which was activated by Ca2+ influx through the ATP receptor-channel complex.

Adenosine Triphosphate↗
PubMed1992

Penicillin-induced triphasic modulation of GABAA receptor-operated chloride current in frog sensory neuron.

Effects of penicillin-G (PCN) on GABA-evoked Cl- current (IGABA) were investigated in freshly dissociated frog sensory neurons by the use of the concentration-clamp technique combined with the suction-pipette method. Under conditions where the internal and external solutions allowed only Cl- permeability, PCN elicited triphasic modulation on IGABA, consisting of two modes of blockade on IGABA and a following rebound (rebound-like transient IGABA). Simultaneously applied PCN and GABA depressed IGABA immediately (phasic blockade), with the depressed IGABA slightly recovering in amplitude to achieve a stable level of blockade (tonic blockade). When a solution containing a mixture or PCN and GABA was quickly replaced by one containing GABA alone, a rebound-like transient Cl- current (IR) was evoked. Each component of the PCN actions on IGABA was PCN- and GABA-concentration-dependent. The reversal potential for each component of the PCN actions on IGABA was close to the chloride equilibrium potential (ECl) calculated using the Nernst equation. The current-voltage (I-V) relations for both the phasic and tonic blockade revealed inward rectification, while I-V curves for the control IGABA and the IR were outwardly rectified. The degree of IGABA-desensitization and the amplitude of the IR correlated well. The data suggest that partial removal of the GABAA receptor-desensitization may result in generation of the IR.

Animals↗
PubMed1992

Effects of Ca2+ antagonists and aminoglycoside antibiotics on Ca2+ current in isolated outer hair cells of guinea pig cochlea.

The effects of various Ca2+ antagonists and aminoglycoside antibiotics on the Ca2+ channel in isolated outer hair cells of the guinea pig were investigated using a whole-cell patch-clamp technique. The inhibitory action was in the order of La3+ much greater than Cd2+ much greater than Ni2+ greater than Co2+ for inorganic Ca2+ antagonists, and flunarizine = nicardipine greater than omega-conotoxin greater than methoxyverapamil = diltiazem much greater than amiloride for organic ones. Aminoglycoside antibiotics also had antagonistic effects on the Ca2+ channel.

Aminoglycosides↗
PubMed1992

Glycine response in isolated dorsal cochlear nucleus of C57BL/6J mouse.

Pharmacological properties of glycine (Gly)-induced Cl- current (ICl) in the dorsal cochlear nucleus (DCN) neurons acutely dissociated from C57BL/6J mouse were investigated in the whole-cell configuration of the patch-clamp technique. Gly-induced ICl increased in a sigmoidal manner with higher Gly concentrations. Strychnine blocked the Gly response competitively at low and non-competitively at high concentrations. Both glutamate (Glu) and N-methyl-D-aspartate (NMDA) responses were augmented by adding 10(-6) M Gly, at which concentration Gly did not induce any ICl. This facilitation was not affected by strychnine. Our results clearly show the existence of strychnine-sensitive and -insensitive glycine receptors in the DCN neurons.

Animals↗
PubMed1992

GABAergic synaptic current in dissociated nucleus basalis of Meynert neurons of the rat.

gamma-Aminobutyric acid (GABA)-mediated spontaneous inhibitory postsynaptic currents (IPSCs) were recorded from dissociated rat nucleus basalis of Meynert neurons which still had their synaptic boutons attached. The membrane currents were recorded by the whole-cell patch-clamp technique. Elevated extracellular K+ concentration and the addition of the calcium ionophore, A23187, enhanced the amplitude and frequency of spontaneous IPSCs. Ryanodine and Ca(2+)-free external solution containing EGTA or BAPTA markedly decreased the spontaneous IPSC activities. Spontaneous IPSC activities were reversibly reduced by baclofen and increased by phaclofen, indicating that the GABAB receptor regulates the release of GABA from nerve terminals and acts as a negative autoreceptor.

Animals↗
PubMed1992

Novel Ca2+ currents in mammalian CNS neurons.

Voltage-dependent Ca2+ currents (ICa) in neurons can be classified into T-, N- and L-types. In the CA1 pyramidal neurons freshly dissociated from rat hippocampus we found an additional tetrodotoxin (TTX)-sensitive Ca2+ current (termed 'TTX-ICa'). The TTX-ICa showed a heterogeneous distribution, preferentially in the dorsal site of CA1 region. Activation and inactivation processes of the TTX-ICa were highly potential-dependent, and the latter was fitted by a double exponential function. The TTX-ICa was activated at a threshold potential of about -55 mV and reached full activation at -30 mV. The steady-state inactivation of TTX-ICa could be fitted by a Boltzmann equation with a slope factor of 6.0 mV and a half-inactivation voltage of -72.5 mV. When the peak amplitudes of TTX-ICa were plotted as a function of extracellular Ca2+ concentration ([Ca2+]o), the current amplitude increased linearly without showing any saturation. The ratio of peak amplitude in the individual I-V relationships of Ca2+, Sr2+ and Ba2+ currents passing through the TTX-sensitive Ca(2+)-conducting channel was 1:0.33:0.05, although the current kinetics were much the same. TTX inhibited the TTX-ICa in time- and concentration-dependent manner without affecting the current kinetics. Lignocaine inhibited the TTX-ICa in a second in a concentration-dependent manner, with accelerating the inactivation process. The concentrations of half-inhibition (IC50) were 3.5 x 10(-9) M for TTX and 3.6 x 10(-4) M for lignocaine. Scorpion toxin prolonged the inactivation phase of TTX-ICa in a time- and concentration-dependent manner. In the toxin-treated neurons, both the slow time constant of inactivation (tau is) and its functional contribution to the total current increased with increasing the toxin concentration.

Animals↗
PubMed1992

Modulation of NMDA receptors by ACh in the central nervous system.

The effect of acetylcholine (ACh) on N-methyl-D-aspartate (NMDA)-induced responses in neurons acutely dissociated from the rat nucleus basalis of Meynert (nBM) was investigated with a conventional patch-clamp technique. The whole-cell recording revealed that NMDA-induced inward current (INMDA) consisted of transient peak and successive steady-state components. With outside-out recording, these components were shown to have the identical single channel conductance. Pretreating the nBM neurons with the low concentration of ACh suppressed the peak component of INMDA, whereas the high concentration potentiated it. The modulatory action of ACh was observed in nBM neurons dissociated from mature rats. The action was deficient, however, in those from immature animals. These results suggest that ACh is either an inhibitory or an excitatory modulator of glutamatergic transmission in the central nervous system.

Acetylcholine↗
PubMed1992

Regional variation of excitatory and inhibitory amino acid-induced responses in rat dissociated CNS neurons.

Regional differences in glutamate (Glu), aspartate (Asp), gamma-aminobutyric acid (GABA) and glycine (Gly) responses in CNS neurons were investigated by means of the whole-cell mode of the patch-clamp technique. The neurons were freshly dissociated from rat cortex, limbic system (hippocampal CA1 region), diencephalon (ventromedial hypothalamus), medulla (nucleus paragigantocellularis lateralis) and spinal cord (spinal dorsal horn). The current amplitudes induced by Glu and GABA did not show any regional differences whereas those of Asp- and Gly-induced responses were significantly different among CNS regions. The enhancement of Asp response by Gly was observed in all regions, and the facilitatory ratio did not differ among these regions. Even though the NMDA response in cortical neurons was significantly greater than that in spinal neurons, the ratios of NMDA response facilitation by Gly were also the same in both regions. When the current amplitudes induced by individual amino acids were estimated for the unit surface area of respective neurons (current density), the Glu, Asp and Gly responses showed regional heterogeneity whereas the GABA response did not.

Amino Acids↗