Actions of Gaba and Ethylenediamine on Ca1 Pyramidal Neurones of the Rat Hippocampus

Blaxter, T. J.; Cottrell, G. A.

doi:10.1113/expphysiol.1985.sp002898

Cited by 15 publications

(8 citation statements)

References 9 publications

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“…The profile of extracellular and intracellular recordings is consistent with previous work showing that somatic applications of GABA and EDA generate bicuculline-sensitive hyperpolarisations, while dendritic applications produce bicuculline-sensitive depolarisations (Blaxter and Cottrell, 1985). The intracellular depolarisation presumably corresponds to the extracellularly recorded depression of fepsps.…”

Section: Discussionsupporting

confidence: 73%

“…When aminophylline was applied by microiontophoresis to spontaneously firing neurones in vivo (Stone and Perkins, 1979) it produced a depression of neuronal firing, leading to the realisation that the inhibition was entirely attributable to the EDA, not the theophylline component of the complex Stone, 1980,1982a;Perkins et al, 1981). This conclusion was confirmed by others studying neuronal activity in the hippocampus (Blaxter and Cottrell 1985), cerebellum and invertebrate CNS (Bokisch et al, 1984).…”

Section: Introductionsupporting

confidence: 68%

“…This response would correspond to the dendritic, bicuculline-resistant, hyperpolarisation observed by Blaxter and Cottrell (1985) when GABA was applied locally to the dendritic region. It has been proposed by others, based on a substantial amount of evidence on uptake, release and actions, that β-alanine could function as an independent neurotransmitter (DeFeudis and del Rio, 1977;Sandberg and Jacobson, 1981).…”

Section: Discussionmentioning

confidence: 99%

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Effects of ethylenediamine – a putative GABA-releasing agent – on rat hippocampal slices and neocortical activity in vivo

Stone

Lui

Addae

2011

European Journal of Pharmacology

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The simple diamine diaminoethane (ethylenediamine, EDA) has been shown to activate GABA receptors in the central and peripheral nervous systems, partly by a direct action and partly by releasing endogenous GABA. These effects have been shown to be produced by the complexation of EDA with bicarbonate to form a carbamate. The present work has compared EDA, GABA and β-alanine responses in rat CA1 neurons using extracellular and intracellular recordings, as well as neocortical evoked potentials in vivo. Superfusion of GABA onto hippocampal slices produced depolarisation and a decrease of field epsps, both effects fading rapidly, but showing sensitivity to blockade by bicuculline. EDA produced an initial hyperpolarisation and increase of extracellular field epsp size with no fade and only partial sensitivity to bicuculline, with subsequent depolarisation, while β-alanine produces a much larger underlying hyperpolarisation and increase in fepsps, followed by depolarisation and inhibition of fepsps. The responses to β-alanine, but not GABA or EDA, were blocked by strychnine. In vivo experiments, recording somatosensory evoked potentials, confirmed that EDA produced an initial increase followed by depression, and that this effect was not fully blocked by bicuculline.Overall the results indicate that EDA has actions in addition to the activation of GABA receptors. These actions are not attributable to activation of β-alanine-sensitive glycine receptors, but may involve the activation of sites sensitive to adipic acid, which is structurally equivalent to the dicarbamate of EDA. The results emphasise the complex pharmacology of simple amines in bicarbonate-containing solutions.

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Section: Discussionsupporting

confidence: 73%

Section: Introductionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

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Effects of ethylenediamine – a putative GABA-releasing agent – on rat hippocampal slices and neocortical activity in vivo

Stone

Lui

Addae

2011

European Journal of Pharmacology

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“…It is well known that GABA produces several effects when applied to pyramidal neurones in the hippocampus (Andersen et al 1980;Djorup, Jahnsen & Mosfeldt Laursen, 1981;Thalmann, Peck & Ayala, 1981;Alger & Nicoll, 1982a;Wong & Watkins, 1982;Blaxter & Cottrell, 1985). The predominant action of GABA when applied in small amounts to the soma is a chloride-dependent hyperpolarization.…”

Section: Discussionmentioning

confidence: 99%

Voltage‐clamp analysis of somatic gamma‐aminobutyric acid responses in adult rat hippocampal CA1 neurones in vitro.

Ashwood

Collingridge

Herron

et al. 1987

The Journal of Physiology

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SUMMARY1. The response of CAI pyramidal neurones to somatic application of yaminobutyric acid (GABA) was studied in adult hippocampal slices using singleelectrode voltage-clamp techniques.2. Small ionophoretic applications of GABA produced a pure outward current at the cell resting potential when recording with potassium-acetate-filled microelectrodes. This response reversed at a membrane potential of -69+5 mV (mean+ 1 S.D.; n = 20). In recordings made with caesium-chloride-filled electrodes the GABA response reversed at -24 + 12 mV (n = 9).3. The effect of different holding potentials on the size of the GABA response was examined in the range of -100 to -40 mV in twenty neurones using potassiumacetate-filled electrodes. In every case outward rectification of the response was observed. For twelve neurones the mean ratio (±1 S.D. of the mean) of the conductance increase produced by GABA at -55 mV compared to -85 mV was 1-9 + 0 5. 4. Step changes in holding potential resulted in shifts in chloride equilibrium potential (EC,), as determined by time-dependent changes in the size of GABAinduced currents. The new value of EC1 was generally reached within a few seconds of altering the membrane potential. Shifts in EC, did not appear to affect the extent of rectification but would cause underestimates of conductance measurements unless these were 'instantaneous'. The mean ratio (± 1 S.D. of the mean) of the 'instantaneous'conductance increase produced by GABA at 13 mV positive to that at 13 mV negative to EC1 was 1-8 + 0 3.5. The outward rectification was greater than that predicted by the constant-field equation. Possible factors that might contribute towards the rectification and its physiological significance are discussed.

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“…Because EDAC acts in this manner, by releasing GABA from GABAergic neurones of the myenteric plexus rather than by directly stimulating GABA receptors, it seems desirable to investigate the possibility that a similar release of GABA from central neurones (Lloyd et al, 1982a;Blaxter & Cottrell, 1985) might also be partly responsible for the GABAmimetic properties of EDA, or EDAC, in the central nervous system. Furthermore, the present results show the ease with which EDAC is formed from EDA in the presence of carbon dioxide; indeed, EDAC can even be formed from EDA with atmospheric carbon dioxide (Frahn & Mills, 1964), which suggests that this conversion would probably occur in any experiments on EDA actions in the presence of bicarbonate buffer, either in vivo or in vitro.…”

Section: Discussionmentioning

confidence: 99%

Bicarbonate‐dependence of responses to ethylenediamine in the guinea‐pig isolated ileum: involvement of ethylenediamine‐monocarbamate

Kerr

Ong

1987

British J Pharmacology

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1 Iy-Aminobutyric-acid (GABA)-mimetic responses were induced by ethylenediamine (EDA) in the isolated ileum of the guinea-pig maintained in bicarbonate buffered Krebs-Henseleit (KBC) GABA from segments maintained in KBC solution. 4 GABA-mimetic responses were induced by EDAC in the isolated ileum maintained in bicarbonate-free KPO solution, as was a 3-aminovalerate-sensitive depression of ileal twitch responses elicited by transmural stimulation, all of which were also sensitive to 3-mercaptopropionic acid. 5 It is concluded that GABA-mimetic responses to EDA in the isolated ileum of the guinea-pig, maintained in normal Krebs bicarbonate medium, result from the release of endogenous GABA by ethylenediamine monocarbamate formed through the rapid reaction of EDA with the carbon dioxide of bicarbonate buffered Krebs solution. Furthermore, in the ileum, HCO3 ions per se are not necessary for this GABA-releasing property of EDA if the latter is first converted to the monocarbamate, since syntheticethylenediamine monocarbamate elicits ileal GABA-mimetic responses in the total absence of bicarbonate.

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Actions of Gaba and Ethylenediamine on Ca1 Pyramidal Neurones of the Rat Hippocampus

Cited by 15 publications

References 9 publications

Effects of ethylenediamine – a putative GABA-releasing agent – on rat hippocampal slices and neocortical activity in vivo

Effects of ethylenediamine – a putative GABA-releasing agent – on rat hippocampal slices and neocortical activity in vivo

Voltage‐clamp analysis of somatic gamma‐aminobutyric acid responses in adult rat hippocampal CA1 neurones in vitro.

Bicarbonate‐dependence of responses to ethylenediamine in the guinea‐pig isolated ileum: involvement of ethylenediamine‐monocarbamate

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