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At least 379 records · Page 21Linked to original sources
PubMed2006

GABAergic signaling at mossy fiber synapses in neonatal rat hippocampus.

In the adult rat hippocampus, granule cell mossy fibers (MFs) form excitatory glutamatergic synapses with CA3 principal cells and local inhibitory interneurons. However, evidence has been provided that, in young animals and after seizures, the same fibers can release in addition to glutamate GABA. Here we show that, during the first postnatal week, stimulation of granule cells in the dentate gyrus gave rise to monosynaptic GABAA-mediated responses in principal cells and in interneurons. These synapses were indeed made by MFs because they exhibited strong paired-pulse facilitation, high sensitivity to the metabotropic glutamate receptor agonist l-AP-4, and short-term frequency-dependent facilitation. MF responses were potentiated by blocking the plasma membrane GABA transporter GAT-1 with NO-711 or by allosterically modulating GABAA receptors with flurazepam. Chemical stimulation of granule cell dendrites with glutamate induced barrages of GABAA-mediated postsynaptic currents into target neurons. Furthermore, immunocytochemical experiments demonstrated colocalization of vesicular GABA transporter with vesicular glutamate transporter-1 and zinc transporter 3, suggesting that GABA can be taken up and stored in synaptic vesicles of MF terminals. Additional fibers releasing both glutamate and GABA into principal cells and interneurons were recruited by increasing the strength of stimulation. Both the GABAergic and the glutamatergic component of synaptic currents occurred with the same latency and were reversibly abolished by l-AP-4, indicating that they originated from the MFs. GABAergic signaling may play a crucial role in tuning hippocampal network during postnatal development. Low-threshold GABA-releasing fibers may undergo elimination, and this may occur when GABA shifts from the depolarizing to the hyperpolarizing direction.

Action Potentials↗
PubMed2006

The effect of intravenous magnesium hypophosphite in calcium borogluconate solution on the serum concentration of inorganic phosphorus in healthy cows.

The goal of this study was to determine the effect of intravenous (IV) administration of phosphite on the serum concentration of inorganic phosphorus in cows. Twelve clinically healthy cows were divided into four groups of three. All cows received 600 mL of a 40% calcium borogluconate solution; three cows each received this as a rapid (20 min) IV infusion with and without 6% magnesium hypophosphite, and three other cows each received this as a slow IV infusion (8 h) with and without 6% magnesium hypophosphite. Samples of blood were collected for the determination of serum concentrations of calcium, inorganic phosphorus and magnesium before and 10, 20, 40, 60 and 90 min and 2, 3, 4, 5, 6, 7, 8, 24, 48 and 72 h after the start of treatment. The concentration of calcium increased after treatment in all cows but the increase was most rapid in cows that received the rapid infusion. In cows that received the rapid IV infusion containing magnesium hypophosphite, the mean concentration of inorganic phosphorus decreased significantly 3-4 h after treatment compared with initial serum levels. The serum concentration of inorganic phosphorus did not change significantly in cows that received the rapid IV solution without magnesium hypophosphite or the slow IV infusion with or without magnesium hypophosphite. The serum concentration of magnesium increased after treatment in all cows receiving magnesium hypophosphite but remained unchanged in the others. The rapid infusion of calcium borogluconate without magnesium hypophosphite made all three cows anorexic and hypercalcaemic and the slow infusion made 1/3 anorexic. It is concluded that the IV administration of a calcium solution containing magnesium hypophosphite does not increase the serum concentration of inorganic phosphorus.

Animals↗
PubMed1994

GABA and glutamate release affected by GABAB receptor antagonists with similar potency: no evidence for pharmacologically different presynaptic receptors.

1. The effects of a series of nine GABAB receptor antagonists of widely varying potencies on electrically stimulated release from cortical slices of [3H]-GABA in the absence or presence of 10 microM of the GABAB agonist, (-)-baclofen and of endogenous glutamate in the presence of (-)-baclofen were compared. 2. The concentrations of the compounds half maximally increasing [3H]-GABA release (EC50's) at a stimulation frequency of 2 Hz correlated well with the IC50 values obtained from the inhibition of the binding of the agonist, [3H]-CGP 27492, to GABAB receptors in rat brain membranes (rank order of potency: CGP 56999 A > or = CGP 55845 A > CGP 52432 > or = CGP 56433 A > CGP 57034 A > CGP 57070 A > or = CGP 57976 > CGP 51176 > CGP 35348). 3. Likewise, the concentrations causing half-maximal increases of [3H]-GABA in the absence or presence of (-)-baclofen, and of endogenous glutamate in the presence of (-)-baclofen, correlated well with each other. Reports in the literature suggesting the CGP 35348 exhibits a 70 fold preference for inhibition of (-)-baclofen's effects on glutamate over [3H]-GABA release, and that CGP 52432 shows a 100 fold preference in the opposite sense, could not be confirmed in our model. 4. Therefore, our results suggest that, if there are pharmacological differences between GABAB autoreceptors and GABAB heteroreceptors on glutamatergic nerve endings in the rat cortex, they are not revealed by this series of compounds of widely different potencies. 5. In particular, our results with CGP 35348 and CGP 52432 do not support the hypothesis that GABAB autoreceptors and GABAB heteroreceptors on glutamatergic nerve endings represent subtypes with different pharmacology.

Animals↗
PubMed1987

An antioxidant-induced life table modification and life-span prolongation in Zaprionus paravittiger (Diptera).

An antioxidant, sodium hypophosphite (SHP-1 X 10(3) microM), when added to the diet of Zaprionus paravittiger, induces various shifts in the age-related biochemical parameters. It maintains the viability of protein synthesis and normal energy-yielding processes through longer intervals besides decelerating the rate of loss of nucleic acids (Sharma and Wadhwa, 1986). Reduced body weight which indicates the low level of food restriction, and adaptive changes in amino acids and proteins, could be the important factors for the favourable effect of this antioxidant on life span.

Amino Acids↗
PubMed2000

Reciprocal modulation of glutamate and GABA release may underlie the anticonvulsant effect of phenytoin.

Although conventional wisdom suggests that the effectiveness of phenytoin as an anticonvulsant is due to blockade of Na+-channels this is unlikely to be it's sole mechanism of action. In the present paper we examined the effects of phenytoin on evoked and spontaneous transmission at excitatory (glutamate) and inhibitory (GABA) synapses, in the rat entorhinal cortex in vitro. Evoked excitatory postsynaptic potentials at glutamate synapses exhibited frequency-dependent enhancement, and phenytoin reduced this enhancement without altering responses evoked at low frequency. In whole-cell patch-clamp recordings the frequency of excitatory postsynaptic currents resulting from the spontaneous release of glutamate was reduced by phenytoin, with no change in amplitude, rise time or decay time. Similar effects were seen on miniature excitatory postsynaptic currents, recorded in the presence of tetrodotoxin. Evoked inhibitory postsynaptic potentials at GABA synapses displayed a frequency-dependent decrease in amplitude. Phenytoin caused a reduction in this decrement without affecting the responses evoked at low frequency. The frequency of spontaneous GABA-mediated inhibitory postsynaptic currents, recorded in whole-cell patch mode, was increased by phenytoin, and this was accompanied by the appearance of much larger amplitude events. The effect of phenytoin on the frequency of inhibitory postsynaptic currents persisted in the presence of tetrodotoxin, but the change in amplitude distribution largely disappeared. These results demonstrate for the first time that phenytoin can cause a simultaneous reduction in synaptic excitation and an increase in inhibition in cortical networks. The shift in balance in favour of inhibition could be a major factor in the anticonvulsant action of phenytoin.

2-Amino-5-phosphonovalerate↗
PubMed2006

NMDA receptor-mediated transmission contributes to network 'hyperexcitability' in the rat insular cortex.

The insular cortex (IC) plays distinct roles under physiological and pathological conditions. However, the mechanisms regulating excitability in this area remain unknown. By employing field potential and sharp-electrode intracellular recordings in horizontal rat brain slices comprising the IC and the perirhinal cortex, we studied here the intrinsic and network characteristics of neurons in the agranular IC. These cells generated regular action potential firing with weak adaptation during intracellular injection of depolarizing current pulses, and were pyramidal in shape when neurobiotin filled. Spontaneous, field events (duration = 2.3 +/- 0.25 s; intervals of occurrence = 44.9 +/- 6.3 s) were identified in 22/52 slices and corresponded in IC neurons to intracellular depolarizations with action potential firing. Similar field and intracellular discharges were elicited in all slices by electrical stimuli. Antagonizing N-methyl-d-aspartate (NMDA) receptors blocked the spontaneous activity and reduced or abolished the stimulus-induced discharges. In the latter cases, stimuli elicited depolarizing events that became hyperpolarizing at about -64 mV, suggesting the contribution of gamma-aminobutyric acid (GABA)(A) receptor-mediated conductances. Our findings identify for the first time some functional properties of agranular IC neurons and point at a powerful NMDA receptor-mediated mechanism implementing network hyperexcitability. This feature may contribute to the role of IC in neurological disorders.

Animals↗
PubMed2001

Modulation of excitatory synaptic transmission by GABA(C) receptor-mediated feedback in the mouse inner retina.

In many vertebrate CNS synapses, the neurotransmitter glutamate activates postsynaptic non-N-methyl-D-aspartate (NMDA) and NMDA receptors. Since their biophysical properties are quite different, the time course of excitatory postsynaptic currents (EPSCs) depends largely on the relative contribution of their activation. To investigate whether the activation of the two receptor subtypes is affected by the synaptic interaction in the inner plexiform layer (IPL) of the mouse retina, we analyzed the properties of the light-evoked responses of ON-cone bipolar cells and ON-transient amacrine cells in a retinal slice preparation. ON-transient amacrine cells were whole cell voltage-clamped, and the glutamatergic synaptic input from bipolar cells was isolated by a cocktail of pharmacological agents (bicuculline, strychnine, curare, and atropine). Direct puff application of NMDA revealed the presence of functional NMDA receptors. However, the light-evoked EPSC was not significantly affected by D(-)-2-amino-5-phosphonopentanoic acid (D-AP5), but suppressed by 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX) or 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine hydrochloride (GYKI 52466). These results indicate that the light-evoked EPSC is mediated mainly by AMPA receptors under this condition. Since bipolar cells have GABA(C) receptors at their terminals, it has been suggested that bipolar cells receive feedback inhibition from amacrine cells. Application of (1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA), a specific blocker of GABA(C) receptors, suppressed both the GABA-induced current and the light-evoked feedback inhibition observed in ON-cone bipolar cells and enhanced the light-evoked EPSC of ON-transient amacrine cells. In the presence of TPMPA, the light-evoked EPSC of amacrine cells was composed of AMPA and NMDA receptor-mediated components. Our results suggest that photoresponses of ON-transient amacrine cells in the mouse retina are modified by the activation of presynaptic GABA(C) receptors, which may control the extent of glutamate spillover.

Amacrine Cells↗
PubMed2004

Identification and quantification of cotton-bound, cyclic polycarboxylic acids by means of isocratic HPLC.

Cotton fabrics are modified by means of polycarboxylic acids (PCA) in combination with an inorganic catalyst in order to impart durable press properties. To evaluate the effectiveness of cyclic PCA, 100% cotton fabrics were treated with 1,2,3,4,5,6-cyclohexanehexacarboxylic acid (CH-HCA), 1,3,5-cyclohexanetricarboxylic acid (CH-TCA), 1,2,3,4-cyclopentanetetracarboxylic acid (CP-TCA), and 1,2,3,4-tetrahydrofurantetracarboxylic acid (THF-TCA) in combination with sodium hypophosphite (SHP) as catalyst. The amount of PCA that reacted with the cellulosic material was determined by means of isocratic HPLC (Aminex HPX-87-H). The results clearly indicate that the cyclic PCA are less effective in respect of durable press performance. CH-TCA does not react with the cellulosic material thus confirming the assumption that the crosslinking reaction between PCA and the cellulose proceeds via a five-membered cyclic anhydride.

Calibration↗
PubMed2005

Melatonin decreases calcium levels in retinotectal axons of Xenopus laevis by indirect activation of group III metabotropic glutamate receptors.

Melatonin is a neuromodulator that binds to receptors in the retinotectal laminae of the amphibian optic tectum. The effect of melatonin on calcium dynamics in Xenopus retinotectal axons was investigated by imaging retinotectal axons labeled with the fluorescent indicator Fluo-4. Melatonin exerted an inhibitory influence on depolarization-evoked calcium increases, and the melatonin receptor antagonist 4-P-PDOT blocked this effect. Blockade of group III metabotropic receptors (mGluRs) counteracted the effect of melatonin on retinotectal axons. Application of the group II/group III mGluR antagonist MSPG or the group III-selective antagonist MSOP abolished the effect of melatonin. Conversely, this effect was not significantly affected by the group I mGluR antagonist LY367385 nor by EGLU or LY341495 at concentrations that specifically inhibit group II mGluRs. Furthermore, a higher concentration of LY341495 that affects group III mGluRs inhibited the effect of melatonin. The data therefore support the hypothesis that, in retinotectal axons, melatonin reduces cAMP levels, thereby relieving PKA-induced inhibition of group III mGluRs; the newly activated mGluRs in turn inhibit voltage-sensitive calcium channels, leading to a decrease in Ca2+ concentrations. The role of GABA(C) receptors in retinotectal responses was also evaluated. GABA(C) receptor antagonists did not block the effects of melatonin but instead were additive. Moreover, while other studies have shown that in Xenopus tectal cells, GABA(C) receptors mediate inhibition, in retinotectal axons, the opposite appears to occur since depolarization-evoked calcium rises in retinotectal axons were inhibited by GABA(C) receptor blockade. This result suggests that activation of GABA(C) receptors produces an increase in the synaptic excitability of retinotectal axon terminals.

Aniline Compounds↗