Enhancement of Endogenous Release of Glutamate and ?-Aminobutyric Acid from Hippocampus CA1 Slices After In Vivo Long-Term Potentiation (original) (raw)
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Neuroscience, 1989
The relationship between long-term potentiation of synaptic transmission and the release of endogenous glutamate and aspartate has been investigated in the CA1 region of the hippocampus and in the fascia dentata of the anaesthetized rat. A high-frequency train of electrical stimulation of afferent pathways produced a long lasting (r2 h) enhancement of the field excitatory postsynaptic potential in CA1 and of the population spike in the fascia dentata. In both regions, this was not associated with a significant long lasting increase in the release of glutamate and aspartate. It is concluded that the maintenance of long-term potentiation is not associated with a sustained increase in the release of excitatory amino acids.
P21. GABA and Glutamate release after LTP, J Neurochem 1992
The effect of long-term potentiation (LTP) on endogenous amino acid release from rat hippocampus slices was studied. LTP was induced in vivo by application of a tetanus (200 H2,200 ms) to the Schaffer collateral fibers in unanesthetized rats. Endogenous release ofglutamate and 7-aminobutyric acid (GABA) was investigated 60 min after tetanization in CAI subslices of potentiated and control rats. No significant effects of LTP were observed in basal and K+-induced Ca2*-independent release components of these amino acids. In contrast, K*-induced Ca2*-dependent release of both elutamate and GABA increased -100% in slices from potentiated rats. No differences were observed in total content of glutamate and GABA between the subslices from control and LTP animals. These results suggest a persistent increase in the recruitment ofthe presynaptic vesicular pool of glutamate and GABA during LTP. Key Words:
Characteristics of GABA release modified by glutamate receptors in mouse hippocampal slices
Neurochemistry International, 2003
The major part of hippocampal innervation is glutamatergic, regulated by inhibitory GABA-releasing interneurons. The modulation of [ 3 H]GABA release by ionotropic and metabotropic glutamate receptors and by nitric oxide was here characterized in superfused mouse hippocampal slices. The ionotropic glutamate receptor agonists kainate, N-methyl-d-aspartate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate potentiated the basal GABA release. These effects were blocked by their respective antagonists 6-nitro-7-cyanoquinoxaline-2,3dione (CNQX), dizocilpine and 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo(f)quinoxaline-7-sulfonamide (NBQX), indicating receptormediated mechanisms. The NO-generating compounds S-nitroso-N-acetylpenicillamine (SNAP), sodiumnitroprusside and hydroxylamine enhanced the basal GABA release. Particularly the sodiumnitroprusside-evoked release was attenuated by the NO synthase inhibitor N G -nitro-l-arginine (l-NNA) and the inhibitor of soluble guanylyl cyclase 1H-(1,2,4)oxadiazolo(4,3a)quinoxalin-1-one (ODQ), indicating the involvement of the NO/cGMP pathway. This inference is corroborated by the enhancing effect of zaprinast, a phosphodiesterase inhibitor, which is known to increase cGMP levels. The K + -stimulated hippocampal GABA release was reduced by the groups I and III agonists of metabotropic glutamate receptors (±)-1-aminocyclopentane-trans-1,3-dicarboxylate (t-ACPD) and l-(+)-2-amino-4-phosphonobutyrate (l-AP4), which effects were abolished by their respective antagonists (RS)-1-aminoindan-1,5-dicarboxylate (AIDA) and (RS)-2-cyclopropyl-4-phosphonophenylglycine (CPPG), again indicating modification by receptor-mediated mechanisms.
Vesicular release of glutamate from hippocampal neurons in culture: an immunocytochemical assay
Experimental Brain Research, 2008
Glutamate, the main excitatory neurotransmitter in the brain, may cause excitotoxic damage through excessive release during a number of pathological conditions. We have developed an immunocytochemical assay to investigate the mechanisms and regulation of glutamate release from intact, cultured neurons. Our results indicate that cultured hippocampal neurons have a large surplus of glutamate available for release upon chemically induced depolarization. Long incubations with high K + -concentrations, and induction of repetitive action potentials with the K + -channel blocker 4-aminopyridine (4-AP), caused a significant reduction in glutamate labeling in a subset of boutons, demonstrating that transmitter release exceeded the capacity for replenishment. The number of boutons where release exceeded replenishment increased continuously with time of stimulation. This depletion was Ca 2+dependent and sensitive to bafilomycin A1 (baf), indicating that it was dominated by vesicular release mechanisms. The depletion of glutamate from cell bodies and dendrites was also Ca 2+ -dependent. Thus, under the present conditions, cytosolic glutamate is taken up in vesicles prior to release, and the main escape route for the amino acid is through vesicular exocytosis. Depolarization with lower concentrations of K + caused sustainable release of glutamate, i.e., without full depletion.
Brain Research, 1977
To study the Ca2+-dependent efltux of GABA (y-aminobutyrate) from hippocampal tissue, superfused slices of the rat dentate gyrus, hippocampus regio inferior and hippocampus regio superior were depolarized with K + in a Ca2+-free medium into which Ca 2+ was then introduced. There was little variation among hippocampal regions in Ca2+-dependent GABA efltux; Ca 2÷ released endogenous GABA from the slices approximately in proportion to their GABA content. In contrast, slices of the dentate gyrus most efficiently accumulated and released exogenous radiolabeled GABA.
Synapse, 2006
We tested the hypothesis that presynaptic GABA B receptors on glutamatergic terminals (GABA B heterosynaptic receptors) decreased in efficacy after partial hippocampal kindling. Rats were implanted with chronically indwelling electrodes and 15 hippocampal afterdischarges were evoked by high-frequency electrical stimulation of hippocampal CA1. Control rats were implanted with electrodes but not given high-frequency stimulations. One to 21 days after the last afterdischarge, excitatory postsynaptic potentials (EPSPs) were recorded in CA1 of hippocampal slices in vitro, following stimulation of the stratum radiatum. Field EPSPs (fEPSPs) were recorded in CA1 stratum radiatum and intracellular EPSPs (iEPSPs) were recorded from CA1 pyramidal cells. GABA B receptor agonist 6 baclofen (10 lM) in the bath suppressed the fEPSPs significantly more in control than kindled rats, at 1 or 21 days after kindling. Similarly, baclofen (10 lM) suppressed iEPSPs more in the control than the kindled group of neurons recorded at 1 day after kindling. Suppression of the fEPSPs by 1 lM N 6 -cyclopentyladenosine, which acted on presynaptic A1 receptors, was not different between kindled and control rats. Activation of the GABA B heteroreceptors by a conditioning burst stimulation of CA3 afferents suppressed the iEPSPs evoked by a test pulse. The suppression of the iEPSPs at 250-500 ms condition-test interval was larger in control than kindled groups of neurons. It was concluded that the efficacy of presynaptic GABA B receptors on the glutamatergic terminals was reduced after partial hippocampal kindling. The reduction in heterosynaptic presynaptic GABA B receptor efficacy will increase glutamate release and seizure susceptibility, particularly during repeated neural activity. Synapse 59: [125][126][127][128][129][130][131][132][133][134] 2006. V V C 2005 Wiley-Liss, Inc.
Release of proteins during long-term potentiation in the hippocampus of the anaesthetized rat
Neuroscience Letters, 1988
Using a push pull device, the release of endogenous proteins in the cxtracellular space was investigated in the CAI region of the hippocampus of anaesthetized rats. With tow-frequency stimulation of the Schaffer collaterals, there was a relatively stable release of 5 proteins (64, 54, 48, 45 and 16 kDa). A train of high-frequency stimulation produced a long-lasting enhancement of the negative field EPSP and a delayed (90 120 min) enhancement of the release of these proteins. An additional 19 kDa protein was present only 90 min after the train. These observations raise the possibility that release of proteins might be involved in the maintenance of LTP. Long-term potentiation (LTP) is a long lasting enhancement of synaptic transmission produced by a train of high-frequency electrical stimulation [8, 28]. This phenomenon has been extensively studied in the hippocampal region and provides a useful experimental model for the study of the cellular mechanisms underlying learning and memory [20, 21]. However, the contribution of pre-and postsynaptic mechanisms to LTP have not been clarified; thus, there is a disagreement as to whether LTP is [9, 13, 15] or is not [4] associated with an increased release of the transmitter candidates glutamate or aspartate. Application of phorbol ester which produces LTP, different from that seen after a train [16], is also not associated with a release of endogenous excitatory amino acids [5]. Biochemical modifications in the hippocampus as well as protein phosphorylation have been reported after LTP [1, 2, 6, 11, 18, 23]. The appearance of newly synthesized proteins [14] in the extracellular fluid (ECF) and the prevention of LTP by inhibitors of protein synthesis [26] or monoclonal antibodies [27] suggest the involvement of macromolecules in this phenomenon. In the present study, using a push-pull cannula, we have examined the release of constituent proteins of the extracellular space
Collateral specific long term potentiation of the output of field CA3 of the hippocampus of the rat
Experimental Brain Research, 1986
Long term potentiation (LTP) in response to brief high frequency trains has been reported for many pathways in the hippocampus. The mechanisms involved are still unclear. The present experiments set out to confirm reports in the literature that LTP of output from CA3 neurons can be specific to particular collaterals. Single pulses delivered to area CA3 produced field responses nearly simultaneously in area CA1 and in the lateral septum (LS). High frequency stimulation of CA3 produced long term potentiation of CA1 but not LS responses. The CA1 response to stimulation of the contralateral hippocampus did not potentiate when the CA] response to CA3 stimulation showed long term potentiation. The CA1 and LS responses to CA3 stimulation showed similar strength-duration, strengthamplitude and frequency following characteristics. Their latencies were comparable to the latencies of antidromic activation of CA3 cells from CA1 and LS. Movement of stimulating electrodes to the region of the Schaffer collaterals increased the latency of the LS response and decraased the latency of the CA1 response but left the sum of these latencies unchanged. It was concluded that the CA3 and Schaffer stimulation were activating LS and CA1 collaterals of the same CA3 neurons. CA I and LS responses to CA3 stimulation showed somewhat different paired pulse and frequency potentiation characteristics. These data confirm reports in the literature that long term potentiation is both inputspecific and collateral-specific. The mechanisms of long term potentiation are likely, therefore, to be limited to changes at specific synaptic junctions, e.g. changes in sensitivity of specific postsynaptic receptor sites or changes in transmitter release, which can depend on functional or organisational differences between two collaterals of the same neuron.