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PubMed1996

Metabotropic glutamate receptor dependent EPSP and EPSP-spike potentiation in area CA1 of the submerged rat hippocampal slice.

1. We reexamined the important areas of conflict in (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD]-induced potentiation of the field excitatory postsynaptic potential (EPSP) and, for the first time, investigated the role of mGluRs in EPSP-spike (E-S) coupling. 2. (1S,3R)-ACPD (10 microM) bath applied for 20 min consistently induced a long-lasting potentiation of the dendritic EPSP in area CA1 of submerged rat hippocampal slices, which was considerably faster in onset than described previously. 3. This effect was not associated with any change in presynaptic fiber volley but was dependent on both an intact CA3 connection, because removal of area CA3 blocked (1S,3R)-ACPD-induced potentiation, and also on functional N-methyl-D-aspartate (NMDA) receptors, because (1S,3R)-ACPD-induced potentiation was blocked by inclusion of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5; 50 microM). 4. (1S,3R)-ACPD induced a long-lasting potentiation of the population spike (PS) amplitude that was consistently larger than that of the EPSP measured in the cell body area. This EPSP-PS (E-S) potentiation was blocked by inclusion of the gamma-aminobuturic acid-A (GABAA) receptor antagonist, picrotoxin (50 microM). 5. E-S potentiation induced by high-frequency stimulation (HFS), which was of the same magnitude as that induced by (1S,3R)-ACPD, was blocked by the mGluR-selective antagonist (+)-alpha-methyl-4-carboxyphenylglycine (+MCPG; 250 microM). +MCPG also blocked HFS-induced long-term potentiation (LTP) of the EPSP measured in the cell body. 6. These results suggest that (1S,3R)-ACPD-induced potentiation is NMDA receptor dependent, contrary to some previous findings, and provide further evidence that both synaptic and E-S potentiation induced by (1S,3R)-ACPD share common mechanisms of expression with HFS-induced LTP. The data emphasize the important role of mGluRs in induction of EPSP LTP and E-S potentiation.

Animals↗
PubMed1992

The I' potential of the brain-stem auditory-evoked potential.

We have consistently recorded a positive wave which precedes wave I, and is called I', within the human brain-stem auditory-evoked potential. It is postulated that I' represents initial neural activity of the auditory nerve, which presumably has as its origin auditory nerve dendrites. Thus, I' may represent a summed far-field dendritic potential from currents of excitatory postsynaptic potentials. We report latency and amplitude values of I'.

Acoustic Stimulation↗
PubMed1993

Effect of denervation on neuromuscular transmission and glutamate sensitivity of the locust wing muscle fibers.

Changes in neuromuscular transmission and ultrastructure of synapses taking place after motor nerve cutting during 20 subsequent days were studied on the wing muscle of the locust (muscle 120) using intracellular recording from phasic fibres. The membrane potential (MP) and the excitatory postsynaptic potential (EPSP) showed practically no changes in comparison with the controls through day 8 after denervation. After the development of a neuromuscular transmission block between days 8 and 14, EPSP and miniature EPSP (MEPSP) disappeared, and the MP level somewhat decreased in comparison with controls. MEPSP frequency and amplitude increased in the first days after denervation. The sensitivity to glutaminic acid (Glu) gradually increased after nerve cutting, reached maximum on day 8 and remained at the same level subsequently (threshold concentration 0.003 mmol/l vs 0.3 mmol/l in the control). At the same time, the maximum amplitude of depolarization produced by Glu increased 1.5-2 times but slightly decreased subsequently. Beginning from day 4 after denervation synaptic vesicles began forming separate groups. On day 14 vesicles were grouped in macroconglomerates at a distance from the presynaptic membrane. On day 20 no axon profiles could be detected. The results suggest a similarity of denervation changes in insect wing and leg muscles.

Animals↗
PubMed2002

Long-term enhancement of excitatory synaptic inputs to layer V parahippocampal neurons by low frequency stimulation in rat brain slices.

Excitatory inputs to layer V neurons of the parasubiculum and medial entorhinal cortex were examined in rat brain slices with intracellular and field potential recordings. Single extracellular stimuli to layer V evoked subthreshold excitatory postsynaptic potentials (EPSPs) or a long duration (>100 ms) depolarization that sustained high frequency firing. Repetitive stimulation at low frequencies (from 1/10 s to 1/min) induced stable long-lasting decreases in the threshold for firing in individual cells or population events, and also induced stable long-lasting increases in evoked intracellular or field response amplitudes. More stimuli were required to produce the equivalent changes in threshold and amplitude in the presence of MCPG (200 microM). Smaller changes in amplitude, but equivalent changes in threshold were elicited in the presence of CPP (10 microM), or CPPG (20 microM). No changes in threshold or amplitude were detected in the presence of CNQX (10 microM), even when used in combination with picrotoxin (100 microM). EPSP facilitation was enhanced greatly by firing in postsynaptic cells. It is suggested that stable changes in excitatory inputs to layer V parahippocampal neurons involve the activation of NMDA and metabotropic glutamate receptors, but requires AMPA receptor activation and postsynaptic cell firing.

Action Potentials↗
PubMed2001

Long-term plasticity in interneurons of the dentate gyrus.

Single interneurons influence thousands of postsynaptic principal cells, and the control of interneuronal excitability is an important regulator of the computational properties of the hippocampus. However, the mechanisms underlying long-term alterations in the input-output functions of interneurons are not fully understood. We report a mechanism of interneuronal plasticity that leads to the functional enhancement of the gain of glutamatergic inputs in the absence of long-term potentiation of the excitatory synaptic currents. Interneurons in the dentate gyrus exhibit a characteristic, limited (approximately 8 mV) depolarization of their resting membrane potential after high-frequency stimulation of the perforant path. The depolarization can be observed with either whole-cell or perforated patch electrodes, and it lasts in excess of 3 h. The long-term depolarization is specific to interneurons, because granule cells do not show it. The depolarization requires the activation of Ca(2+)-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and the rise of intracellular Ca(2+), but not N-methyl-d-aspartate (NMDA) receptor activation. Data on the maintenance of the depolarization point to a major role for a long-term change in the rate of electrogenic Na(+)/K(+)-ATPase pump function in interneurons. As a result of the depolarization, interneurons after the tetanus respond with action potential discharges to previously subthreshold excitatory postsynaptic potentials (EPSPs), even though the EPSPs are not potentiated. These results demonstrate that the plastic nature of the interneuronal resting membrane potential underlies a unique form of long-term regulation of the gain of excitatory inputs to gamma-aminobutyric acid (GABA)ergic neurons.

Animals↗
PubMed1993

Large, deep layer pyramid-pyramid single axon EPSPs in slices of rat motor cortex display paired pulse and frequency-dependent depression, mediated presynaptically and self-facilitation, mediated postsynaptically.

1. In slices of rat sensorimotor cortex, dual intracellular recordings were obtained from 1,952 pairs of deep layer pyramidal neurons. Where action potentials in one neurone elicited excitatory postsynaptic potentials (EPSPs, n = 56) in the other, responses to different presynaptic firing rates and patterns and at different postsynaptic membrane potentials were recorded and on some occasions both neurons were filled with biocytin. 2. Slices were fixed, sectioned again at 60 microns, and incubated with Avidin horseradish peroxidase (HRP), which was then visualized using the 3,3'-diaminobenzidine tetrahydrochloride (DAB) method. All neurones reported here that were identified histologically were pyramidal cells with their somata in the deep layers (V and VI). 3. One in 70 of the tests performed revealed a synaptic connection, 25 of which were studied in detail. Mean EPSP amplitude was 1.67 +/- 1.66 (SD) mV, with some single sweep events as large as 9 mV. For some of the smaller EPSPs the amplitude distributions contained a clear peak around 0 mV, the coefficient of variation (CV) was large, and paired pulse facilitation was apparent. EPSPs with large average amplitudes displayed no apparent failures of transmission, EPSP amplitudes were fairly evenly distributed around the mean, CVs were small, and paired pulse depression was apparent in 2.5 mM extracellular Ca2+. When single sweeps were selected according to the size of the first EPSP, large second EPSPs were found to follow small first EPSPs and small second EPSPs to follow large first EPSPs. Paired pulse effects appeared, in the majority of tests, to be due to a change in presynaptic release probability. 4. Two EPSPs were recorded in three different extracellular Ca2+ concentrations. In 1 mM Ca2+, the first EPSP of a short interval pair was small and paired pulse facilitation was apparent. In 5 mM Ca2+, first EPSPs were between 2.5 and 4 times larger than in 1 mM Ca2+ and paired pulse depression was apparent. In all Ca2+ concentrations however, averaged third and fourth EPSPs of brief bursts were of similar amplitudes and smaller than second EPSPs. If presynaptic inhibition does contribute to paired pulse effects here, it is not overcome by a combination of raised extracellular Ca2+ and repetitive presynaptic firing. 5. These EPSPs displayed a wide range of time courses. The mean 10-90% rise time was 2.49 +/- 1.08 ms, the mean width at half amplitude was 15.39 +/- 5.42 ms (n = 22), and the mean EPSP latency was 1.59 +/- 0.68 ms (n = 18). (ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

Synaptic properties of neocortical neurons in epileptic mice lacking the Otx1 gene.

PURPOSE: The murine homeobox-containing Otx gene is required for correct nervous system and sense organ development. Otx1-/1 mice obtained by replacing Otx with the lac Z gene show developmental abnormalities of the cerebellum, mesencephalon, and cerebral cortex associated with spontaneous epileptic seizures (1). The epileptogenic mechanisms accounting for these seizures were investigated by means of electrophysiological recordings made from neocortical slices. METHODS: The 400-microm slices were prepared from the somatosensory cortex of Otx1-/- and Otx1+/+ mice, and the current clamp intracellular recordings were obtained from layer V pyramidal neurons by means of pipettes containing K+ acetate 1.5 mol/L and biocytin 2% (pH 7.3). RESULTS: Synaptic responses could be evoked in the neocortical pyramidal neurons by electrically stimulating the underlying white matter. gamma-Aminobutyric acid A/B-mediated inhibitory postsynaptic potentials were more pronounced in the Otx1-/- than in the control pyramidal neurons from the earliest postnatal period; multisynaptic excitatory postsynaptic potentials were significantly more expressed in the Otx1-/- mice also at the end of the first postnatal month, when they were only rarely encountered in controls. CONCLUSION: Excessive excitatory amino acid-mediated synaptic driving may lead to a hyperexcitable condition that is responsible for the epileptic manifestations occurring in Otx1-/- mice. This excess of excitation is not counteracted by well-developed gamma-aminobutyric acid activity, which seems to be involved in the synchronization of cell discharges. Our ongoing and more extensive comparative analysis of the mutants and controls should help to clarify the way in which the putative rearrangement taking place in Otx1-/- neocortex may lead to the excitatory hyperinnervation of layer V pyramidal neurons.

Animals↗
PubMed2001

Noise-tolerant stimulus discrimination by synchronization with depressing synapses.

Some synapses between cortical pyramidal neurons exhibit a rapid depression of excitatory postsynaptic potentials for successive presynaptic spikes. Since depressing synapses do not transmit information on sustained presynaptic firing rates, it has been speculated that they are favorable for temporal coding. In this paper. we study the dynamical effects of depressing synapses on stimulus-induced transient synchronization in a simple network of inhibitory interneurons and excitatory neurons, assuming that the recurrent excitation is mediated by depressing synapses. This synchronization occurs in a temporal pattern which depends on a given stimulus. Since the presence of noise is always a potential hazard in temporal coding, we investigate the extent to which noise in stimuli influences the synchronization phenomena. It is demonstrated that depressing synapses greatly contribute to suppressing the influences of noise on the stimulus-specific temporal patterns of synchronous firing. The timing-based Hebbian learning revealed by physiological experiments is shown to stabilize the temporal patterns in cooperation with synaptic depression. Thus, the times at which synchronous firing occurs provides a reliable information representation in the presence of synaptic depression.

Action Potentials↗
PubMed1976

Effect of temperature on postsynaptic potentials of cat spinal motoneurones.

The effect of spinal cord temperature on excitatory postsynaptic potentials (EPSP) and inhibitory postsynaptic potentials (IPSP) were measured by means of intracellular recordings from lumbar motoneurones of 43 cats. While body temperature and oil bath temperature were maintained between 37 and 38 degrees C, the temperature of the spinal segment under investigation was changed separately in the range between 30 and 42 degrees C. Cooling consistently produced an increase in amplitude and duration of both, mono- and poly-synaptic EPSPs and recurrent and direct IPSPs. Warming caused the opposite effect. The input resistance of the motoneurones was inversely related to the spinal cord temperature, while the latency of action potentials produced by intracellular injection of outward current was directly and exponentially related to spinal temperature. Although the data do not provide a quantitative differentiation of pre- versus postsynaptic temperature effects, they are consistent with the notion that temperature dependent changes on postsynaptic membrane properties contribute to the observed PSP changes. It is further suggested that similar postsynaptic temperature effects may be concerned in temperature sensitivity of proposed specific central neurones.

Animals↗
PubMed1996

Shared calcium signaling pathways in the induction of long-term potentiation and synaptic disinhibition in CA1 pyramidal cell dendrites.

1. Calcium signaling pathways were examined in the induction of long-term synaptic disinhibition following tetanization. Effects of tetanization on gamma-aminobutyric acid-A (GABAA receptor-mediated inhibitory responses were measured and compared with excitatory responses under experimental conditions previously used for examining induction mechanisms of N-methyl-D-aspartate (NMDA)-dependent long-term potentiation (LTP). Intracellular recordings were performed in current-clamp and discontinuous single-electrode voltage-clamp (dSEVC) modes in CA1 pyramidal cell apical dendrites in hippocampal slices of adult guinea pigs with the use of sharp electrodes. Test pulses and tetanic stimuli were applied to the Schaffer collateral fibers in stratum radiatum. 2. Under standard control conditions [3 M K Ac in the recording pipette and artificial cerebrospinal fluid as extracellular solution], tetanization-induced sustained increases of excitatory responses were accompanied by marked decreases of parameters of GABAA-mediated synaptic inhibition: at 40 min after tetanization [posttetanus 40 (PT 40)], orthodromically evoked excitatory postsynaptic potential (EPSP) peak amplitudes were on average 195 +/- 15% (mean +/- SE) and excitatory postsynaptic currents (IPSPs) were 166 +/- 10% of pretetanus controls. Peak amplitudes of orthodromically evoked inhibitory postsynaptic potentials (IPSPs) were 30 +/- 5% and inhibitory postsynaptic currents (IPSCs) were 21 +/- 4% at PT 40. Synaptic GABAA conductances (measured as chord conductances) were reduced to 22 +/- 4% at PT 40. Iontophoretic GABAA responses measured as conductance changes were 28 +/- 4% of pretetanus controls at PT 40. 3. A role of NMDA receptors in induction of long-term synaptic disinhibition was tested by preventing NMDA receptor activation 1) by pharmacological means and 2) by holding the membrane clamped at -80 mV (in dSEVC) during tetanization. In the presence of the NMDA-receptor antagonist D-2-amino5-phosphonopentanoic acid (D-AP5) 10-40 microM), orthodromically evoked EPSP amplitudes were 107 +/- 9%, EPSCs were 104 +/- 6%, GABAA-mediated IPSPs were 88 +/- 8%, IPSCs were 97 +/- 8%, synaptic GABAA conductances were 84 +/- 9%, and iontophoretic GABAA conductances were 102 +/- 13% at PT 40. In recordings in which the dendritic membrane potential was clamped at -80 mV during tetanization, orthodromically evoked peak amplitudes of EPSPs were 105 +/- 11%, EPSCs were 102 +/- 8, IPSPs were 103 +/- 4%, IPSCs were 102 +/- 5%, GABAA chord conductances were 101 +/- 9%, and iontophoretically evoked GABAA conductances were 105 +/- 5% at PT 40. 4. In recordings in which the intracellular pipette was preloaded with the Ca2+ chelator 1,2-bis(2-aminophenoxy) ethane-N,N,N'N"-tetraacetic acid (BAPTA) (5mM), long-term changes of synaptic transmission (increases of excitation, decreases of synaptic inhibition) were prevented. At PT 40, EPSP peak amplitudes were 93 +/- 7%, EPSCs were 115 +/- 6%, IPSPs were 115 +/- 9%, IPSCs were 117 +/- 8%, and synaptic GABAA conductances were 108 +/- 17%. Iontophoretic conductances at PT 40 were 109 +/- 9% over pretetanus controls when recorded with BAPTA-containing electrodes. 5. In recordings in which the intracellular pipette was preloaded with cypermethrin, a potent and selective inhibitor of phosphatase 2B, respective long-term changes of synaptic transmission (increases of excitation, decreases of synaptic inhibition) were prevented. At PT 40, EPSP peak amplitudes were 98 +/- 6%, EPSCs were 105 +/- 10%, IPSPs were 99 +/- 5%, IPSCs were 104 +/- 7%, synaptic GABAA conductances were 97 +/- 6% and iontophoretic GABAA conductances were 113 +/- 18% over pretetanus controls in cypermethrin-containing recordings. 6. In conclusion, the data presented demonstrate shared cellular pathways in the induction of both LTP and long-term synaptic disinhibition in apical dendrites of CA1 pyramidal cells after tetanization of the Schaffer collaterals.

Animals↗
PubMed2001

Substance P and neurokinin A mediate sensory synaptic transmission in young rat dorsal horn neurons.

Spinal nociceptive transmission is mediated by glutamate and neuropeptides such as substance P (SP) and neurokinin A (NKA). The neuropeptide-mediated excitatory postsynaptic potentials (EPSPs) had a slow onset and long duration. Here, we demonstrate SP- and NKA-mediated excitatory postsynaptic currents (EPSCs) in dorsal horn neurons of young rats using whole-cell patch-clamp recording techniques. After complete blockade of glutamate receptor-mediated currents, we observed a small residual EPSC. The residual EPSCs exhibited temporal summation in response to a train of stimulation (six pulses delivered at 10-50 Hz). High intensity stimulation (the same or greater than the stimulation threshold for nociceptive fibers in vivo) was required for evoking these summated EPSCs. Summated EPSCs were attenuated or abolished by capsaicin pretreatment, which depletes SP and NKA from presynaptic terminals; SP and NKA pretreatment; NK(1) or NK(2) receptor antagonists; and inhibition of postsynaptic G proteins. EPSCs were neither blocked by a metabotropic glutamate receptor antagonist nor a gamma-aminobutyric acid(B) receptor antagonist. The summated EPSCs were also sensitive to voltage-gated calcium channel antagonists or mu-opioid receptor activation by DAMGO. The present study provides electrophysiological evidence that suggests the possible contribution of SP and NKA to sensory synaptic transmission between primary afferent fibers and dorsal horn neurons.

2-Amino-5-phosphonovalerate↗
PubMed2004

Properties of horizontal axo-axonic cells in stratum oriens of the hippocampal CA1 area of rats in vitro.

Local-circuit gamma-aminobutyric acid (GABA)ergic interneurons constitute a diverse population of cells, which remain poorly defined into functionally distinct subclasses. Traditionally, dendritic and axonal arbors have been used to describe cell classes. In the present report, we characterize a set of hippocampal interneurons, horizontal axo-axonic cells, located in stratum oriens. They displayed the pattern of axonal arborization characteristic of axo-axonic cells with radially aligned rows of boutons making synapses exclusively on axon initial segments of pyramidal cells, as shown by electron microscopy. However, in contrast to previously described axo-axonic cells, which have radial dendrites spanning all layers, the dendrites of the horizontal axo-axonic cells were restricted to stratum oriens and ran parallel with the layers for several hundred micrometers. Single action potentials elicited by depolarizing current steps in these cells were often followed by a fast- and medium-duration afterhyperpolarization, distinguishing them from fast-spiking interneurons. In two out of four cells, trains of action potentials showed prominent early spike frequency adaptation and a characteristic "accommodative hump." Excitatory postsynaptic potentials (EPSPs) could be evoked by stimuli delivered to stratum oriens. Paired recordings unequivocally confirmed direct synaptic inputs from CA1 pyramidal cells. The kinetics of the EPSPs were fast (rise time 1.7 +/- 0.6 ms, mean +/- SD, n = 3; decay time constant 19.3 +/- 2.4 ms). They showed paired-pulse depression with inter-stimulus intervals of 10-50 ms. One pair showed a reciprocal connection establishing a direct feedback loop. The axo-axonic cell-evoked inhibitory postsynaptic potentials (IPSPs) were reliable (failure rate approximately 10%). Our data show that the laminar distribution of the dendrites of axo-axonic cells can vary, suggesting distinct synaptic inputs. However, this remains to be shown directly, and we cannot exclude the possibility that all axo-axonic cells may gather similar synaptic input, leaving them as one distinct class of interneuron.

Action Potentials↗
PubMed1998

Large frequency potentiation induced by 2 Hz stimulation in the hippocampus of epileptic El mice.

El mouse has been found to be characteristics with hippocampal disinhibition, and has been suggested decrease in GABAergic synaptic transmission [Ono et al., Brain Res. 745 (1997) 165-172; Fueta et al. , Brain Res. 779 (1998) 324-328]. The efficacy of GABAergic synapses can be modulated in response to trains of low frequency stimulation. The frequency potentiation of a population spike (PS) and the field excitatory postsynaptic potential (fEPSP) induced by a low frequency stimulation (2 Hz for 15 s) were recorded for the CA3 subfield, and PS alone for the CA1 subfield and dentate gyrus. PS frequency potentiation was greater in El mice than in non-epileptic control ddY mice. Especially the CA3 subfield exhibited a high PS frequency potentiation (300+/-73%) compared to age-matched ddY mice (64+/-24%). However, EPSP frequency potentiation was similar in El and ddY mice. The degree of PS frequency potentiation in CA3 was decreased by the reduction of extracellular Ca2+ from 2 to 1 mM in both strains, suggesting presynaptic involvement. The potentiation in El mice was suppressed by AMPA/kainate type receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dion (CNQX), but more than half of the control value remained at 5 microM, whereas the potentiation in ddY mice was abolished at this concentration. N-methyl-d-aspartate (NMDA) type receptor antagonist 3-3 (2-carboxypiperazine-4-yl) propyl-1-phosphonate (10 microM; CPP) did not affect the potentiation. Bicuculline (5 microM), GABAA receptor antagonist, did not increase the amplitude of PS during stimulation but induced epileptic (multiple PSs) potentials. High PS frequency potentiation of El mice was mimicked to the degree of that in ddY mice by a low dose of GABAB receptor agonist baclofen (3 microM). The suppression by baclofen was partially reversed by the antagonist saclofen (500 microM). The large frequency potentiation in young El mice, which do not have seizure-susceptibility, indicates an intrinsic property in El mice. It is suggested that the high synchronization of CA3 neurons in El mice is due to a little activation of GABAB receptor activation and also to enhancement of non-NMDA type synaptic transmission.

Animals↗
PubMed2006

Excitatory amino acid receptor-mediated responses in periaqueductal gray neurons are increased during ethanol withdrawal.

The ventrolateral periaqueductal gray (PAG) is critical for propagation in the neuronal network for ethanol withdrawal (ETX) seizures, and ethanol is known to alter glutamate effects. This study evaluated changes in glutamate antagonist effects on PAG neurophysiology in brain slices from rats treated with ethanol in vivo. Spontaneous action potentials were rare in control PAG neurons but common during ETX. Spontaneous excitatory postsynaptic potential (EPSP) frequency was increased during ETX, and an AMPA antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX) was more effective in suppressing this activity than an NMDA antagonist, 2-amino-7-phosphonoheptanoate (AP7). EPSPs evoked by stimulation of dorsolateral PAG were decreased by AP7 or DNQX in ETX and control neurons. EPSPs of ETX neurons were significantly less sensitive than controls to blockade by AP7 and DNQX. Paired-pulse facilitation of EPSPs was significantly increased during ETX, but paired-pulse inhibition occurred in controls. Thus, PAG hyperexcitability during ETX results from alterations of both NMDA and AMPA receptor-mediated neurotransmission, which may contribute importantly to ETX seizures. These results differ from previous findings in the seizure-initiating site for ETX seizures, inferior colliculus (IC), where NMDA receptor-mediated mechanisms dominate excitability increases during ETX. This dichotomy may be related to the different role played by IC and PAG in the ETX seizure network.

Action Potentials↗
PubMed2000

Influence of an extracellular acidosis on excitatory synaptic transmission and long-term potentiation in the CA1 region of rat hippocampal slices.

The effects of extracellular acidification on the synaptic function and neuronal excitability were investigated on the hippocampal CA1 neurons. A decrease of extracellular pH from 7.4 to 6.7 did not alter either the resting membrane potential or the neuronal membrane input resistance. Extracellularly recorded field excitatory postsynaptic potentials (fEPSPs) and population spikes (PSs) were significantly reduced by acidosis. Additionally, the amplitude of presynaptic fiber volley was also reduced. The sensitivity of postsynaptic neurons to N-methyl-D-aspartate, but not to alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, was depressed by acidosis. Lowering of extracellular pH did not significantly affect the magnitude of paired-pulse facilitation (PPF) of synaptic transmission. Acidosis also reversibly limited the sustained repetitive firing (RF) of Na(+)-dependent action potentials elicited by injection of depolarizing current pulses into the pyramidal cells. The limitation of RF by extracellular acidification was accompanied by the reduction of the maximal rate of rise (;V(max)) of the action potentials and the amplitude of afterhyperpolarization. Neither the Na (+)/H (+) antiporter blocker 5-(N -ethyl -N -isopropyl)-amiloride nor the selective adenosine A (1) receptor antagonist 1,3-dipropyl -8-cyclopentylxanthine, however, affected the acidosis -induced synaptic depression. It was also found that acidosis did not affect either the induction r maintenance of long -term potentiation (LTP) at Schaffer collateral -CA 1 synapses. These results suggest that the extracellular acidosis -induced synaptic depression is likely to result from an inhibition of presynaptic Na (+) conductance, thereby decreasing the amplitude of action potentials in individual afferent fibers or the number of afferent fiber activation to stimuli and then indirectly affecting the signaling processes contributing to trigger neurotransmitter release.

Acidosis↗
PubMed2002

Lack of effects of vitamin E on aluminium-induced deficit of synaptic plasticity in rat dentate gyrus in vivo.

Aluminium (Al), has the potential to be neurotoxic in humans and animals, and is present in many manufactured foods and medicines and is also added to drinking water for purification purposes. Our previous study demonstrated that chronic Al exposure induced deficits of both long-term potentiation (LTP) and long-term depression (LTD) of excitatory postsynaptic potential (EPSP) and population spike (PS) in rat dentate gyrus (DG) of hippocampus in vivo (Wang et al., 2001). The purpose of the present study was to investigate whether the Al-induced impairment of synaptic plasticity could be reversed by dietary supplementation with vitamin E (Vit E; alpha-tocopherol). Neonatal Wistar rats were exposed to Al from parturition throughout life by drinking 0.3% aluminium chloride (AlCl3) solution or a diet supplemented with Vit E at 500 microg/g/day with 0.3% AlCl3. The input/output (I/O) function, EPSP and PS were measured in DG area of adult rats (80-100 days of age) in response to stimulation applied to the lateral perforant path. The results showed that: (1) chronic Al exposure reduced the amplitudes of both EPSP LTP (control: 130.4+/-3%, n=7; Al-exposed: 110+/-2%, n=9, P<0.001) and PS LTP (control: 241+/-19%, n=7; Al-exposed: 130+/-7%, n=9, P<0.001) significantly. Vit E had no significant effects on the Al-induced deficits of EPSP LTP (Al-exposed: 110+/-2%, n=9; Al-exposed+Vit E: 112+/-2%, n=8, P>0.05) and PS LTP (Al-exposed: 130+/-7%, n=9; Al-exposed+Vit E: 129+/-4%, n=8; P>0.05); (2) the amplitudes of EPSP LTD (control: 84+/-4%, n=7; Al-exposed: 92+/-7%, n=9, P<0.01) and PS LTD (control: 81+/-4%, n=7; Al-exposed: 98+/-5%, n=9, P<0.001) were also decreased by Al treatment. The impaired EPSP LTD (Al-exposed: 92+/-7%, n=9; Al-exposed+Vit E: 93+/-4%, n=8, P>0.05) and PS LTD (Al-exposed: 98+/-5%, n=9; Al-exposed+Vit E: 94+/-6%, n=8, P>0.05) were also not significantly affected by Vit E treatment. It was suggested that dietary supplementation with Vit E did not reverse the impairment of synaptic plasticity induced by Al in DG in vivo.

Aluminum↗
PubMed2001

Electrophysiological effects of GABA on cat pancreatic neurons.

In mammalian peripheral sympathetic ganglia GABA acts presynaptically to facilitate cholinergic transmission and postsynaptically to depolarize membrane potential. The GABA effect on parasympathetic pancreatic ganglia is unknown. We aimed to determine the effect of locally applied GABA on cat pancreatic ganglion neurons. Ganglia with attached nerve trunks were isolated from cat pancreata. Conventional intracellular recording techniques were used to record electrical responses from ganglion neurons. GABA pressure microejection depolarized membrane potential with an amplitude of 17.4 +/- 0.7 mV. Electrically evoked fast excitatory postsynaptic potentials were significantly inhibited (5.4 +/- 0.3 to 2.9 +/- 0.2 mV) after GABA application. GABA-evoked depolarizations were mimicked by the GABA(A) receptor agonist muscimol and abolished by the GABA(A) receptor antagonist bicuculline and the Cl(-) channel blocker picrotoxin. GABA was taken up and stored in ganglia during preincubation with 1 mM GABA; beta-aminobutyric acid application after GABA loading significantly (P < 0.05) increased depolarizing response to GABA (15.6 +/- 1.0 vs. 7.8 +/- 0.8 mV without GABA preincubation). Immunolabeling with antibodies to GABA, glial cell fibrillary acidic protein, protein gene product 9.5, and glutamic acid decarboxylase (GAD) immunoreactivity showed that GABA was present in glial cells, but not in neurons, and that glial cells did not contain GAD, whereas islet cells did. The data suggest that endogenous GABA released from ganglionic glial cells acts on pancreatic ganglion neurons through GABA(A) receptors.

Aminobutyrates↗
PubMed1997

Biphasic effect of hydrogen peroxide on field potentials in rat hippocampal slices.

In the CA1 region of rat hippocampal slices, H2O2 (0.294-2.94 mM) caused initial augmentation, and subsequent long-lasting depression, of population spikes and excitatory postsynaptic potentials. The effect of H2O2 may not be mediated by its degradation product, hydroxyl radicals, because an iron chelator deferoxamine did not block the effect. A catalase inhibitor 3-amino-1,2,4-triazole only modestly attenuated the initial augmentation, suggesting that the effect of H2O2 is not attributable to catalase-dependent O2 generation, either. An N-methyl-D-aspartate receptor antagonist DL-2-amino-5-phosphonovaleric acid had no influence on the effect of H2O2, whereas a gamma-aminobutyric acid type A receptor channel blocker picrotoxin attenuated long-lasting depression, indicating that gamma-aminobutyric acid-mediated inhibition is altered during the depression phase. The initial augmentation but not subsequent depression was attenuated by a phospholipase A2/C inhibitor 4-bromophenacyl bromide, suggesting the involvement of lipid signaling molecule(s) in the enhancement of excitatory synaptic transmission. These results suggest that H2O2 regulates hippocampal synaptic transmission via multiple mechanisms.

Action Potentials↗