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At least 883 records · Page 49Linked to original sources
PubMed2005

Opposite effects of lead exposure on taurine- and HFS-induced LTP in rat hippocampus.

The effect of lead exposure on taurine-induced long-term potentiation (LTP(TAU)) was examined and compared with high-frequency stimulation-induced one (LTP(HFS)). Field excitatory postsynaptic potentials (fEPSP) and fiber volley (FV) in area CA1 of hippocampal slice were recorded in control and lead-exposed rats. In contrast to the inhibitory effects of lead exposure on LTP(HFS), the amplitude of LTP(TAU) in the lead-exposed rats (199.3+/-13.7%, n=12) was significantly larger than that in controls (152.3+/-17.0%, n=12). It was also observed that taurine induced greater FV potentiation in lead-exposed rats (162.6+/-9.0%, n=10) than controls (132.1+/-6.9%, n=11). In addition, after a previous HFS, sequent perfusion of taurine could further increase the synaptic efficacy in lead-exposed rats. These results provide the first evidence that chronic lead exposure has opposite effects on the two types of LTP resulting from different lead toxicity sites.

Analysis of Variance↗
PubMed2001

Vestibuloocular reflex of the adult flatfish. III. A species-specific reciprocal pattern of excitation and inhibition.

In juvenile flatfish the vestibuloocular reflex (VOR) circuitry that underlies compensatory eye movements adapts to a 90 degrees relative displacement of vestibular and oculomotor reference frames during metamorphosis. VOR pathways are rearranged to allow horizontal canal-activated second-order vestibular neurons in adult flatfish to control extraocular motoneurons innervating vertical eye muscles. This study describes the anatomy and physiology of identified flatfish-specific excitatory and inhibitory vestibular pathways. In antidromically identified oculomotor and trochlear motoneurons, excitatory postsynaptic potentials (EPSPs) were elicited after electrical stimulation of the horizontal canal nerve expected to provide excitatory input. Electrotonic depolarizations (0.8-0.9 ms) preceded small amplitude (<0.5 mV) chemical EPSPs at 1.2-1.6 ms with much larger EPSPs (>1 mV) recorded around 2.5 ms. Stimulation of the opposite horizontal canal nerve produced inhibitory postsynaptic potentials (IPSPs) at a disynaptic latency of 1.6-1.8 ms that were depolarizing at membrane resting potentials around -60 mV. Injection of chloride ions increased IPSP amplitude, and current-clamp analysis showed the IPSP equilibrium potential to be near the membrane resting potential. Repeated electrical stimulation of either the excitatory or inhibitory horizontal canal vestibular nerve greatly increased the amplitude of the respective synaptic responses. These observations suggest that the large terminal arborizations of each VOR neuron imposes an electrotonic load requiring multiple action potentials to maximize synaptic efficacy. GABA antibodies labeled axons in the medial longitudinal fasciculus (MLF) some of which were hypothesized to originate from horizontal canal-activated inhibitory vestibular neurons. GABAergic terminal arborizations were distributed largely on the somata and proximal dendrites of oculomotor and trochlear motoneurons. These findings suggest that the species-specific horizontal canal inhibitory pathway exhibits similar electrophysiological and synaptic transmitter profiles as the anterior and posterior canal inhibitory projections to oculomotor and trochlear motoneurons. Electron microscopy showed axosomatic and axodendritic synaptic endings containing spheroidal synaptic vesicles to establish chemical excitatory synaptic contacts characterized by asymmetrical pre/postsynaptic membrane specializations as well as gap junctional contacts consistent with electrotonic coupling. Another type of axosomatic synaptic ending contained pleiomorphic synaptic vesicles forming chemical, presumed inhibitory, synaptic contacts on motoneurons that never included gap junctions. Altogether these data provide electrophysiological, immunohistochemical, and ultrastructural evidence for reciprocal excitatory/inhibitory organization of the novel vestibulooculomotor projections in adult flatfish. The appearance of unique second-order vestibular neurons linking the horizontal canal to vertical oculomotor neurons suggests that reciprocal excitation and inhibition are a fundamental, developmentally linked trait of compensatory eye movement circuits in vertebrates.

Abducens Nerve↗
PubMed2005

Excitatory synaptic potentials in spastic human motoneurons have a short rise-time.

This study assessed whether changes in size or time-course of excitatory postsynaptic potentials (EPSPs) in motoneurons innervating spastic muscle could induce a greater synaptic response, and thereby contribute to reflex hyperexcitability. We compared motor unit (MU) firing patterns elicited by tendon taps applied to both spastic and contralateral (nonspastic) biceps brachii muscle in hemiparetic stroke subjects. Based on recordings of 115 MUs, significantly shortened EPSP rise times were present on the spastic side, but with no significant differences in estimated EPSP amplitude. These changes may contribute to hyperexcitable reflex responses at short latency, but the EPSP amplitude changes appear insufficient to account for global differences in reflex excitability.

Excitatory Postsynaptic Potentials↗
PubMed2007

Properties of basal dendrites of layer 5 pyramidal neurons: a direct patch-clamp recording study.

Basal dendrites receive the majority of synapses that contact neocortical pyramidal neurons, yet our knowledge of synaptic processing in these dendrites has been hampered by their inaccessibility for electrical recordings. A new approach to patch-clamp recordings enabled us to characterize the integrative properties of these cells. Despite the short physical length of rat basal dendrites, synaptic inputs were electrotonically remote from the soma (>30-fold excitatory postsynaptic potential (EPSP) attenuation) and back-propagating action potentials were significantly attenuated. Unitary EPSPs were location dependent, reaching large amplitudes distally (>8 mV), yet their somatic contribution was relatively location independent. Basal dendrites support sodium and NMDA spikes, but not calcium spikes, for 75% of their length. This suggests that basal dendrites, despite their proximity to the site of action potential initiation, do not form a single basal-somatic region but rather should be considered as a separate integrative compartment favoring two integration modes: subthreshold, location-independent summation versus local amplification of incoming spatiotemporally clustered information.

Action Potentials↗
PubMed2001

Effects of pituitary adenylate cyclase activating polypeptide on lumbosacral preganglionic neurons in the neonatal rat spinal cord.

The effects of PACAP-38 on phasic and tonic preganglionic neurons (PGN) in L6 and S1 spinal cord slices from neonatal rats (5--11 days old) were studied using the whole-cell patch clamp technique. PGN were identified by retrograde axonal transport of a fluorescent dye (Fast Blue, 5 microl of 4% solution) injected into the intraperitoneal space 3--7 days prior to the study. Bath application of pituitary adenylate cyclase activating polypeptide (PACAP) (20 nM) increased the frequency of spontaneous excitatory postsynaptic potentials (EPSPs) and spontaneous firing in both types of PGN. PACAP markedly increased the number (200--800%) and frequency of action potentials elicited by depolarizing current pulses in phasic PGN, but had a smaller effect on tonic PGN. PACAP decreased the threshold for action potential generation by approximately 25% in both types of neurons (e.g. -34.0+/-1.5 to -38.4+/-1.7 mV from a holding potential of -50 mV in phasic PGN, P<0.005). PACAP did not affect the duration of the action potential. The amplitude of the spike after hyperpolarization was not changed but the duration was significantly reduced by PACAP from 204.4+/-12.2 to 106.2+/-8.1 ms in tonic but not in phasic PGN. PACAP suppressed a transient outward current that was also suppressed by 4-aminopyridine (0.5 mM). These results coupled with the immunohistochemical identification of a dense collection of PACAP fibers in the region of the PGN, raises the possibility that PACAP may function as an excitatory transmitter in lumbosacral parasympathetic reflex pathways in the neonatal rat.

4-Aminopyridine↗
PubMed2002

Synaptic mechanisms regulating the activation of a Ca(2+)-mediated plateau potential in developing relay cells of the LGN.

Using intracellular recordings in an isolated (in vitro) rat brain stem preparation, we examined the synaptic responses of developing relay neurons in the dorsal lateral geniculate nucleus (LGN). In newborn rats, strong stimulation of the optic tract (OT) evoked excitatory postsynaptic potentials (EPSPs) that gave rise to a sustained (300-1,300 ms), slow-decaying (<0.01 mV/s), depolarization (25-40 mV). Riding atop this response was a train of spikes of variable amplitude. We refer to this synaptically evoked event as a plateau potential. Pharmacology experiments indicate the plateau potential was mediated by the activation of high-threshold L-type Ca(2+) channels. Synaptic activation of the plateau potential relied on N-methyl-D-aspartate (NMDA) receptor-mediated activity and the spatial and/or temporal summation of retinally evoked EPSPs. Inhibitory postsynaptic responses (IPSPs) did not prevent the expression of the plateau potential. However, GABA(A) receptor activity modulated the intensity of optic tract stimulation needed to evoke the plateau potential, while GABA(B) receptor activity affected its duration. Expression of the plateau potential was developmentally regulated, showing a much higher incidence at P1-2 (90%) than at P19-20 (1%). This was in part due to the fact that developing relay cells show a greater degree of spatial summation than their mature counterparts, receiving input from as many as 7-12 retinal ganglion cells. Early spontaneous retinal activity is also likely to trigger the plateau potential. Repetitive stimulation of optic tract in a manner that approximated the high-frequency discharge of retinal ganglion cells led to a massive temporal summation of EPSPs and the activation of a sustained depolarization (>1 min) that was blocked by L-type Ca(2+) channel antagonists. These age-related changes in Ca(2+) signaling may contribute to the activity-dependent refinement of retinogeniculate connections.

2-Amino-5-phosphonovalerate↗
PubMed2000

Actions of histamine on muscle and ganglia of the guinea pig gallbladder.

Histamine is an inflammatory mediator present in mast cells, which are abundant in the wall of the gallbladder. We examined the electrical properties of gallbladder smooth muscle and nerve associated with histamine-induced changes in gallbladder tone. Recordings were made from gallbladder smooth muscle and neurons, and responses to histamine and receptor subtype-specific compounds were tested. Histamine application to intact smooth muscle produced a concentration-dependent membrane depolarization and increased excitability. In the presence of the H(2) antagonist ranitidine, the response to histamine was potentiated. Activation of H(2) receptors caused membrane hyperpolarization and elimination of spontaneous action potentials. The H(2) response was attenuated by the ATP-sensitive K(+) (K(ATP)) channel blocker glibenclamide in intact and isolated smooth muscle. Histamine had no effect on the resting membrane potential or excitability of gallbladder neurons. Furthermore, neither histamine nor the H(3) agonist R-alpha-methylhistamine altered the amplitude of the fast excitatory postsynaptic potential in gallbladder ganglia. The mast cell degranulator compound 48/80 caused a smooth muscle depolarization that was inhibited by the H(1) antagonist mepyramine, indicating that histamine released from mast cells can activate gallbladder smooth muscle. In conclusion, histamine released from mast cells can act on gallbladder smooth muscle, but not in ganglia. The depolarization and associated contraction of gallbladder smooth muscle represent the net effect of activation of both H(1) (excitatory) and H(2) (inhibitory) receptors, with the H(2) receptor-mediated response involving the activation of K(ATP) channels.

Adenosine Triphosphate↗
PubMed1985

Excessive glutamate as an inhibitor of excitatory transmission in rat hippocampal slice.

Exposure of rat hippocampal slices to perfusate containing 1-2 mM glutamate (GLU) induces reversible and relatively selective blockade of excitatory transmission. Intracellular recordings from 20 region CA1 hippocampal cells demonstrated only transient and mild effects on resting membrane properties and action potentials. In contrast, in 2 mM GLU excitatory postsynaptic potentials declined to 28% of control (P less than 0.001); inhibitory postsynaptic potentials remained robust at 88% of control. This suggests that excess exposure to GLU may result in a selective 'down-regulation' of excitatory synaptic transmission, while preserving inhibitory pathways. These observations may have practical implications for development of new anticonvulsant drugs.

Animals↗
PubMed1999

Dendritic GABA release depresses excitatory transmission between layer 2/3 pyramidal and bitufted neurons in rat neocortex.

GABAergic, somatostatin-containing bitufted interneurons in layer 2/3 of rat neocortex are excited via glutamatergic excitatory postsynaptic potentials (EPSPs) by pyramidal neurons located in the same cortical layer. Pair recordings showed that short bursts of backpropagating dendritic action potentials (APs) reduced the amplitude of unitary EPSPs. EPSP depression was dependent on a rise in dendritic [Ca2+]. The effect was blocked by the GABA(B) receptor (GABA(B)-R) antagonist CGP55845A and was mimicked by the GABA(B)-R agonist baclofen. As presynaptic GABA(B)-Rs were activated neither by somatostatin nor by GABA released from axon collaterals of the bitufted cell, we conclude that GABA(B)-Rs were activated by a retrograde messenger, most likely GABA, released from the dendrite. Because synaptic depression was prevented by loading bitufted neurons with GDP-beta-S, it is likely to be caused by exocytotic GABA release from dendrites.

Action Potentials↗
PubMed1992

Reversal learning of the rabbit nictitating membrane response following kindling-induced potentiation within the hippocampal dentate gyrus.

The following experiment examined the effects of kindled seizures on reversal learning and the effects of both kindling and classical conditioning of the rabbit nictitating membrane on granule cell responsivity to perforant path input. Kindling resulted in significant potentiation of the population spike, the excitatory postsynaptic potential (EPSP) and the magnitude of twin pulse inhibition. Following kindling, rabbits were trained in a discrimination-reversal paradigm with either a tone or light paired with a corneal airpuff. Kindling did not affect acquisition of the initial discriminative response but did retard the rate of reversal learning. Kindling-induced potentiation, within dentate excitatory and inhibitory circuits, persisted for the duration of training. Thus, these results do not distinguish between the contribution of kindling-induced potentiation within dentate excitatory and inhibitory circuits to discrimination-reversal training. Spikes evoked during tone presentations were of reduced amplitude compared to spikes evoked either between trials or during light trials. The EPSP was not affected by stimulus conditions. In control rabbits, the magnitude of both the spike and EPSP increased across training. Training-related potentiation, in kindled rabbits, could not be separated from kindling-induced potentiation. These results demonstrate that an LTP-like effect of both the population spike and EPSP occurs with discrimination-reversal training.

Animals↗
PubMed1991

Commissural responses of rat retrohippocampal neurons.

Synaptic responses of commissurally activated rat subicular and entorhinal neurons were studied intracellularly in vivo by stimulating the contralateral dentate gyrus. The most prominent synaptic responses in both subicular and entorhinal neurons were inhibitory postsynaptic potentials (IPSPs). IPSPs were generated in combination with antidromic spikes and/or excitatory postsynaptic potentials (EPSPs) and orthodromic spikes. No dependency between any two response types were found. Commissurally projecting subicular neurons (identified by the presence of antidromic spikes evoked by contralateral stimulation) were found, extending previous anatomical studies. Commissurally projecting entorhinal neurons were found in layer II, confirming previous anatomical studies. Positive correlations between antidromic spike latency and depth of recording sites supported the interpretation that axons projected along the fiber bundles of the hippocampal commissures and angular bundle to distribute to their targets. Possible circuits that could have mediated the excitatory and inhibitory responses of these retrohippocampal neurons are considered.

Animals↗
PubMed1999

Analysis of potentiation in the cerebral ganglion of Aplysia.

Quantal analysis was used to characterize synaptic transmission between A and B neurons in the cerebral ganglion of Aplysia in control and during slow developing potentiation, a form of synaptic plasticity exhibited by these synapses. Control values of mean quantal content (m) and quantal size (q) estimated by the method of coefficient of variation (CV) were m approximately 6, q approximately 56 microV in the solution with Ca2+/Mg2+ = 5/200 and m approximately 18, q approximately 41 microV in the solution with Ca2+/Mg2+ = 55/150. There was a good correlation between an increase in the amplitude of excitatory synaptic potential and an increase in calculated quantal content (m(cv)) during potentiation. A decrease of Ca2+/Mg2+ ratio in the bath solution allowed observation of transmission failures and in some cases regular peaks on excitatory postsynaptic potential amplitude histograms. The latter provided more direct estimate of the quantal size. Induction of the potentiation in this solution, however, became difficult. In cases of successful potentiation induction, probability of failures was less than in control; distances between histogram peaks, reflecting quantal size remained the same. The results obtained in this study support a hypothesis that potentiation of the synaptic transmission between A and B neurons of Aplysia is primarily due to an increase of transmitter release.

Animals↗
PubMed2004

Long-term potentiation in the optic tectum of rainbow trout.

We examined synaptic plasticity in the optic tectum of rainbow trout by extracellular recordings. We found that the field-excitatory postsynaptic potential in the retinotectal synapses was potentiated by repetitive stimuli of 1.0 Hz for 20 s to the retinotectal afferents. The long-term potentiation (LTP) developed slowly, and was maintained for at least 2 h. Applications of an antagonist for N-methyl-D-aspartic acid (NMDA) receptors or Mg2+ -free saline showed that activation of NMDA receptors was required to form the LTP beyond the induction period. The present findings indicate that presynaptic stimulation in the retinotectal synapses causes LTP mediated by NMDA receptors in the optic tectum of rainbow trout.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2000

A model for pleiotropic muscarinic potentiation of fast synaptic transmission.

The predominant form of muscarinic excitation in the forebrain and in sympathetic ganglia arises from m1 receptors coupled to the G(q/11) signal transduction pathway. Functional components of this system have been most completely mapped in frog sympathetic B neurons. Presynaptic stimulation of the B neuron produces a dual-component muscarinic excitatory postsynaptic potential (EPSP) mediated by suppression of voltage-dependent M-type K(+) channels and activation of a voltage-insensitive cation current. Evidence from mammalian systems suggests that the cation current is mediated by cyclic GMP-gated channels. This paper describes the use of a computational model to analyze the consequences of pleiotropic muscarinic signaling for synaptic integration. The results show that the resting potential of B neurons is a logarithmic function of the leak conductance over a broad range of experimentally observable conditions. Small increases (<4 nS) in the muscarinically regulated cation conductance produce potent excitatory effects. Damage introduced by intracellular recording can mask the excitatory effect of the muscarinic leak current. Synaptic activation of the leak conductance combines synergistically with suppression of the M-conductance (40 --> 20 nS) to strengthen fast nicotinic transmission. Overall, this effect can more than double synaptic strength, as measured by the ability of a fast nicotinic EPSP to trigger an action potential. Pleiotropic muscarinic excitation can also double the temporal window of summation between subthreshold nicotinic EPSPs and thereby promote firing. Activation of a chloride leak or suppression of a K(+) leak can substitute for the cation conductance in producing excitatory muscarinic actions. The results are discussed in terms of their implications for synaptic integration in sympathetic ganglia and other circuits.

Action Potentials↗
PubMed1996

Localized calcium signalling and neuronal integration in cerebellar Purkinje neurones.

The use of high resolution imaging techniques has revealed new forms of dendritic signal integration in neurones. In contrast to electrical signals that have a more widespread influence on the cell, brief Ca2+ transients resulting from synaptic activation are often restricted to a small part of the dendritic tree. In cerebellar Purkinje neurones, different levels of Ca2+ signalling have been observed that may involve the entire neurone or be spatially limited to fine dendritic structures. The Ca2+ signals accompanying subthreshold excitatory postsynaptic potentials resulting from stimulation of the excitatory parallel fibre input can be restricted to regions as small as a spiny dendrite or a single dendritic spine. With the recruitment of increasing numbers of inputs there is a summation of Ca2+ signals in highly restricted regions of the spiny dendrites that is independent of electrical summation at the soma. Of a number of potential sources that could provide the Ca2+ responsible for the postsynaptic changes, Ca2+ entry through voltage-gated Ca2+ channels has received the most support, although other sources like Ca2+ entry through ligand-gated channels and especially Ca2+ release from intracellular stores need to be considered.

Animals↗
PubMed1990

In vivo intracellular analysis of rat dentate granule cells.

In vivo intracellular recordings and dentate EEG were obtained in urethanized-curarized rats. Granule cells (GCs) were identified by antidromic activation as well as by intracellular staining with Lucifer yellow (LY). GCs fired spikes which, in 43.6% of the cases, had brief post-hyperpolarization. Slow spikes were recorded at hyperpolarized levels during the rebound of hyperpolarizing pulses or during inhibitory postsynaptic potentials (IPSPs). Medial septal nucleus or perforant pathway stimulation evoked an excitatory postsynaptic potential (EPSP)-IPSP sequence. During theta (theta) rhythm, the membrane potential of 80.3% of the GCs showed rhythmic sine-like waves of up to 15 mV at a theta frequency which were phase-locked with extracellular theta. GCs were classified into 3 types: type 1 (67.1%) showed intracellular theta and rhythmic firing; type 2 (13.2%) revealed intracellular theta and random firing, but spikes tended to occur at a preferred phase of the dentate theta; and type 3 (19.7%) had neither intracellular theta nor rhythmic firing. Intracellular theta amplitude was wider during injection of the hyperpolarizing current and narrower during depolarizing ones, indicating that rhythmic EPSPs contribute to theta genesis. Intracellular theta was unaffected by Cl- or Cs+ diffusion, suggesting that IPSP is not essential to theta genesis.

Action Potentials↗
PubMed2000

Afferent high strength tetanizations favour potentiation of the NMDA vs. AMPA receptor-mediated component of field EPSP in CA1 hippocampal slices of rats.

Long-term potentiation (LTP) of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated components of 'dual-component' field excitatory postsynaptic potentials (fEPSP-A and fEPSP-N) was studied in the CA1 stratum radiatum in hippocampal slices of rats. Relative degrees of LTP of these fEPSP components were compared for tetanizations with low and high strengths. Magnitudes of fEPSP-A and fEPSP-N were estimated in parallel with a least-square fitting of a short-latent (0.1-8.8 ms) fragment of evoked responses by a weighted sum of 'basic' fEPSP-A and fEPSP-N, obtained during a short preliminary application of d-2-amino-5-phosphonovalerate (APV). We found that low-strength tetanizations selectively potentiated fEPSP-A, while high strength tetanizations potentiated both fEPSP components. These results demonstrate in the experiments with parallel measurements of fEPSP-A and fEPSP-N that LTP of these components differ depending on the strength of afferent tetanization. Unequal potentiation of the commissural-collateral and excitatory local-circuit synapses, which presumably contain different amounts of the AMPA and NMDA receptors, is discussed as the most probable explanation for these results.

Animals↗
PubMed2006

5-HT4 receptor activation induces long-lasting EPSP-spike potentiation in CA1 pyramidal neurons.

Recent studies implicated involvement of the 5-hydroxytryptamine4 (5-HT4) receptor in cognitive and emotional processes. The highest 5-HT4 receptor densities in the brain are found in the limbic system including the hippocampus. Here we used the selective 5-HT4 receptor full agonist, N-pentyl-N'-aminoguanidine carbazimidamide (SDZ-216454) to characterize effects of 5-HT4 receptor activation in whole-cell and field recordings in the area CA1 in hippocampal slices prepared from 3 to 4- and 6 to 9-week-old rats, respectively. Extracellular recordings showed that transient 5-HT4 receptor activation by 10-20 min application of SDZ-216454 induces field excitatory postsynaptic potential (fEPSP)-population spike potentiation (ESP(5-HT4)), which persisted for as long as we held the recordings (> 2 h). ESP(5-HT4) displayed characteristics different from EPSP-spike potentiation that accompanies long-term potentiation; it developed without an associated increase in synaptic transmission, was independent on afferent input, activity of postsynaptic neurons and N-methyl-d-aspartate receptor activation; and was expressed in the presence of GABA receptor antagonists. ESP(5-HT4) was also induced by transient application of the natural neurotransmitter, 5-HT. The increase in the evoked population spike (PS) induced by SDZ-216454 was not prevented by blockers of hyperpolarization-activated cation current (Ih), Cs+ and ZD-7288, but was mimicked and occluded by 150 microm Ba2+. Whole-cell voltage-clamp recordings from pyramidal neurons demonstrated that SDZ-216454 application increases membrane resistance with a concomitant decrease in a Ba2+-sensitive inwardly rectifying K+ current and the Ba2+-insensitive K+ current underlying slow afterhyperpolarization (I(sAHP)). We conclude that 5-HT4 receptor activation may cause a long-lasting excitability increase in CA1 pyramidal neurons by inhibition of a Ba2+-sensitive inwardly rectifying K+ current.

Action Potentials↗