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PubMed2000

Timing-based LTP and LTD at vertical inputs to layer II/III pyramidal cells in rat barrel cortex.

Experience-dependent plasticity in somatosensory (S1) and visual (V1) cortex involves rapid depression of responses to a deprived sensory input (a closed eye or a trimmed whisker). Such depression occurs first in layer II/III and may reflect plasticity at vertical inputs from layer IV to layer II/III pyramids. Here, I describe a timing-based, associative form of long-term potentiation and depression (LTP/LTD) at this synapse in S1. LTP occurred when excitatory postsynaptic potentials (EPSPs) led single postsynaptic action potentials (APs) within a narrow temporal window, and LTD occurred when APs led EPSPs within a significantly broader window. This long LTD window is unusual among timing-based learning rules and causes EPSPs that are uncorrelated with postsynaptic APs to become depressed. This behavior suggests a simple model for depression of deprived sensory responses in S1 and V1.

2-Amino-5-phosphonovalerate↗

PubMed1986

Dorsal horn potentials and current source densities evoked by single action potentials in single slowly adapting type I axons.

The slow-wave response of cat dorsal horn, elicited by single action potentials in single slowly adapting type I (SAI) axons, was mapped by averaging the slow wave recorded from each locus in a rectangular array of recording loci in the transverse plane. Current source-density (CSD) waveforms were computed from these averages. Evoked potentials always included N-waves, with mean latency = 4.9 ms, rise time (base line to peak) = 2.3 ms, and duration (base line-peak-base line) = 13.1 ms. In some planes, the N-wave was followed by a longer P-wave. The N-wave timing corresponded to previously described excitatory postsynaptic potentials (EPSPs) recorded intracellularly and excitatory discharges recorded extracellularly from single units evoked by single SAI spikes. The P-wave timing corresponded to a previously described postexcitatory suppression of SAI spike-evoked EPSPs and discharges following single conditioning SAI action potentials. The current sink during the N-wave had the following properties: It occurred in a column of tissue, perpendicular to the laminar borders, less than 600 microns wide; this is similar to the terminal domain of a single SAI collateral. It remains stationary during the N-wave, indicating that the excited population of dorsal horn elements does not spread or shift within the transverse plane during the response. It is somatotopically organized in the mediolateral dimension, in a manner similar to the somatotopic organization of primary afferent terminations and of dorsal horn cell receptive fields.

Action Potentials↗

PubMed2001

The supramammillary nucleus contributes to associative EPSP-spike potentiation in the rat dentate gyrus in vivo.

The supramammillary nucleus (SUM) of the hypothalamus sends neural projections to the hippocampus and is supposed to be involved in learning and memory. To test the possibility that SUM afferents modulate hippocampal functions, we investigated the effect of electrical stimulation of the SUM on the induction of long-term potentiation (LTP) at medial perforant path (PP)--granule cell synapses in the dentate gyrus (DG) of anaesthetized rats. High-frequency stimulation of the SUM (100 pulses at 100 Hz) alone did not change PP--DG field potentials. However, when the SUM stimulation was applied simultaneously with weak tetanic stimulation of the PP (20 pulses at 20 Hz) which alone did not induce any potentiation, it produced a long-lasting potentiation of the population spike, without an accompanying increase in the population excitatory postsynaptic potential (EPSP). The EPSP-spike (E-S) potentiation induced by pairing SUM and PP stimulation was abolished by lesions of the fimbria--fornix, a major pathway of SUM afferents. SUM stimulation applied 1 s before or after PP stimulation failed to produce E-S potentiation, and SUM stimulation augmented PP--DG field potentials during tetanic stimulation. Furthermore, the E-S potentiation was abolished by blocking GABAergic neurotransmission with picrotoxin. These results suggest that coactivation of SUM and PP inputs produces a long-lasting increase of granule cell excitability by modulating GABAergic inhibition. SUM afferents may contribute to associative memory processing by modulating hippocampal excitability.

Animals↗

PubMed2000

Muscarinic agonist carbachol depresses excitatory synaptic transmission in the rat basolateral amygdala in vitro.

Intracellular recordings in slice preparations of the basolateral amygdala were used to test which excitatory amino acid receptors mediate the excitatory postsynaptic potentials due to stimulation of the external capsule. These recordings were also used to examine the action of muscarinic agonists on the evoked excitatory potentials. Intracellular recordings from amygdaloid pyramidal neurons revealed that carbachol (2-20 microM) suppressed, in a dose-dependent manner, excitatory postsynaptic responses evoked by stimulation of the external capsule (EC). This effect was blocked by atropine. The estimated effective concentration to produce half-maximal response (EC(50)) was 6.2 microM. Synaptic suppression was observed with no changes in the input resistance of the recorded cells, suggesting a presynaptic mechanism. In addition, the results obtained using the paired-pulse protocol provided additional support for a presynaptic action of carbachol. To identify which subtype of cholinergic receptors were involved in the suppression of the EPSP, four partially selective muscarinic receptor antagonists were used at different concentrations: pirenzepine, a compound with a similar high affinity for muscarinic M1 and M4 receptors; gallamine, a noncompetitive antagonist for M2; methoctramine, an antagonist for M2 and M4; and 4-diphenylacetoxy-N-methylpiperidine, a compound with similar high affinity for muscarinic receptors M1 and M3. None of them independently antagonized the suppressive effect of carbachol on the evoked EPSP completely, suggesting that more than one muscarinic receptor subtype is involved in the effect. These experiments provide evidence that in the amygdala muscarinic agonists block the excitatory synaptic response, mediated by glutamic acid, by acting on several types of presynaptic receptors.

Amygdala↗

PubMed2006

Target-specific regulation of synaptic efficacy in the feeding central pattern generator of Aplysia: potential substrates for behavioral plasticity?

The contributions to this symposium are unified by their focus on the role of synaptic plasticity in sensorimotor learning. Synaptic plasticities are also known to operate within the central pattern generator (CPG) circuits that produce repetitive motor programs, where their relation to adaptive behavior is less well understood. This study examined divergent synaptic plasticity in the signaling of an influential interneuron, B20, located within the CPG that controls consummatory feeding-related behaviors in Aplysia. Previously, B20 was shown to contain markers for catecholamines and GABA (Díaz-Ríos et al., 2002), and its rapid synaptic signaling to two follower motor neurons, B16 and B8, was found to be mediated by dopamine (Díaz-Ríos and Miller, 2005). In this investigation, two incremental forms of increased synaptic efficacy, facilitation and summation, were both greater in the signaling from B20 to B8 than in the signaling from B20 to B16. Manipulation of the membrane potentials of the two postsynaptic motor neurons did not affect facilitation of excitatory postsynaptic potentials (EPSPs) to either follower cell. Striking levels of summation in B8, however, were eliminated at hyperpolarized membrane potentials and could be attributed to distinctive membrane properties of this postsynaptic cell. GABA and the GABAB agonist baclofen increased facilitation and summation of EPSPs from B20 to B8, but not to B16. The enhanced facilitation was not affected when the membrane potential of B8 was pre-set to hyperpolarized levels, but GABAergic effects on summation were eliminated by this manipulation. These observations demonstrate a target-specific amplification of synaptic efficacy that can contribute to channeling the flow of divergent information from an intrinsic interneuron within the buccal CPG. They further suggest that GABA, acting as a cotransmitter in B20, could induce coordinated and target-specific pre- and postsynaptic modulation of these signals. Finally, we speculate that target-specific plasticity and its modulation could be efficient, specific, and flexible substrates for learning-related modifications of CPG function.

Animals↗

PubMed1983

Effects of juxta- and intracellular microinjection of ethanol on trigeminal motoneurons in the chronic cat.

The direct cellular effects of ethanol on trigeminal motoneurons were studied in chronic cats during sleep and wakefulness. Intracellular and extracellular recordings were obtained while simultaneously injecting ethanol microdroplets onto the surface (juxtacellularly) or within the soma (intracellularly) of these motoneurons. Juxtacellular ethanol injection resulted in a suppression of neuronal excitability as well as a reduction in the amplitude of action potentials and monosynaptically-induced excitatory postsynaptic potentials. Intracellular ethanol injection led to a slight increase in excitability (i.e. membrane depolarization); concurrently, however, there was a reduction in the amplitude of spike and synaptic potentials. We conclude that the predominant response of trigeminal motoneurons to the direct application of ethanol entails a dose-dependent reduction in membrane excitability in addition to a depression of excitatory synaptic transmission. This pattern of ethanol action was observed throughout the states of quiet sleep and active sleep as well as when the animal was awake.

Animals↗

PubMed1998

Electrical characteristics and responses to jejunal distension of neurons in Remak's juxta-jejunal ganglia of the domestic fowl.

1. Remak's nerve is a ganglionated nerve trunk found only in birds that runs parallel to the gut from the duodenal-jejunal junction to the cloaca. We report the first electrophysiological characterization of these neurons and their responses to gut distension. 2. A segment of chicken jejunum with attached Remak's nerve was pinned in an electrophysiological chamber. Neurons in Remak's ganglia were impaled with microelectrodes. The adjacent segment of gut was distended with fluid. 3. One hundred and thirty neurons were characterized into three electrophysiological classes: (i) tonic neurons (74%) fired action potentials spontaneously (frequency 3.5 Hz) and continuously (up to 40 Hz) throughout a depolarizing current pulse; (ii) AD neurons (22%) fired a brief burst of action potentials (1-10), which were followed by a prolonged after-depolarization (AD) of duration 2.8 +/- 0.3 s; and (iii) phasic neurons (4%) fired an initial burst of action potentials followed by an after-hyperpolarization (duration, 520.0 +/- 32.0 ms). Tetrodotoxin (1 microM) abolished action potentials in tonic and AD neurons as well as the after-depolarization. 4. Spontaneous fast excitatory postsynaptic potentials (FEPSPs) occurred in all classes of neurons; they were not observed, however, in ganglia isolated from the jejunum. 5. Intracellular injection of biocytin revealed that neurons could be characterized into four morphological classes. Tonic neurons, which had long and extensive dendritic trees, were Remak's Type I, II and IV neurons. AD neurons also comprised Remak's type II neurons. Phasic neurons were Remak's Type III neurons. Most neurons had axons that projected orally along Remak's nerve. 6. Distension of the jejunum evoked FEPSPs and action potentials in tonic neurons, and repetitive bursts of action potentials (1-4) followed by an after-depolarization in AD neurons. All responses to distension were blocked by hexamethonium (300 microM) and tetrodotoxin (1 microM). 7. In conclusion, neurons in Remak's juxta-jejunal nerve appear to regulate gut motility. Three distinct electrophysiological classes of neurons were observed, all of which appear to be activated by distension sensitive cholinergic intestinofugal neurons in the jejunum.

Action Potentials↗

PubMed2000

Myelination defects and neuronal hyperexcitability in the neocortex of connexin 32-deficient mice.

Morphological and electrophysiological studies were performed on neocortices of adult Connexin 32 (Cx32)-deficient mice and wild-type mice to investigate the consequences of a lack of the gap junction subunit Cx32 on neocortical structure and function. Morphometrical analysis revealed a reduced volume fraction of myelin within the neuropil and a decreased thickness of the axonal myelin sheaths in the neocortex of Cx32-deficient mice. Intracellular recordings from neurons in neocortical slice preparations provided evidence for an increased membrane input resistance in neurons of Cx32-null mutant mice as compared to neurons of wild-type mice. Consequently, neurons of Cx32-deficient mice displayed an enhanced intrinsic excitability. In addition, approximately 50% of the neurons investigated in slices of Cx32-deficient mice responded to afferent stimulation with delayed and large glutamatergic excitatory postsynaptic potentials resembling paroxysmal depolarizations. GABAergic inhibition sufficient to efficiently control synaptic excitability was virtually absent in these cells. The changes in intrinsic membrane properties observed in neurons of Cx32-null mutant mice were independent of the alterations in synaptic function, since increased membrane resistances were observed also in neurons with normal synaptic response pattern. Thus, in the neocortex, lack of Cx32 correlates with myelination defects, alterations in intrinsic membrane properties and dysfunction of inhibitory synaptic transmission.

Action Potentials↗

PubMed1999

Regulation of action potential size and excitability in substantia nigra compacta neurons: sensitivity to 4-aminopyridine.

Slow, pacemaker-like firing is due to intrinsic membrane properties in substantia nigra compacta (SNc) neurons in vitro. How these properties interact with afferent synaptic inputs is not fully understood. In this study, intracellular recordings from SNc neurons in brain slices showed that spontaneous action potentials (APs) were attenuated when generated from lower than normal threshold. Such APs were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and could be related to non-N-methyl-D-aspartate (NMDA) receptor-mediated spontaneous excitatory postsynaptic potentials (EPSPs). The AP attenuation was reproduced by stimulus-evoked EPSPs and by current injections to the soma. APs evoked from holding potentials between -40 and -60 mV were reduced in width by Cd(2+) (0. 2 mM). Tetraethylammonium chloride (TEA, 10 mM) or 4-aminopyridine (4-AP, 5 mM) increased the AP width. However, at more negative holding potentials, Cd(2+) and TEA were inefficacious, whereas 4-AP enlarged the AP, partly via induction of a Cd(2+)-sensitive component. A monophasic afterhyperpolarization (AHP), following attenuated APs, was little affected by either Cd(2+) or TEA, but inhibited by 4-AP, which induced an additional, slow component, sensitive to Cd(2+) or apamin (100 nM). The AP delay showed a discontinuous relation to the amplitude or slope of the injected current (delay shift), which was sensitive to low doses of 4-AP (0. 05 mM). The initial time window before the delay shift was longer than the rise time of EPSPs. It is suggested that a 4-AP-sensitive current prevents or postpones discharge during slow depolarization's, but allows direct excitation by fast EPSPs. Fast excitation leads to AP attenuation, primarily due to strong activation of 4-AP-sensitive current. This seems to cause inhibition of the Ca(2+) current during the AP and reduction of Ca(2+)-dependent K(+) currents. Together, these properties are likely to influence the excitability and the local, somatodendritic effects of the AP, in a manner that discriminates between firing induced by the intrinsic pacemaker mechanism and fast synaptic potentials.

4-Aminopyridine↗

PubMed2006

Cortical network modeling: analytical methods for firing rates and some properties of networks of LIF neurons.

The circuitry of cortical networks involves interacting populations of excitatory (E) and inhibitory (I) neurons whose relationships are now known to a large extent. Inputs to E- and I-cells may have their origins in remote or local cortical areas. We consider a rudimentary model involving E- and I-cells. One of our goals is to test an analytic approach to finding firing rates in neural networks without using a diffusion approximation and to this end we consider in detail networks of excitatory neurons with leaky integrate-and-fire (LIF) dynamics. A simple measure of synchronization, denoted by S(q), where q is between 0 and 100 is introduced. Fully connected E-networks have a large tendency to become dominated by synchronously firing groups of cells, except when inputs are relatively weak. We observed random or asynchronous firing in such networks with diverse sets of parameter values. When such firing patterns were found, the analytical approach was often able to accurately predict average neuronal firing rates. We also considered several properties of E-E networks, distinguishing several kinds of firing pattern. Included were those with silences before or after periods of intense activity or with periodic synchronization. We investigated the occurrence of synchronized firing with respect to changes in the internal excitatory postsynaptic potential (EPSP) magnitude in a network of 100 neurons with fixed values of the remaining parameters. When the internal EPSP size was less than a certain value, synchronization was absent. The amount of synchronization then increased slowly as the EPSP amplitude increased until at a particular EPSP size the amount of synchronization abruptly increased, with S(5) attaining the maximum value of 100%. We also found network frequency transfer characteristics for various network sizes and found a linear dependence of firing frequency over wide ranges of the external afferent frequency, with non-linear effects at lower input frequencies. The theory may also be applied to sparsely connected networks, whose firing behaviour was found to change abruptly as the probability of a connection passed through a critical value. The analytical method was also found to be useful for a feed-forward excitatory network and a network of excitatory and inhibitory neurons.

Action Potentials↗

PubMed2003

Decoding of synaptic voltage waveforms by specific classes of recombinant high-threshold Ca(2+) channels.

Studies suggest that the preferential role of L-type voltage-sensitive Ca(2+) channels (VSCCs) in coupling strong synaptic stimulation to transcription is due to their selective activation of local chemical events. However, it is possible that selective activation of the L-type channel by specific voltage waveforms also makes a contribution. To address this issue we have examined the response of specific Ca(2+) channel types to simulated complex voltage waveforms resembling those encountered during synaptic plasticity (gamma and theta firing frequency). L-, P/Q- and N-type VSCCs (alpha1C, alpha1A, alpha1B/beta1B/alpha2delta, respectively) were all similarly activated by brief action potential (AP) waveforms or sustained step depolarization. When complex waveforms containing large excitatory postsynaptic potentials (EPSPs), APs and spike accommodation were applied under voltage clamp we found that the integrated L-type VSCC current was approximately three times larger than that produced by the P/Q- or N-type Ca(2+) channels (gamma frequency 1 s stimulation). For P/Q- or N-type channels the complex waveforms led to a smaller current than that expected from the response to a simple 1 s step depolarization to 0 or +20 mV. EPSPs present in the waveforms favoured the inactivation of P/Q- and N-type channels. In contrast, activation of the L-type channel was dependent on both EPSP- and AP-mediated depolarization. Expression of P/Q-type channels with reduced voltage-dependent inactivation (alpha1A/beta2A/alpha2delta) or the use of hyperpolarized intervals between AP stimuli greatly increased their response to complex voltage stimuli. We propose that in response to complex synaptic voltage waveforms P/Q- and N-type channels can undergo selective voltage-dependent inactivation leading to a Ca(2+) current mediated predominantly by L-type channels.

Action Potentials↗

PubMed1999

The RULER model. Is this how the somatosensory cortex works?

Despite a wealth of information, it is still not known how neurones in the different neocortical layers interact to produce a conscious perception. We now put forward a model for the somatosensory cortex in which a touch is perceived whenever superficial cortical pyramidal cells (in layers II and III) are made to discharge by a recurrent input from deep pyramidal neurones (in layer V). The superficial cells act as biological amplifiers and the number discharging will depend both on the strength of the message from the thalamus and on the variable background depolarisation of their apical dendrites. The recurrent volley arises in the layer V neurones at the end of an IPSP (inhibitory postsynaptic potential), which itself follows an excitatory response induced by the incoming thalamic signal; the IPSP is generated by local basket cells. The duration of the initial excitation--IPSP--late excitation sequence corresponds to a time chunk, that is, the period over which neural activity is integrated to produce a perception. During the time chunk, the superficial cortical pyramids, unlike the deeper ones, can accumulate information as subthreshold excitatory postsynaptic potentials (EPSPs). The relative time at which the information arrived in the cortex is roughly coded by the gradient of EPSPs among cells in an axis perpendicular to the cortical surface. Although developed for the somatosensory cortex, the basic features of the model may well apply to other sensory receiving areas of the cortex.

Attention↗

PubMed1981

Morphine and opioid peptides reduce inhibitory synaptic potentials in hippocampal pyramidal cells in vitro without alteration of membrane potential.

We used intracellular recording in the hippocampal slice in vitro to characterize further the mechanisms behind the unusual excitatory action of opiates and opioid peptides on hippocampal pyramidal cells in vivo. No significant effect on resting membrane potential, input resistance, or action potential size in cortical area 1 (CA1) pyramidal cells was observed with morphine sulfate, beta-endorphin, [Met5]enkephalin, or [D-Ala2, D-Leu5]enkephalin at 1-50 microM. However, in all cells studied, these agents markedly reduced the size of inhibitory postsynaptic potentials generated by stimulation of the stratum radiatum or alveus. Excitatory postsynaptic potentials were also diminished in many of these cells. The effects of the opioids were antagonized by naloxone. These results are consistent with excitation of pyramidal neurons by a disinhibitory mechanism.

Animals↗

PubMed1991

Postsynaptic and presynaptic effects of the calcium chelator BAPTA on synaptic transmission in rat hippocampal dentate granule neurons.

When applied to rat hippocampal slices, the permeable calcium chelator, BAPTA-AM, caused a reduction of both post-spike train slow afterhyperpolarizations (AHPs) and spike-frequency adaptation in dentate granule cells. This indicated that BAPTA-AM can, like microinjected EGTA, block calcium-activated potassium channels. At perforant pathway synapses, BAPTA-AM caused a reduction of inhibitory postsynaptic potentials (IPSPs) and an initial increase and later decrease of excitatory postsynaptic potentials (EPSPs). The initial increase in EPSPs may be caused by presynaptic spike-broadening owing to inhibition of calcium-activated potassium channels which normally regulate the duration of the presynaptic action potential. These channels may be affected at lower doses of chelator than synaptic transmitter release. BAPTA salt injected into individual dentate granule cells caused, as expected, decreased AHPs and spike-frequency adaptation. Also, paradoxically, both excitatory and inhibitory synaptic potentials were increased although input resistance was not.

Action Potentials↗

PubMed1998

The anticonvulsant actions of sigma receptor ligands in the Mg2+-free model of epileptiform activity in rat hippocampal slices.

1. The anticonvulsant potency of a series of structurally-dissimilar compounds which possess nanomolar affinities for high-affinity sigma binding sites was examined in the Mg2+-free model of epileptiform activity in rat hippocampal slices. Extracellular field potential recordings in the CA1 region were employed to examine the effects of test compounds on spontaneous epileptiform activity and multiple population spikes evoked by stimulation of the Schaffer collateral-commissural pathway. 2. Applied at sigma site-selective (i.e. nanomolar) concentrations, dextromethorphan, ditolylguanidine, caramiphen and opipramol failed to modify Mg2+-free epileptiform activity; neither pro- nor anticonvulsant effects were observed. However, applied at micromolar concentrations, these and additional test compounds reversibly inhibited orthodromically-evoked epileptiform field potentials with a rank order potency (IC50 values in microM): dextrorphan (1.5) > ifenprodil (6.3) > dextromethorphan (10) > ditolylguanidine (15) > loperamide (28) > carbetapentane (38) > caramiphen (46) > opipramol (52). Micromolar concentrations of the same compounds also inhibited spontaneous epileptiform bursts recorded during perfusion with Mg2+-free medium. 3. Co-application of ropizine (10 microM), an allosteric modulator of dextromethorphan binding to high-affinity sigma receptors, failed to endow dextromethorphan 10 nM with anticonvulsant properties and did not modify the anticonvulsant potency of 10 microM dextromethorphan. 4. The effects of dextrorphan (10 microM), ifenprodil (20 microM), loperamide (50 microM) and caramiphen (100 microM) were examined in the presence of external Mg2+ on field potential input/output (I/O) relationships and paired-pulse facilitation (PPF) of field excitatory postsynaptic potentials. Only caramiphen elicited effects on these parameters, affecting synaptic transmission at the point of synaptic transfer and depressing PPF ratios to below baseline values. The effects of caramiphen on I/O relationships mimicked those of the established anticonvulsant adenosine: in contrast, adenosine evoked an increase in PPF ratios. 5. Because anticonvulsant activity was observed only at micromolar concentrations of the sigma ligands tested, the results indicate that their anticonvulsant actions should not be ascribed to their occupancy, observed at nanomolar concentrations, of high-affinity sigma binding sites. Rather, anticonvulsant activity more likely reflects functional NMDA receptor antagonism and/or blockade of high voltage-activated Ca2+ channels, effects which are associated with micromolar concentrations of the test compounds. Modulation of GABAergic inhibitory mechanisms may also contribute to the anticonvulsant properties of caramiphen.

Animals↗

PubMed2004

Mechanosensory S-neurons rather than AH-neurons appear to generate a rhythmic motor pattern in guinea-pig distal colon.

Simultaneous intracellular recordings were made from myenteric neurons and circular muscle (CM) cells in isolated, stretched segments of guinea-pig distal colon. We have shown previously that maintained stretch generates a repetitive and coordinated discharge of ascending excitatory and descending inhibitory neuronal reflex pathways in the distal colon. In the presence of nifedipine (1-2 microm) to paralyse the muscle, simultaneous recordings were made from 25 pairs of AH (after-hyperpolarization)-neurons and CM cells separated by 100-500 microm. In all 25 AH-neurons, proximal process potentials (PPPs) were never recorded, even though at the same time, all recordings from neighbouring CM cells showed an ongoing discharge of inhibitory junction potentials (IJPs) anally, or excitatory junction potentials (EJPs) orally. In fact, 24 of 25 AH-neurons were totally silent, while in one AH-cell, some spontaneous fast excitatory postsynaptic potentials (FEPSPs) were recorded. All 10 electrically silent AH-cells that were injected with neurobiotin were found to be multipolar Dogiel type II neurons. In contrast, when recordings were made from myenteric S-neurons, two distinct electrical patterns of electrical activity were recorded. Recordings from 25 of 48 S-neurons showed spontaneous FEPSPs, the majority of which (22 of 25) showed periods when discrete clusters of FEPSPs (mean duration 88 ms) could be temporally correlated with the onset of EJPs or anal IJPs in the CM. Nine S-neurons were electrically quiescent. The second distinct electrical pattern in 14 S-neurons consisted of bursts, or prolonged trains of action potentials, which could be reduced to proximal process potentials (PPPs) in six of these 14 neurons during membrane hyperpolarization. Unlike FEPSPs, PPPs were resistant to a low Ca(2+)-high Mg(2+) solution and did not change in amplitude during hyperpolarizing pulses. Mechanosensory S-neurons were found to be uniaxonal or pseudounipolar filamentous neurons, with morphologies consistent with interneurons. No slow EPSPs were ever recorded from AH- or S-type neurons when IJPs or EJPs occurred in the CM. In summary, we have identified a population of mechanosensory S-neurons in the myenteric plexus of the distal colon which appear to be largely stretch sensitive, rather than muscle-tension sensitive, since they generate ongoing trains of action potentials in the presence of nifedipine. No evidence was found to suggest that in paralysed preparations, the repetitive firing in ascending excitatory or descending inhibitory nerve pathways was initiated by myenteric AH-neurons, or slow synaptic transmission.

Action Potentials↗

PubMed2002

Dendritic K+ channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons.

We investigated the role of A-type K(+) channels for the induction of long-term potentiation (LTP) of Schaffer collateral inputs to hippocampal CA1 pyramidal neurons. When low-amplitude excitatory postsynaptic potentials (EPSPs) were paired with two postsynaptic action potentials in a theta-burst pattern, N-methyl-d-aspartate (NMDA)-receptor-dependent LTP was induced. The amplitudes of the back-propagating action potentials were boosted in the dendrites only when they were coincident with the EPSPs. Mitogen-activated protein kinase (MAPK) inhibitors PD 098059 or U0126 shifted the activation of dendritic K(+) channels to more hyperpolarized potentials, reduced the boosting of dendritic action potentials by EPSPs, and suppressed the induction of LTP. These results support the hypothesis that dendritic K(+) channels and the boosting of back-propagating action potentials contribute to the induction of LTP in CA1 neurons.

Action Potentials↗

PubMed1988

Sodium valproate decreases synaptic potentiation and epileptiform activity in hippocampus.

The actions of sodium valproate (NaVP) were studied in the in vitro hippocampus using extracellular, intracellular and voltage-clamp recording techniques. In the CA1 region, concentrations of 30-200 microM NaVP reduced the amplitude but not the time course of post-tetanic potentiation (PTP) of dendritic field excitatory postsynaptic potentials (EPSPs). Epileptiform discharges were studied intracellularly in CA3 cells after pharmacological blockade of synaptic inhibition and repeated tetanic stimulation. NaVP (100 microM) blocked evoked paroxysmal depolarizing shift (PDS) discharges through a mechanism of increasing the threshold for burst-firing. When the PDS current was studied under voltage-clamp, application of NaVP (100 microM) resulted in a graded reduction of the PDS waveform. All of the actions of NaVP may result from inhibition of excitatory synaptic transmission following repetitive cell firing. A hypothesis is proposed that NaVP may act to decrease excitatory synaptic potentiation necessary for network synchronization.

Action Potentials↗