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PubMed1989

DTG and (+)-3-PPP inhibit a ligand-activated hyperpolarization in mammalian neurons.

The effects of three compounds with high affinity for the haloperidol-sensitive alpha-binding site were studied with intracellular recordings in the vitro neuronal preparations of the rat locus ceruleus, rat dorsal raphe and the guinea pig submucous plexus. Both (+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine [(+)-3-PPP] and 1,3-di-o-tolylguanidine (DTG) inhibited the hyperpolarization induced by a ligand-activated potassium conductance. In the locus ceruleus, (+)-3-PPP and DTG produced a maximal 40 to 45% inhibition of the [Met5]enkephalin hyperpolarization, and had EC50 values of 6.6 and 2.2 microM, respectively. In the submucous plexus, the two compounds had a similar action on the alpha-2 adrenoceptor agonist UK14304 hyperpolarization, producing a maximal 50% inhibition with EC50 values of 140 and 32 nM, respectively. In addition, DTG inhibited the alpha-2-mediated inhibitory postsynaptic potential in both preparations. In contrast, (+)-3-PPP increased and prolonged the inhibitory postsynaptic potential. This action is qualitatively similar to the actions of cocaine on locus ceruleus and submucous plexus neurons. Haloperidol (1-10 microM) shared none of these actions. It is concluded that DTG and (+)-3-PPP are inhibitors of the opiate and alpha-2-mediated hyperpolarization at a postreceptor site, possibly the potassium channel. In addition, (+)-3-PPP, but not DTG, inhibits norepinephrine reuptake. None of these effects appear to be related to the sigma -binding site, because haloperidol acted as neither an agonist nor an antagonist.

Animals↗

PubMed1994

Homogeneity of intracellular electrophysiological properties in different neuronal subtypes in medial preoptic slices containing the sexually dimorphic nucleus of the rat.

The sexually dimorphic nucleus of the preoptic area (SDN-POA) is larger in male than in female rats, the male phenotype requiring the presence of circulating androgens perinatally. These experiments investigated the intracellular electrophysiology and morphology of SDN-POA neurons and compared these properties with those of other medial preoptic area (MPOA) neurons. Biocytin-injected cells in the SDN-POA either had one or two primary dendrites, or they had multipolar dendritic arrays; dendrites were aspiny or sparsely spiny and displayed limited branching. Neurons in other parts of the MPOA were similar morphologically. Regardless of morphology, neurons situated in either the SDN-POA or surrounding MPOA had low-threshold potentials and linear or nearly linear current-voltage relations. In most (73%) cells, stimulation of the dorsal preoptic region evoked a fast excitatory postsynaptic potential followed by a fast inhibitory postsynaptic potential (IPSP). Bicuculline blocked the fast IPSPs, which reversed near the Cl2 equilibrium potential (-71 +/- 5 mV), indicating their mediation by gamma-aminobutyric acid (GABA)A receptors. Neurons in the SDN-POA have electrophysiological properties similar to those of other medial preoptic cells. When compared with the hypothalamic paraventricular nucleus, the MPOA appears relatively homogeneous electrophysiologically. This is despite the morphological variability within this population of neurons and heterogeneities that are also apparent at other levels of analysis. Finally, GABA-mediated, inhibitory synaptic contacts are widespread among medial preoptic neurons, consistent with indications from earlier reports that GABA provides a link in the feedback actions of gonadal steroids on the release of gonadotropic hormones.

Animals↗

PubMed2000

2-Deoxyglucose-induced long-term potentiation of monosynaptic IPSPs in CA1 hippocampal neurons.

In previous experiments on excitatory synaptic transmission in CA1, temporary (10-20 min) replacement of glucose with 10 mM 2-deoxyglucose (2-DG) consistently caused a marked and very sustained potentiation (2-DG LTP). To find out whether 2-DG has a similar effect on inhibitory synapses, we recorded pharmacologically isolated mononosynaptic inhibitory postsynaptic potentials (IPSPs; under current clamp) and inhibitory postsynaptic currents (IPSCs; under voltage clamp); 2-DG was applied both in the presence and the absence of antagonists of N-methyl-D-aspartate (NMDA). In spite of sharply varied results (some neurons showing large potentiation, lasting for >1 h, and many little or none), overall there was a significant and similar potentiation of IPSP conductance, both for the early (at approximately 30 ms) and later (at approximately 140 ms) components of IPSPs or IPSCs: by 35.1 +/- 10.25% (mean +/- SE; for n = 24, P = 0.0023) and 36.5 +/- 16.3% (for n = 19, P = 0.038), respectively. The similar potentiation of the early and late IPSP points to a presynaptic mechanism of LTP. Overall, the LTP was statistically significant only when 2-DG was applied in the absence of glutamate antagonists. Tetanic stimulations (in presence or absence of glutamate antagonists) only depressed IPSPs (by half). In conclusion, although smaller and more variable, 2-DG-induced LTP of inhibitory synapses appears to be broadly similar to the 2-DG-induced LTP of excitatory postsynaptic potentials previously observed in CA1.

2-Amino-5-phosphonovalerate↗

PubMed1983

Integration of biphasic synaptic input by electrotonically coupled neuroendocrine caudodorsal cells in the pond snail.

The ovulation hormone-producing caudodorsal cells (CDCs) of the pond snail Lymnaea stagnalis form two clusters of electrotonically coupled cells, each containing a few specialized (ventral) cells that connect the clusters. The hormone is secreted during a pacemaker-driven discharge. The CDCs receive a biphasic cholinergic postsynaptic potential (PSP), consisting of a rapid excitatory postsynaptic potential (EPSP) and a slow inhibitory postsynaptic potential (IPSP) that is elicited by stimulation of nerves. The effect of the synaptic input on the discharge of the CDCs is described and the location of the synapse investigated by a combination of electrophysiological recordings and morphological techniques. The PSP interrupts the discharge and hastens its termination. In addition, it causes a reversal of the temporal order of the spikes of ventral cells (that normally lead) and dorsal cells (that lead only after the PSP). Ion-substitution experiments indicate that the ionic mechanism underlying the biphasic PSP is conventional, involving a conductance increase for Na+ (EPSP) and K+ (IPSP). Receptors mediating the inhibitory component occur only on the proximal axons of the ventral cells, both components are larger and reverse more readily in ventral cells. These findings suggest that the PSP is generated in the ventral cells. The biphasic PSP has no effect on electrical coupling, suggesting that it is not generated along the electrical pathways among the cells. Horseradish peroxidase (HRP) staining reveals that the lateral branches emerge from the proximal axons of the ventral cells only. In HRP-filled preparations processed for electron microscopy (EM) acetylcholinesterase is demonstrated at these branches where it occurs associated with synapses. The location on fine branches of the ventral cells explains the absence of an effect on electrotonic transmission, whereas the reluctance of components of the PSP to reverse at the expected potentials is due to the distribution of the synapses over more than one cell. It is concluded that the biphasic PSP is received only by the ventral cells and that it is conveyed electrotonically to the other cells.

Acetylcholinesterase↗

PubMed1994

Serotonin2 receptor-mediated excitation of interneurons in piriform cortex: antagonism by atypical antipsychotic drugs.

Rat piriform cortex contains a subpopulation of presumed GABAergic interneurons located near the border of layers 2 and 3 that express excitatory serotonin2 receptors. These serotonin2-responsive interneurons send axons to layer 2 pyramidal cells. Using an in vitro brain slice preparation, serotonin2 receptor-mediated excitation can be assessed either by directly recording from the interneurons or by recording the increase in inhibitory postsynaptic potentials in the pyramidal cells. Intracellular recordings from the interneurons demonstrated that compared to pyramidal cells they had a more depolarized resting membrane potential, a higher input resistance and shorter action potential duration. The serotonin2 receptor-mediated excitation was associated with a strong depolarization (range 3-22 mV). We found that the atypical antipsychotic drugs, risperidone and clozapine, which have relatively high affinity for serotonin2 receptors, each dose-dependently inhibited the serotonin2-mediated excitation of the interneurons with IC50 values of 7 nM and 1.4 microM, respectively. This antagonism was specific to the extent that excitation mediated by agonists at excitatory amino acid receptors were not blocked at concentrations of risperidone and clozapine that completely antagonized the serotonin2 receptor-mediated excitation. The typical antipsychotic drug, chlorpromazine, inhibited the serotonin2-mediated excitation of the interneurons with an IC50 of 14 microM. Haloperidol, another typical antipsychotic drug, decreased the serotonin2 response to about half of baseline at a concentration of 10 microM (the exact IC50 could not be calculated because higher concentrations produced non-specific effects on cells). Both risperidone and clozapine blocked the serotonin-elicited inhibitory postsynaptic potentials in layer 2 pyramidal cells at concentrations that approximated the IC50 for antagonizing the serotonin2-mediated excitation of the interneurons. Chlorpromazine and haloperidol, in the concentration range that blocked serotonin2 receptor-mediated excitation of interneurons, also blocked the serotonin-elicited inhibitory postsynaptic potentials in the pyramidal cells. The IC50 values for risperidone and clozapine, but not for chlorpromazine or haloperidol, for blocking serotonin2 receptor-mediated actions in rodent piriform cortical slice are in the range of the plasma concentrations of the drug that are clinically efficacious. Our data suggest that a potential site of action of the atypical antipsychotic drugs risperidone and clozapine could be antagonism of serotonin acting through serotonin2 receptors on GABAergic interneurons in cerebral cortex.

Action Potentials↗

PubMed1991

Intracellular study of rat entopeduncular nucleus neurons in an in vitro slice preparation: response to subthalamic stimulation.

Responses of rat entopeduncular nucleus (EP) neurons after stimulation of the subthalamic nucleus (STh) and the morphology of the EP neurons were studied using brain slice preparations. EP neurons were classified into two types based on their electrophysiological properties as reported previously. Of 87 EP neurons, 72 were Type I and the rest were Type II. Synaptic responses to STh stimulation were different in these two cell types. STh stimulation evoked excitatory postsynaptic potentials (EPSPs) followed by strong inhibitory postsynaptic potentials (IPSPs) in Type I neurons and EPSPs without strong IPSPs in Type II neurons. The EPSPs were considered to be monosynaptic because no large change in the latency (1.7 +/- 0.5 ms) resulted by alteration of stimulus intensity. The EPSPs were reversibly suppressed by kynurenic acid in a dose-dependent manner. Bath application of (+)-tubocurarine (10-50 microM) had no effect on EPSPs or IPSPs. Bath application of bicuculline methiodide (50-100 microM) markedly suppressed IPSPs evoked by STh stimulation and at the same time increased the amplitude and duration of EPSPs without affecting the latency. In the presence of bicuculline methiodide, EPSPs could induce plateau potentials and slow action potentials. Some type I and Type II neurons were intracellularly labeled by biocytin. Type I neurons were located throughout the EP but Type II neurons were located mainly in the dorsal portion of the EP. Medium sized somata of both Type I and Type II neurons were spine-free and fusiform or round in shape. They had 3-4 thick primary dendrites with diameters of 2-5 micron that branched into thin secondary dendrites.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

PubMed1987

Transcallosal evoked potentials in relation to behavior in the rat: effects of atropine, p-chlorophenylalanine, reserpine, scopolamine and trifluoperazine.

Single pulse electrical stimulation of the sensorimotor cortex in waking rats produced an evoked response in the contralateral sensorimotor cortex. The slow wave response consisted of: (1) an early component that was negative at the pial surface and in layer V, and was associated with multiunit discharge; and (2) a late component that was mainly negative at the surface, positive in layer V, and was associated with multiunit suppression. Previous research suggests that the early component represents summed excitatory postsynaptic potentials; the late component summed inhibitory postsynaptic potentials. Both components could be elicited by direct stimulation of the corpus callosum and both were abolished by midline callosal section. The amplitude and duration of the late component varied with concurrent motor activity in a striking manner. It was large during waking immobility and also during face-washing, licking the paws, chewing food and drinking water, but was much reduced or absent during head movements, walking and changes in posture. Only minor changes were associated with the transition from waking immobility to slow wave sleep. A series of pharmacological experiments indicated that the behavior-related variation in the late component of the transcallosal evoked response was dependent on both cholinergic and serotonergic transmission.

Animals↗

PubMed1992

Adenosine inhibits the synaptic potentials in rat septal nucleus neurons mediated through pre- and postsynaptic A1-adenosine receptors.

Intracellular and voltage-clamp recordings were made from neurons in rat brain slices containing dorsolateral septal nucleus (DLSN), in vitro. Bath application of adenosine (100 microM) produced a hyperpolarization (2-15 mV) in 46% of DLSN neurons (AH-neurons); in the remaining 54% neurons (non-AH-neurons), no hyperpolarization to adenosine was observed. Adenosine (1-300 microM) depressed not only the excitatory postsynaptic potential (EPSP) but also the inhibitory postsynaptic potential (IPSP) and the late hyperpolarizing potential (LHP) evoked by stimulation of the hippocampal CA3 area or the fimbria/fornix pathway in both AH- and non-AH-neurons. In non-AH-neurons, adenosine did not block current responses resulting from glutamate, muscimol or baclofen applied directly to DLSN neurons. In AH-neurons, adenosine partially depressed the baclofen-induced outward current. Adenosine did not block the directly-evoked IPSP (monosynaptic IPSP) as well as the glutamate-induced (hyperpolarizing) postsynaptic potential (PSP) that is mediated by GABA released from interneurons. These results suggest that adenosine does not directly inhibit the release of GABA. The effects of adenosine was mimicked by selective A1-receptor agonists and was blocked by selective A1-receptor antagonists. Pertussis toxin (PTX) blocked the hyperpolarization induced by adenosine or baclofen applied exogenously. Adenosine consistently produced presynaptic inhibition of the EPSP even in DLSN neurons treated with PTX. We conclude that adenosine inhibits neurotransmission between the hippocampus and septum through activation of pre- and postsynaptic A1-receptors which couple with G-proteins of different PTX-sensitivity or with distinct transduction processes at pre- vs. postsynaptic sites.

Adenosine↗

PubMed2002

Ethanol withdrawal results in aberrant membrane properties and synaptic responses in periaqueductal gray neurons associated with seizure susceptibility.

The midbrain periaqueductal gray (PAG) is implicated as a component of the neuronal network for ethanol withdrawal (ETX) seizures and in other forms of audiogenic seizure (AGS) in rats. Previous in vivo experiments suggest that neurons in the ventrolateral PAG (VL PAG) are required for generation of the clonic and tonic seizure behaviors of AGS. During these seizures, PAG neuronal firing rates increase markedly, but the intracellular events, contributing to this phenomenon, have not been characterized. In the present in vitro study, intracellular current-clamp recordings were obtained from 115 control VL PAG neurons and 71 neurons during ETX. The amount of depolarizing current that needed to be injected into ETX neurons in order to generate an action potential (AP) (N=40) was significantly less than control (N=52). ETX also yielded a significant leftward shift in the frequency-current curve of VL PAG neurons. VL PAG neurons during ETX had significantly enhanced spike firing tendencies, but the firing pattern was similar in ETX and control. ETX significantly increased the incidence of spontaneous APs and the frequency of firing above those in control. A number of cellular properties [e.g. resting membrane potential (RMP), amplitude of AP, AP width at half-height, input resistance and time constant] did not differ significantly between ETX and control neurons. The current-voltage (I-V) relationships of the ETX and control VL PAG neurons were nearly linear between RMP and 80 mV more negative than RMP, whereas the I-V relation was non-linear beyond this range. Stimulation in the dorsolateral PAG in either ETX or control neurons evoked a fast excitatory postsynaptic potential (EPSP) and a slow inhibitory postsynaptic potential (IPSP). The stimulus intensities required to evoke EPSPs were significantly lower than control in neurons during ETX. Epileptiform firing was observed commonly (20%) during ETX but was never seen in control rats. Paired-pulse responses evoked paired-pulse inhibition in approximately 80% of VL PAG neurons from control rats (N=38), which was significantly above the incidence (12%) of this pattern during ETX (N=25). Paired-pulse facilitation was significantly more common (88%) in VL PAG neurons (N=25) during ETX compared to approximately 20% in controls (N=38). These aberrant membrane and synaptic properties provide direct evidence regarding the basis of the hyperexcitability observed in VL PAG neurons in vivo that contribute to propagation mechanisms of clonic and tonic convulsions, occurring during ETX.

Action Potentials↗

PubMed1988

Synaptic activation of N-methyl-D-aspartate receptors in the Schaffer collateral-commissural pathway of rat hippocampus.

1. The involvement of N-methyl-D-aspartate (NMDA) receptors in the response to single-shock (0.033 Hz) stimulation of the Schaffer collateral-commissural pathway in hippocampal slices has been investigated using current- and voltage-clamp techniques. 2. In the presence of Mg2+ (1 or 2 mM) at membrane potentials near rest, the selective NMDA antagonist D-2-amino-5-phosphonovalerate (APV) had no effect on the excitatory postsynaptic potential (EPSP) and the biphasic inhibitory postsynaptic potential (IPSP) evoked by Schaffer collateral-commissural stimulation. The recurrent IPSP evoked by antidromic stimulation of alvear fibres was also unaffected by APV. 3. The introduction of a Mg2+-free perfusate led, at high stimulus intensity, to an orthodromically evoked epileptiform discharge but little change in the recurrent IPSP. APV suppressed a large proportion of the enhanced response in Mg2+-free perfusate. 4. EPSPs and excitatory postsynaptic currents (EPSCs) evoked in Mg2+-free perfusate invariably had both APV-resistant and APV-sensitive components. Both synaptic components had similar thresholds and latencies to onset. The APV-sensitive component had a long time to peak and long duration. 5. Under current-clamp conditions in Mg2+-containing medium, an APV-sensitive component was recorded at membrane potentials of between -30 and -10 mV, but not at potentials more negative than -55 mV. 6. Under voltage-clamp, but not current-clamp, conditions in Mg2+-containing medium, a small APV-sensitive component was recorded at resting membrane potentials and increased with membrane depolarization. The difference between the current- and voltage-clamp data is attributed to the hyperpolarizing influence of conjointly activated IPSPs. 7. In the presence of Mg2+ and picrotoxin, a dual-component EPSC was recorded between -30 and +30 mV in all cells examined. The APV-resistant and APV-sensitive components had similar latencies to onset. They both had reversal potentials of between -8 and 0 mV. The APV-sensitive component had a longer latency to peak and duration than the APV-resistant component. 8. It is suggested that NMDA receptors can contribute a low-threshold and long-duration monosynaptic component of the response evoked by low-frequency stimulation of the Schaffer collateral-commissural pathway. However, under physiological conditions significant expression of this component is prevented by concurrently activated IPSPs which rapidly hyperpolarize neurones into a region where Mg2+ substantially blocks NMDA channels.

2-Amino-5-phosphonovalerate↗

PubMed1984

Intracellular recordings from vagally innervated intramural neurons in opossum stomach.

Intracellular recordings were made from intramural neurons in parafascicular ganglia in the opossum stomach. These ganglia were situated between the myenteric and subserosal plexuses and were found lying adjacent to vagal nerve fascicles. The neurons at these ganglia showed active and passive electrical properties similar only to S/type I enteric neurons. They received a complex innervation from preganglionic vagal fibers. These parasympathetic nerves elicited three distinct transmission processes in intramural neurons: fast and slow excitation (excitatory postsynaptic potentials, EPSP) and slow inhibition (inhibitory postsynaptic potential, IPSP). Fast EPSPs were cholinergically mediated via postjunctional nicotinic receptors, with convergence of numerous cholinergic fibers in several vagal fascicles to individual neurons. When seen, slow EPSPs increased neuronal excitability, whereas slow IPSPs decreased excitability.

Animals↗

PubMed2006

Properties of propriospinal neurons in the C3-C4 segments mediating disynaptic pyramidal excitation to forelimb motoneurons in the macaque monkey.

Candidate propriospinal neurons (PNs) that mediate disynaptic pyramidal excitation to forelimb motoneurons were studied in the C3-C4 segments in anesthetized macaque monkeys (n = 10). A total of 177 neurons were recorded (145 extracellularly, 48 intracellularly, and 16 both) in laminae VI-VII. Among these, 86 neurons (73 extracellularly, 14 intracellularly and 1 both) were antidromically activated from the forelimb motor nucleus or from the ventrolateral funiculus just lateral to the motor nucleus in the C6/C7 segments and thus are identified as PNs. Among the 73 extracellularly recorded PNs, 60 cells were fired by a train of four stimuli to the contralateral pyramid with segmental latencies of 0.8-2.2 ms, with most of them (n = 52) in a monosynaptic range (<1.4 ms including one synaptic delay and time to firing). The firing probability was only 21% from the third pyramidal volley but increased to 83% after intravenous injection of strychnine. In most of the intracellularly recorded PNs, stimulation of the contralateral pyramid evoked monosynaptic excitatory postsynaptic potentials (EPSPs, 12/14) and disynaptic inhibitory postsynaptic potentials (14/14), which were found to be glycinergic. In contrast, cells that did not project to the C6-Th1 segments where forelimb motoneurons are located were classified as segmental interneurons. These were fired from the third pyramidal volley with a probability of 71% before injection of strychnine. It is proposed that some of these interneurons mediate feed-forward inhibition to the PNs. These results suggest that the C3-C4 PNs receive feed-forward inhibition from the pyramid in addition to monosynaptic excitation and that this inhibition is stronger in the macaque monkey than in the cat. Another difference with the cat was that only 26 of the 86 PNs (30%, as compared with 84% in the cat) with projection to the forelimb motor nuclei send ascending collaterals terminating in the lateral reticular nucleus (LRN) on the ipsilateral side of the medulla. Thus we identified C3-C4 PNs that could mediate disynaptic pyramidal excitation to forelimb motoneurons in the macaque monkey. The present findings explain why it was difficult in previous studies of the macaque monkey to evoke disynaptic pyramidal excitation via C3-C4 PNs in forelimb motoneurons and why-as compared with the cat-the monosynaptic EPSPs evoked from the LRN via C3-C4 PNs were smaller in amplitude.

Animals↗

PubMed1988

Voltage-dependent currents prolong single-axon postsynaptic potentials in layer III pyramidal neurons in rat neocortical slices.

1. Using isolated slices of rat cingulate and sensorimotor cortex, intracellular recordings were obtained from pyramidal neurons in layer III. Simultaneous extracellular recordings were obtained from neurons in ventral layer III and layer IV. Spike-triggered averaging was employed to investigate synaptic connections from neurons in layers III/IV to pyramidal cells in layer III. 2. Of 701 simultaneously recorded pairs of neurons, comprising 699 extracellularly and 128 intracellularly recorded neurons, synaptic connections were demonstrated in 30 pairs. Of these, 29 were excitatory postsynaptic potentials (EPSPs) and 1, an inhibitory postsynaptic potential (IPSP). Single-axon EPSPs with a wide variety of amplitudes were recorded: the range recorded at membrane potentials between -68 and -72 mV was 0.079-2.3 mV. Comparing recordings obtained from different cells, EPSP amplitude was found to be independent of both the membrane resistance of the postsynaptic neuron and the EPSP time course; i.e., the largest EPSPs were not necessarily those recorded from neurons with the highest input resistance, nor those with the briefest time course. 3. Shape indices: width at half amplitude and rise-time, indicative of both proximal and distal synaptic locations were obtained. Normalized rise-times were between 0.1 and 2 times the membrane time constant and half-widths between 0.8 and 20 times. 4. The majority of postsynaptic neurons displayed nonlinear voltage relations typical of pyramidal neurons, and the contribution to EPSP shape of voltage-dependent currents was investigated. EPSP amplitude and duration were found to be dependent on membrane potential. The majority of single-axon EPSPs (26 of 29), increased in amplitude and duration with membrane depolarization over the range -95 - -50 mV, despite the significant decrease in driving force for the EPSP that would be expected to accompany such large depolarizations. This increase coincided with an increase in the amplitude of voltage responses to small injected current pulses. 5. It is concluded that the amplitude and time course of single-axon EPSPs recorded in cortical pyramidal somata are affected not only by the amplitude of the postsynaptic current and the location(s) of the synapse(s) relative to the soma, but also by voltage-dependent currents. The possibility that the increase in amplitude and duration of these EPSPs with membrane depolarization is due to N-methyl-D-aspartate receptor involvement is discussed.

Animals↗

PubMed1988

Postsynaptic potentials recorded in neurons of the cat's lateral geniculate nucleus following electrical stimulation of the optic chiasm.

1. We recorded intracellularly from X and Y cells of the cat's lateral geniculate nucleus and measured the postsynaptic potentials (PSPs) evoked from electrical stimulation of the optic chiasm. We used an in vivo preparation and computer averaged the PSPs to enhance their signal-to-noise ratio. 2. The vast majority (46 of 50) of our sample of X and Y cells responded to stimulation of the optic chiasm with an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP); these were tentatively identified as relay cells. We quantified several parameters of these PSPs, including amplitude, latency, time to peak (i.e., rise time), and duration. 3. Among the relay cells, the latencies of both the EPSP and action potential evoked by optic chiasm stimulation were shorter in Y cells than in X cells. Furthermore, the difference between the latencies of the EPSP and action potential was shorter for Y cells than for X cells. This means that the EPSPs generated in Y cells reached threshold for generation of action potentials faster than did those in X cells. The EPSPs of Y cells also displayed larger amplitudes and faster rise times than did those in X cells, but neither of these distinctions was sufficient to explain the shorter latency difference between the EPSP and action potential for Y cells. 4. The EPSPs recorded in relay Y cells had longer durations than did those in relay X cells. Our data suggest that the subsequent IPSP actively terminates the EPSP, which, in turn, suggests that the time interval between EPSP and IPSP onsets is longer in Y cells than in X cells. Furthermore, we found that, for individual Y cells, the latency and duration of the evoked EPSP were inversely related. These observations lead to the conclusion that the latency of IPSPs activated from the optic chiasm is relatively constant among Y cells and thus independent of the EPSP latencies. Thus the excitation and inhibition produced in individual geniculate Y cells may originate from different populations of retinogeniculate axons. 5. The IPSPs recorded in geniculate relay cells following optic chiasm stimulation could be divided into three groups based on their durations. The majority of both X and Y cells showed short-duration IPSPs, whereas the remainder of Y cells displayed medium-duration IPSPs, and the remaining X cells displayed long-duration IPSPs. A positive correlation was seen between the time to peak and duration of these IPSPs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Induction of long-term potentiation without participation of N-methyl-D-aspartate receptors in kitten visual cortex.

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.

2-Amino-5-phosphonovalerate↗

PubMed1992

Connections between utricular nerve and dorsal neck motoneurons of the decerebrate cat.

1. We studied connections between the utricular (UT) nerve and dorsal neck motoneurons in decerebrate cats. Electrodes were fixed in place on the UT nerve under visual observation; the other branches of the vestibular nerve were transected. 2. The N1 field potential evoked by UT nerve stimulation was recorded in the vestibular nuclei at the start of each experiment. The potential typically grew until it reached a plateau. Stimulus spread (if any) to the central ends of other nerve branches was revealed by an additional increase in N1 amplitude after the plateau was reached. 3. We recorded intracellularly from 55 motoneurons in C1-C3. Some were identified as having axons in the dorsal rami, which innervate dorsal neck muscles. Others projected in nerves that were not available for stimulation. 4. UT nerve stimulation evoked synaptic potentials in essentially all motoneurons studied. The predominant pattern consisted of disynaptic excitatory postsynaptic potentials in ipsilateral motoneurons and inhibitory postsynaptic potentials that were at least trisynaptic in contralateral motoneurons. 5. The results demonstrate the presence of short-latency connections between the utricular nerve and dorsal neck motoneurons. The functional role of this pathway remains to be investigated.

Animals↗

PubMed1997

Glutamate currents in morphologically identified human dentate granule cells in temporal lobe epilepsy.

Glutamate-receptor-mediated synaptic transmission was studied in morphologically identified hippocampal dentate granule cells (DGCs; n = 31) with the use of whole cell patch-clamp recording and intracellular injection of biocytin or Lucifer yellow in slices prepared from surgically removed medial temporal lobe specimens of epileptic patients (14 specimens from 14 patients). In the current-clamp recording, low-frequency stimulation of the perforant path generated depolarizing postsynaptic potentials that consisted of excitatory postsynaptic potentials and phase-inverted inhibitory postsynaptic potentials mediated by the gamma-aminobutyric acid-A (GABA(A)) receptor at a resting membrane potential of -62.7 +/- 2.0 (SE) mV. In the voltage-clamp recording, two glutamate conductances, a fast alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-receptor-mediated excitatory postsynaptic current (EPSC; AMPA EPSC) and a slowly developing N-methyl-D-aspartate (NMDA)-receptor-mediated EPSC (NMDA EPSC), were isolated in the presence of a GABA(A) receptor antagonist. NMDA EPSCs showed a voltage-dependent increase in conductance with depolarization by exhibiting an N-shaped current-voltage relationship. The slope conductance of the NMDA EPSC ranged from 1.1 to 9.4 nS in 31 DGCs, reaching up to twice the size of the AMPA conductance. This widely varying size of the NMDA conductance resulted in the generation of double-peaked EPSCs and a nonlinear increase of the slope conductance of up to 37.5 nS with positive membrane potentials, which resembled "paroxysmal currents," in a subpopulation of the neurons. In contrast, AMPA EPSCs, which were isolated in the presence of an NMDA receptor antagonist (2-amino-5-phosphonovaleric acid), showed voltage-independent linear changes in the current-voltage relationship and were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione. The AMPA conductance showed little variance, regardless of the size of the NMDA conductance of a given neuron. The average AMPA slope conductance was 5.28 +/- 0.65 (SE) nS in 31 human DGCs. This value was similar to AMPA EPSC conductances in normal rat DGCs (5.35 +/- 0.52 nS, mean +/- SE; n = 55). Dendritic morphology and spine density were quantified in the individual DGCs to assess epileptic pathology. Dendritic spine density showed an inverse correlation (r2 = 0.705) with a slower rise time and a longer half-width of the excitatory postsynaptic potentials mediated by the NMDA receptor. It is concluded that both AMPA and NMDA EPSCs contribute to human DGC synaptic transmission in epileptic hippocampus. However, a wide range of changes in the slope conductance of the NMDA EPSCs suggests that the NMDA-receptor-mediated conductance could be altered in human epileptic DGCs. These changes may influence the generation of chronic subthreshold epileptogenic synaptic activity and give rise to pathological excitation leading to epileptic seizures and dendritic pathology.

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PubMed1997

Diencephalic projection to reticulospinal neurons involved in the initiation of locomotion in adult lampreys Lampetra fluviatilis.

Morphological and electrophysiological techniques were used to characterize a diencephalic projection from the ventral thalamus to reticulospinal neurons and its role in initiating rhythmic locomotor activity in the spinal cord of adult lampreys (Lampetra fluviatilis). Injection of fluorescein-coupled dextran amine (FDA) into the rhombencephalic reticular nuclei labeled neurons in the ventral thalamus region on both the ipsilateral side and the contralateral side. Injection of FDA into the ventral thalamus labeled axonal projections in all reticular nuclei, but no direct projections were found to the spinal cord. Extracellular stimulation of the ventral thalamus elicited monosynaptic excitatory postsynaptic potentials (EPSPs), polysynaptic EPSPs, and inhibitory postsynaptic potentials (IPSPs) in reticulospinal neurons in the posterior (prrn) and middle (mrrn) rhombencephalic reticular nuclei. The monosynaptic EPSPs were blocked by the glutamate antagonist kynurenic acid and can be considered glutamatergic. The monosynaptic EPSPs were potentiated (up to 12 minutes) following a brief high-frequency stimulation. Stimulation of the ventral thalamus induced rhythmic firing of reticulospinal neurons and elicited rhythmic burst activity in the spinal ventral roots. The projections from the ventral thalamus to the reticulospinal neurons in the prrn and mrrn thus provide excitatory inputs to the reticulospinal neurons, which, in turn, can activate the spinal circuits underlying locomotion. Also, the input nuclei to the ventral thalamus were labeled following injection of FDA into this nucleus. Labeled cells were found in the olfactory bulb, pallial areas, striatum, preoptic nucleus, hypothalamus, dorsal thalamus, optic tectum, and dorsal isthmic gray. The ventral thalamus, therefore, receives inputs from several different regions in the brain and controls the level of excitability in reticulospinal neurons.

Animals↗