Synaptic potentials, after-potentials, and slow rhythms of lateral geniculate neurones.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
1. Spontaneous subthreshold potentials have been recorded with an intracellular electrode from neurones of the isolated spinal cord of the frog.2. Records of both depolarizing and hyperpolarizing potentials were obtained from cells in normal Ringer solution and also when impulse conduction in the cord had been abolished by tetrodotoxin (TTX).3. Comparisons of results before and after TTX show that the majority of the spontaneous potentials are analogous to miniature end-plate potentials.
1. Intracellular recordings have been made from neurones lying in the submucous plexus of guinea-pig mid small intestine. 2. Most neurones in this plexus receive an extensive excitatory input which could be abolished by tubocurarine. 3. A proportion of neurones also received a single inhibitory input which was activated by transmural stimulation. 4. Some of the characteristics of the inhibitory potentials evoked by transmural stimulation are described. 5. The observations are discussed in relation to the concept of descending excitation (Hirst, Holman & McKirdy, 1975).
1. The monosynaptic projection of single Ia muscle spindle afferents to motoneurones of identified type has been examined by spike triggered averaging in barbiturate anaesthetized cats. 2. The amplitude of averaged individual monosynaptic e.p.s.p.s in medical gastrocnemius motoneurones from homonymous Ia afferents was clearly related to the motor unit mechanical properties. It was largest in type S units, intermediate in type FR and smallest in type FF. 3. The projection frequency of homonymous Ia afferents to medial gastrocnemius motoneurones followed the same order. 4. Similar trends were evident in both respects for the heteronymous projections of triceps surae. 5. The mechanical property of units which related most directly to e.p.s.p. size was muscle unit contraction strength, a single continuous relation existing throughout all three unit types. 6. On the basis of motor axon conduction velocity measurements, it appeared that motoneurone size could provide a simple explanation for e.p.s.p. size in type S and type FR units, but not in type FF. The latter had unduly small e.p.s.p.s relative to their axon conduction velocity, indicating a qualitatively different presynaptic organization for FF motoneurones from the others. 7. The data make it possible to predict that Ia afferent excitation alone would cause recruitment of units in order of increasing contraction strength and that this order would also obtain if a substantial part of the excitation came from other sources with uniform effect on all unit types. 8. It is shown that a consequence of the observed organization is that the gain of the Ia mediated stretch reflex would be approximately proportional to the developed force.
1. The discharges of muscle spindle afferents from the external intercostal muscles of anaesthetized, paralysed cats were recorded from dorsal roots in continuity. The dynamic responses, regularities of firing and conduction velocities of the afferents were measured and used to characterize the afferents as primary-like or secondary-like. 2. The synchronization of afferent discharges was investigated by the construction of cross-correlation histograms from the simultaneously recorded discharges of pairs of afferents. The discharges of primary-like afferents with high dynamic responses were found to be synchronized within a few msec. The cardiac pulse was a strong contributary factor in this synchronization. 3. Intracellular recordings were made from external intercostal motoneurones, and spike-triggered averaging was used to reveal unitary e.p.s.p.s evoked by muscle spindle afferents which were from the same spinal cord segment. Dorsal roots other than the rootlet containing the afferent were cut to prevent the synchronization of afferent discharges from affecting the averaged e.p.s.p.s. 4. For primary-like afferents the mean amplitude of the e.p.s.p.s was 171 microV and the mean connectivity (the proportion of motoneurones connected by one afferent) was between 42 and 48%. 5. The amplitudes and shapes of the e.p.s.p.s varied with the respiratory phase, usually being larger in inspiration than in expiration and sometimes also having a longer time course. In particular some e.p.s.p.s showed that components, only represent in inspiration, which were interpreted as indicating polysynaptic connexions gated by the respiratory cycle. 6. The results are discussed in comparison with the connexions of individual muscle spindle afferents from other muscles, with particular reference to the conduction velocities of the afferents.
1. Intracellular recordings were made from locus coeruleus neurones in a slice of tissue cut from the rat pons. A depolarizing postsynaptic potential (PSP) followed electrical stimulation of the slice surface; the latency was 1-3 ms and the duration was 50-200 ms. 2. The reversal potential of the PSP (estimated by extrapolation from potentials between -60 and -90 mV) was -27 mV when the recording electrodes contained potassium chloride, and -36 mV when electrodes contained potassium acetate or methylsulphate. 3. Kynurenic acid depressed the PSP amplitude by up to 60%. The residual PSP reversed polarity at -50 mV (extrapolated, potassium chloride in electrodes) or -70 mV (observed, potassium methylsulphate in electrodes): it was blocked by bicuculline (10 microM). 4. Exogenously applied gamma-aminobutyric acid (GABA) depolarized cells when the recording electrode contained potassium chloride (reversal potential was -45 mV) and hyperpolarized cells when the recording electrode contained potassium methylsulphate (reversal potential was -70 mV). 5. In the presence of bicuculline, the residual PSP was blocked by kynurenic acid, whereas DL-2-amino-5-phosphonovaleric acid (2-APV) reduced its amplitude to 80% of control. 6. Exogenously applied glutamate, quisqualate and N-methyl-D-aspartate (NMDA) all caused a membrane depolarization (or an inward current under voltage clamp) which reversed polarity at about 0 mV. These effects were blocked by kynurenic acid (500 microM); 2-APV (50 microM) selectively blocked the effect of NMDA. 7. The results indicate that the PSP evoked by focal stimulation within the nucleus locus coeruleus results from an excitatory amino acid acting predominantly at non-NMDA receptors, and from GABA acting at GABAA receptors.
1. Excitatory postsynaptic potentials (EPSPs) evoked by impulses in single group I muscle afferents were recorded intracellularly in dorsal spinocerebellar tract (DSCT) neurones in the spinal cords of anaesthetized cats. 2. In the same experiments, electrotonic membrane properties of DSCT neurones were measured using the voltage response of each cell to a brief intracellular current pulse. 3. Single group I fibre EPSPs were found to exhibit a large range of amplitudes, from 210 microV to 3.4 mV. All of these EPSPs exhibited uniformly rapid rise times, in contrast to the wide range of time courses exhibited by group I a EPSPs recorded in motoneurones. 4. Electrotonic analysis of DSCT neurones indicated that the time constants of these cells ranged from 5.9 to 18.2 ms, with an average value of 10.9 ms. 5. Current pulse responses of the majority (approximately three-quarters) of DSCT neurones were well described by a simple cable model. Equivalent dendritic cable lengths were calculated for DSCT neurones and found to have an average value of 1.0 space constants, which is considerably less than that calculated for motoneurones. 6. Application of the simple cable model of DSCT neurones demonstrated that the rapid rise-times of single group I EPSPs can be explained by a substantial somatic input to these cells. However, in addition to this strong somatic component, there may also be a contribution from dendritic synapses which prolong the initial decay phase of these EPSPs. The final decay of single fibre EPSPs in DSCT neurones is explained simply by the passive membrane time constant of these cells.
1. Intracellular recordings were made from rat CA3 hippocampal neurones in vitro during the first eighteen days of postnatal life. The cells had resting membrane potentials more negative than -51 mV, action potentials greater than 55 mV and membrane input resistances of 117 +/- 12 M omega. An unusual characteristic of these cells was the presence of spontaneous giant depolarizing potentials (GDPs) which were observed during the first eight postnatal (P) days in over 85% of neurones. They were less frequent between P9 and P12 (48%) and disappeared after P12. 2. The GDPs were synchronously generated by a population of neurones; they reversed polarity at -27 mV when recorded with KCl-containing electrodes and at -51 mV with potassium acetate- or potassium methylsulphate-filled electrodes. 3. The GDPs were blocked by bath application of bicuculline (10 microM) or picrotoxin (100-200 microM). Exogenously applied gamma-aminobutyric acid (GABA; 0.2-1 mM) induced at resting membrane potential a bicuculline-sensitive membrane depolarization which reversed polarity at -25 and -51 mV when recorded with KCl- or potassium methylsulphate-filled electrodes respectively. 4. The GDPs were reduced in frequency or blocked by the N-methyl-D-aspartate (NMDA) receptor antagonists DL-2-amino-7-phosphonoheptanoate (AP-7; 50 microM), D(-)2-amino-5-phosphonovalerate (AP-5, 10-50 microM) and (+-)3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP, 10-50 microM) or NMDA channel blockers phencyclidine (2 microM) and ketamine (20 microM). 5. Stimulation of the hilus during the first week of life evoked a GDP followed by a hyperpolarization. The GDPs were generated by a population of synchronized neurones and reversed polarity at -27 mV with KCl-filled electrodes and at -52 mV with potassium acetate- or potassium methylsulphate-containing electrodes. 6. Bath application of bicuculline (1-10 microM) or picrotoxin (100-200 microM) reversibly blocked the evoked GDPs in the majority of cells. The NMDA receptor antagonists AP-5 (50 microM), AP-7 (50 microM) and CPP (30 microM) usually reduced the amplitude and the duration of the evoked GDPs. In neurones in which evoked GDPs were blocked by bicuculline, a NMDA-mediated component was revealed by increasing the strength or the frequency of stimulation. 7. During the second week of postnatal life, when spontaneous GDPs were extremely rare or absent, superfusion with bicuculline (10 microM) induced, as in adult slices, interictal discharges. These reversed polarity near 0 mV with KCl- or potassium acetate-containing electrodes and were reduced in amplitude and duration by AP-5 (50 microM).(ABSTRACT TRUNCATED AT 400 WORDS)
Whole-cell voltage recordings were made in vivo from excitatory neurons (n = 23) in layer 4 of the barrel cortex in urethane-anaesthetised rats. Their receptive fields (RFs) for a brief whisker deflection were mapped, the position of the cell soma relative to barrel borders was determined for 15 cells and dendritic and axonal arbors were reconstructed for all cells. Three classes of neurons were identified: spiny stellate cells and pyramidal cells located in barrels and pyramidal cells located in septa. Dendritic and, with some exceptions, axonal arborisations of barrel cells were mostly restricted to the borders of a column with a cross sectional area of a barrel, defining a cytoarchitectonic barrel-column. Dendrites and axons of septum cells, in contrast, mostly extended across barrel borders. The subthreshold RFs measured by evoked postsynaptic potentials (PSPs) comprised a principal whisker (PW) and several surround whiskers (SuWs) indicating that deflection of a single whisker is represented in multiple barrels and septa. Barrel cells responded with larger depolarisation to stimulation of the PW (13.7 +/- 4.6 mV (mean +/- S.D.), n = 10) than septum cells (5.7 +/- 2.4 mV, n = 5), the gradient between peak responses to PW and SuW deflection was steeper and the latency of depolarisation onset was shorter (8 +/- 1.4 ms vs. 11 +/- 2 ms). In barrel cells the response onset and the peak to SuW deflection was delayed depending on the distance to the PW thus indicating that the spatial representation of a single whisker deflection in the barrel map is dynamic and varies on the scale of milliseconds to tens of milliseconds. Septum cells responded later and with comparable latencies to PW and SuW stimulation. Spontaneous (0.053 +/- 0.12 action potentials (APs) s(-1)) and evoked APs (0.14 +/- 0.29 APs per principal whisker (PW) stimulus) were sparse. We conclude that PSPs in ensembles of barrel cells represent dynamically the deflection of a single whisker with high temporal and spatial acuity, initially by the excitation in a single PW-barrel followed by multi-barrel excitation. This presumably reflects the divergence of thalamocortical projections to different barrels. Septum cell PSPs preferably represent multiple whisker deflections, but less dynamically and with less spatial acuity.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
1. Plasticity could be induced in (S1) barrel cortex of adolescent rats by reducing the complement of vibrissae on one side of the muzzle to a single whisker for a period of 7, 20, or 60 days. The effect of deprivation was assessed by quantitatively by measuring cortical responses to stimulation of the spared and regrown deprived vibrissae. Vibrissa responses were evoked using a standard stimulus generated by an electromechanical stimulator and measured using poststimulus time histogram analysis. 2. Cells located in layers II/III were found to be plastic beyond postnatal day 28 (P28), whereas cells located in layer IV were not. The vibrissa dominance distribution was shifted significantly toward the spared vibrissa after 7, 20, and 60 days of deprivation for cells located in layers II/III of barrel columns surrounding the D1 column (P < 0.0001, 2-factor analysis of variance). The vibrissa dominance distribution did not shift significantly for cells located in layer IV of surrounding barrels for any of the durations of deprivation tested (P > 0.1). After 7 days of deprivation, 37% of the cells located in layers II/III of the columns deprived vibrissae showed greater responses to the spared vibrissae than to their deprived principal vibrissa, compared with 11% in normally reared adolescent animals and 3% in adults. The percentage of cells dominated by the spared vibrissa was 65% after 20 days of deprivation and 43% after 60 days. 3. For cells located in layers II/III, short-term deprivation (7 days) caused a decrease in the absolute magnitude of response to stimulation of the deprived vibrissa (reduction to approximately 28% of control levels). However, no change could be detected in the spared (D1) vibrissa input to the same deprived columns. Therefore the increase in D1 dominance registered in the deprived columns was mainly due to a decrease in principal vibrissa response and no change in the spared D1 vibrissa response. 4. The first increase in spared vibrissa response was seen after 20 days of deprivation. The response magnitude cells located in layers II/III increased to 70% above control levels. Responses to deprived vibrissa stimulation were depressed at 20 days of deprivation (reduction to 35% of control), implying that the vibrissa dominance shift at 20 days was due to both an increase in spared vibrissa response and a decrease in deprived vibrissa response. 5. The spared vibrissa response was increased after 60 days of deprivation (110% above control) in both near and far halves of the barrel columns surrounding D1. On average, the deprived vibrissa response was depressed at 60 days (84% of control), although less than at 20 or 7 days, because of recovery of responsiveness in the far half of the deprived barrel column. Layer II/III cells located in the half of the barrel column farthest from the spared D1 barrel column showed normal levels of deprived vibrissa input, whereas cells located in the half of the barrel column closest to the spared D1 barrel column still exhibited depressed levels of deprived vibrissa input (54% of control). 6. Control experiments suggested that depression of the deprived vibrissa response could not be explained by nonspecific effects. Depression was not a function of animal's age, because normally reared P28 and adult animals showed similar principal vibrissa response levels. It was not a result of nonspecific depression of cortical responses. because the decreased response only occurred in cells of deprived barrel columns and not spared barrel columns (recorded in the same animals). Depression was not due to altered vibrissa mechanics, because the spared vibrissa response was similarly depressed in animals in which the vibrissae had been trimmed rather than removed. Finally, depression was input specific at 7 and 20 days, because only the deprived vibrissa responses were depressed, whereas spared vibrissa responses were either at control levels or at elevated levels for the same cells. 7.
We have investigated the contribution of GABA(A) receptor activation to swimming in Xenopus tadpoles during the first day of postembryonic development. Around the time of hatching stage (37/8), bicuculline (10-50 microM) causes a decrease in swim episode duration and cycle period, suggesting that GABA(A) receptor activation influences embryonic swimming. Twenty-four hours later, at stage 42, GABA(A) receptor activation plays a more pronounced role in modulating larval swimming activity. Bicuculline causes short, intense swim episodes with increased burst durations and decreased cycle periods and rostrocaudal delays. Conversely, the allosteric agonist, 5beta-pregnan-3alpha-ol-20-one (1-10 microM) or the uptake inhibitor, nipecotic acid (200 microM) cause slow swimming with reduced burst durations and increased cycle periods. These effects appear to be mainly the result of GABA release from the spinal terminals of midhindbrain reticulospinal neurons but may also involve spinal GABAergic neurons. Intracellular recordings were made using KCl electrodes to reverse the sign and enhance the amplitude of chloride-dependent inhibitory postsynaptic potentials (IPSPs). Recordings from larval motoneurons in the presence of strychnine (1-5 microM), to block glycinergic IPSPs, provided no evidence for any GABAergic component to midcycle inhibition. GABA potentials were observed during episodes, but they were not phase-locked to the swimming rhythm. Bicuculline (10-50 microM) abolished these sporadic potentials and caused an apparent decrease in the level of tonic depolarization during swimming activity and an increase in spike height. Finally, in most larval preparations, GABA potentials were observed at the termination of swimming. In combination with the other evidence, our data suggest that midhindbrain reticulospinal neurons become involved in an intrinsic pathway that can prematurely terminate swim episodes. Thus during the first day of larval development, endogenous activation of GABA(A) receptors plays an increasingly important role in modulating locomotion, and GABAergic neurons become involved in an intrinsic descending pathway for terminating swim episodes.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In the identified molluscan neuron, the presynaptic stimulation evokes a histaminergic inhibition of long duration (HILD), resulting from an increase in K conductance followed by a conductance-independent hyperpolarizing process. The latter component of HILD was enhanced by cyclic AMP but depressed by cyclic GMP. However, neither agent alone altered the resting membrane potential nor the conductance.