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PubMed1979

Potentials evoked by alvear tract in hippocampal CA1 region of rats. I. Topographical projection, component analysis, and correlation with unit activities.

1. The field potentials and unit activities evoked by the alvear tract (AT) in CA1 region of the dorsal hippocampus of rats were studied under sodium pentobarbital anesthesia. 2. The localized activity evoked anterior to an AT stimulus began as a compound action potential, followed by a slower negative wave, and ended in a long-lasting, slow positive wave. Observed with a 64-electrode recording array, topographical projections of the AT in CA1 were seen as parallel strips inclined at an angle of 5-30 degrees medially from the sagittal plane. 3. Three overlapping components in the averaged evoked potentials (AEPs) were distinguished. The first event (component I) was a brief compound antidromic action potential of pyramidal cells. The second field event (component II) reversed from surface negative to deep positive at 200 micrometer from the ventricular surface, increased rapidly with stimulus intensity, potentiated with double shocks, and followed stimulus frequency up to 50/s. The third component was long lasting (up to 200 ms), surface positive and ventral negative (turnover at 150 micron below the pyramidal layer), followed stimulus frequency up to about 10/s, and saturated at a low stimulus intensity (about 3 x threshold). 4. In some preparations, another fast negative peak of about 2 ms duration was found to follow the axon compound action potential on the hippocampal surface and appeared to propagate from the pyramidal layer to the ventricular surface. It was probably of nonsynaptic origin, perhaps due to the centrifugal basal dendritic spikes of the pyramidal cells. 5. Single units were recorded in CA1. Antidromic units were identified by their firing at a fixed latency (1.5 ms) and ability to follow high stimulus frequencies. Units firing at about 2.7 ms latency possessed characteristics of monosynaptic excitation. Under light anesthesia, many of the latter units also showed a late, prolonged suppression of background firing. Tentative interneuronal types fired with peak latencies of 4-5 ms or showed prolonged increase in firing rate. 6. From the correlation with unit post-stimulus time histograms, AEP component II was inferred to be the extracellular, monosynaptic, excitatory postsynaptic potentials, and component III the di- or polysynaptic inhibitory postsynaptic potentials. These postsynaptic potentials were generated by the pyramidal cells and interneurons.

Animals↗

PubMed1998

Net interaction between different forms of short-term synaptic plasticity and slow-IPSPs in the hippocampus and auditory cortex.

Paired-pulse plasticity is typically used to study the mechanisms underlying synaptic transmission and modulation. An important question relates to whether, under physiological conditions in which various opposing synaptic properties are acting in parallel, the net effect is facilitatory or depressive, that is, whether cells further or closer to threshold. For example, does the net sum of paired-pulse facilitation (PPF) of excitatory postsynaptic potentials (EPSPs), paired-pulse depression (PPD) of inhibitory postsynaptic potentials (IPSPs), and the hyperpolarizing slow IPSP result in depression or facilitation? Here we examine how different time-dependent properties act in parallel and examine the contribution of gamma-aminobutyric acid-B (GABAB) receptors that mediate two opposing processes, the slow IPSP and PPD of the fast IPSP. Using intracellular recordings from rat CA3 hippocampal neurons and L-II/III auditory cortex neurons, we examined the postsynaptic responses to paired-pulse stimulation (with intervals between 50 and 400 ms) of the Schaffer collaterals and white matter, respectively. Changes in the amplitude, time-to-peak (TTP), and slope of each EPSP were analyzed before and after application of the GABAB antagonist CGP-55845. In both CA3 and L-II/III neurons the peak amplitude of the second EPSP was generally depressed (further from threshold) compared with the first at the longer intervals; however, these EPSPs were generally broader and exhibited a longer TTP that could result in facilitation by enhancing temporal summation. At the short intervals CA3 neurons exhibited facilitation of the peak EPSP amplitude in the absence and presence of CGP-55845. In contrast, on average L-II/III cells did not exhibit facilitation at any interval, in the absence or presence of CGP-55845. CGP-55845 generally "erased" short-term plasticity, equalizing the peak amplitude and TTP of the first and second EPSPs at longer intervals in the hippocampus and auditory cortex. These results show that it is necessary to consider all time-dependent properties to determine whether facilitation or depression will dominate under intact pharmacological conditions. Furthermore our results suggest that GABAB-dependent properties may be the major contributor to short-term plasticity on the time scale of a few hundred milliseconds and are consistent with the hypothesis that the balance of different time-dependent processes can modulate the state of networks in a complex manner and could contribute to the generation of temporally sensitive neural responses.

Animals↗

PubMed1999

Ionic mechanisms underlying depolarizing responses of an identified insect motor neuron to short periods of hypoxia.

Hypoxia can dramatically disrupt neural processing because energy-dependent homeostatic mechanisms are necessary to support normal neuronal function. In a human context, the long-term effects of such disruption may become all too apparent after a "stroke," in which blood-flow to part of the brain is compromised. We used an insect preparation to investigate the effects of hypoxia on neuron membrane properties. The preparation is particularly suitable for such studies because insects respond rapidly to hypoxia, but can recover when they are restored to normoxic conditions, whereas many of their neurons are large, identifiable, and robust. Experiments were performed on the "fast" coxal depressor motoneuron (Df) of cockroach (Periplaneta americana). Five-minute periods of hypoxia caused reversible multiphasic depolarizations (10-25 mV; n = 88), consisting of an initial transient depolarization followed by a partial repolarization and then a slower phase of further depolarization. During the initial depolarizing phase, spontaneous plateau potentials normally occurred, and inhibitory postsynaptic potential frequency increased considerably; 2-3 min after the onset of hypoxia all electrical activity ceased and membrane resistance was depressed. On reoxygenation, the membrane potential began to repolarize almost immediately, becoming briefly more negative than the normal resting potential. All phases of the hypoxia response declined with repeated periods of hypoxia. Blockade of ATP-dependent Na/K pump by 30 microM ouabain suppressed only the initial transient depolarization and the reoxygenation-induced hyperpolarization. Reduction of aerobic metabolism between hypoxic periods (produced by bubbling air through the chamber instead of oxygen) had a similar effect to that of ouabain. Although the depolarization seen during hypoxia was not reduced by tetrodotoxin (TTX; 2 microM), lowering extracellular Na+ concentration or addition of 500 microM Cd2+ greatly reduced all phases of the hypoxia-induced response, suggesting that Na influx occurs through a TTX-insensitive Cd2+-sensitive channel. Exposure to 20 mM tetraethylammonium and 1 mM 3,4-diaminopyridine increased the amplitude of the hypoxia-induced depolarization, suggesting that activation of K channels may normally limit the amplitude of the hypoxia response. In conclusion we suggest that the slow hypoxia-induced depolarization on motoneuron Df is mainly carried by a TTX-resistant, Cd2+-sensitive sodium influx. Ca2+ entry may also make a direct or indirect contribution to the hypoxia response. The fast transient depolarization appears to result from block of the Na/K pump, whereas the reoxygenation-induced hyperpolarization is largely caused by its subsequent reactivation.

Adenosine Triphosphate↗

PubMed1999

Neural architecture of the electrosensory lateral line lobe: adaptations for coincidence detection, a sensory searchlight and frequency-dependent adaptive filtering

The electrosensory lateral line lobe (ELL) of weakly electric fish is the only nucleus that receives direct input from peripheral electroreceptor afferents. This review summarises the neurotransmitters, receptors and second messengers identified in the intrinsic circuitry of the ELL and the extrinsic descending direct and indirect feedback pathways, as revealed by recent in vitro and in vivo studies. Several hypotheses of circuitry function are examined on this basis and on the basis of recent functional evidence: (1) fast primary afferent excitatory postsynaptic potentials (EPSPs) and fast granule cell 2 GABAA inhibitory postsynaptic potentials (IPSPs) suggest the involvement of basilar pyramidal cells in coincidence detection; (2) voltage-dependent EPSPs and IPSPs, dendritic spike bursts and frequency-dependent synaptic facilitation support a sensory searchlight role for the direct feedback pathway; and (3) the contributions of distal and proximal inhibition, anti-Hebbian plasticity and beam versus isolated fiber activity patterns are discussed with reference to an adaptive spatio-temporal filtering role for the indirect descending pathway.

Journal Article↗

PubMed1997

Reduction in amplitude of the ventral root elicited small spike by dorsal root stimulation in cat motoneurons.

Ventral root stimulation is known to produce two spikes, large and small, in the alpha-motoneuron. Since it is the small spike that triggers the outgoing impulse from the cell it is regarded as the key potential in information processing of the cell and referred to either as the IS-spike or as the A-spike depending upon whether one considers it as a purely single spike or as a composite spike. The small spike was elicited by stimulating the L 7 or S 1 ventral root in cats anesthetized with pentobarbital sodium and immobilized with d-tubocurarine. During the later phase of the excitatory prostsynaptic potential and thereto following inhibitory postsynaptic potential (IPSP) produced by stimulating the corresponding dorsal root the amplitude of the small spike was reduced by about 20%. This could be either explained as due to reduction in impedance of the membrane generating the small spike or interpreted as suggesting that the small spike is a composite spike and some of its components were inhibited by the IPSP. This interpretation was favored because the reduction occurred not when the safety factor for antidromic impulse transmission was high, but when it was low.

Action Potentials↗

PubMed2001

The identification of the sympathetic neurons innervating the hamster submandibular gland and their electrophysiological membrane properties.

The neuron innervating the hamster submandibular (SM) gland was identified in the superior cervical ganglion (SCG) in vitro by recording the antidromic response using the intracellular recording technique. After the cellular response was recorded, methylene blue was injected iontophoretically into the neuron from the recording electrode, and the location of the cell soma was determined. The salivatory neurons of the SM gland were in the small- to medium-sized group of the entire cell population of the SCG. The cell size was 36.3 x 24.4 microm (mean, n=45). The postganglionic fibers were entirely unmyelinated (mean: 0.34 m/sec at 28-30 degrees C, n=141). Eighty-seven percent of the cells were distributed in the central one-third of area between the external carotid nerve origin and the caudal pole in the SCG. The resting membrane potential, membrane input resistance, membrane time constant and membrane input capacitance of the salivatory neuron were as follows: -49.2+/-7.6 mV (n=102), 52.9+/-23.6 Mohms (n=71), 8.0+/-3.4 msec (n=71) and 147+/-50 pF (n=71). Fast- and slow-excitatory postsynaptic potentials (EPSPs) were evoked, but not slow-inhibitory postsynaptic potentials (IPSPs). The fast EPSP was 13.1+/-5.7 mV in amplitude and 46.2+/-17.1 msec in duration (n=35). The slow EPSP (20 Hz, 5 sec) was 6.9+/-11 .9 mV in amplitude and 101+/-43 sec in duration (n=16). The directly-evoked spike was 63.0+/-11.9 mV in amplitude and 5.9+/-1.3 msec in duration (n=54). The spike after-hyperpolarization (AHP) was 12.5+/-3.5 mV in amplitude and 353+/-161 msec in duration. Na+ and Ca+ channels were involved in the spike generation. The voltage-dependent K+ channels (delayed rectifier), A channels and rapidly Ca2+-activated K+ channels (BK channels) regulated the spike-falling phase. The delayed rectifiers, A channels, and BK and SK (slowly Ca2+-activated) channels were involved in generation of spike-AHP. Muscarine suppressed the Ca2+ component of spike via muscarinic receptors.

4-Aminopyridine↗

PubMed2001

Optical recording of the spatiotemporal propagation of neuronal excitation in the rat hippocampal CA2-CA1 pathway.

Changes in the membrane potential of neurons in the hippocampal CA2 and CA1 regions were recorded by optical recording techniques. After stimulation of the Schaffer collaterals at the hippocampal CA2 region, excitatory optical signals first occurred adjacent stimulus electrode and then flamed-up signals spread toward the hippocampal CA1 region. The optical signal was blocked by tetrodotoxin (TTX) (1 microM). Propagation of the optical signal was blocked in an artificial cerebrospinal fluid (ACSF) containing 0 mM Ca2+ and 6 mM Mg2+. 6,7-Dinitroquinoxaline-2,3 (1H,4H)-dione (DNQX) (20 microM) also blocked the optical signals that spread to the hippocampal CA1 region. The time course of the optical signal recorded at a unit area (49 pixels) on the propagation pathway was characterized by fast and slow components. TTX (1 microM) blocked both fast and slow components of the optical signal. The slow component of the optical signal was preferentially depressed by either removal of external Ca2+ or by bath-application of DNQX (20 microM). When bicuculline (15 microM) was applied to the bath-solution, the intensity and propagation area of the optical signal were increased. The results indicate that stimulation of the Schaffer collaterals in the hippocampal CA2 region produces the propagation of the optical signal to the hippocampal CA1 region, and that the optical signal involves the action potential and excitatory and inhibitory postsynaptic potentials.

Action Potentials↗

PubMed1988

The formation of chemical synapses between cell-cultured neuronal somata.

The study of the development and plasticity of chemical synaptic connections is frequently restricted by the lack of access to the synaptic terminals. This can, in part, be overcome by plating neurons into cell culture where all regions of a neuron are made experimentally accessible. However, the small size of synaptic terminals still makes direct experimental manipulation difficult. In this study we have found in the absence of neurite extension, directly contacting cell somata (diameter 50-100 mumol) will form chemical synapses. Identified neurons B5 and B19 of Helisoma were plated into culture under conditions that promote adhesion between cell pairs. Under these conditions, neurite outgrowth was absent, but action potentials in B5 evoked inhibitory postsynaptic potentials in B19 that were reversed in sign by the injection of chloride ions and were blocked by tubocurare (10(-5) M), reduced extracellular Ca2+, and Cd2+ ions. Such synapses exhibited classical properties of chemical synapses, including the spontaneous release of neurotransmitter. Since somatic synapses represent an appropriate model of synaptic transmission, this system was utilized to study the role of mutual neuronal contact in the development of transmitter release capabilities. Future pre- and postsynaptic somata were cultured separately for 3 d, the period required for the development of synaptic transmission under conditions of maintained contact. Then, neurons were made to contact and intracellular recordings taken within 0 to 4 hours. Postsynaptic potentials were detected as early as 10 sec following contact. Thus, qualitatively the development of transmitter release capabilities does not require maintained contact.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Calcium channel involvement in GABAB receptor-mediated inhibition of GABA release in area CA1 of the rat hippocampus.

1. Experiments were performed in rat hippocampal slices to examine the nature of GABAergic inhibition of inhibitory synaptic transmission. In these experiments the effects of the gamma-aminobutyric acid-B (GABAB) receptor agonist, baclofen, and of subtype-selective calcium channel blockers were tested with the use of intracellular recordings of evoked inhibitory postsynaptic potentials (IPSPs) and whole cell recordings of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs). 2. Baclofen inhibited evoked and spontaneous (action-potential-dependent) monosynaptic GABAA-mediated IPSPs and IPSCs but had no effect on the frequency of tetrodotoxin-resistant (action-potential-independent) miniature IPSCs recorded in CA1 pyramidal neurons. 3. Depolarizing GABAergic synaptic terminals by raising the extracellular potassium concentration caused an increase in action-potential-independent miniature IPSC frequency that could be inhibited by either baclofen or cadmium, a blocker of voltage-dependent calcium channels. In addition, under these depolarizing conditions, cadmium occluded the baclofen inhibition of miniature IPSCs. These data suggest that baclofen reduces only depolarization-induced, not quantal, GABA release and that it does so by decreasing presynaptic voltage-dependent calcium influx. 4. Experiments with subtype-selective calcium channel blockers demonstrate that the presynaptic action of baclofen was mediated through both omega-conotoxin-GVIA-sensitive and omega-agatoxin-IVA-sensitive, but not dihydropyridine-sensitive calcium channels.

Action Potentials↗

PubMed1991

Noradrenaline receptors participate in the regulation of GABAergic inhibition in area CA1 of the rat hippocampus.

1. Standard intracellular recordings from CA1 pyramidal neurones in in vitro hippocampal slices have been used to investigate the effects of excitatory amino acid antagonists and adrenergic agents on evoked synaptic potentials. 2. Ortho- and antidromic stimulation were conducted with remotely placed electrodes in order to minimize the possibility of stimulating the interneurones directly. In addition to the excitatory postsynaptic potential (EPSP), orthodromic stimulation evoked an inhibitory sequence consisting of a fast and slow inhibitory postsynaptic potential (IPSP). The slow-IPSP was blocked by intracellular injection of QX 314. Antidromic stimulation evoked a relatively pure fast-IPSP. 3. In seven neurones the differential effects of glutamatergic receptor blockers on the fast-IPSP were investigated. The N-methyl-D-aspartate (NMDA) receptor blocker, DL-2-amino-5-phosphonovaleric acid (APV) was added after the full effect of the non-NMDA receptor blocker, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) had been achieved. In three neurones, APV had no additional blocking effect, while in the remaining four neurones, both the ortho- and antidromically evoked IPSPs were reduced by 20-50%. This suggests that NMDA receptors participate in the activation of some GABAergic interneurones, which was further confirmed by showing that the IPSP was enhanced by Mg(2+)-free medium. 4. In the presence of CNQX (10 microM) and APV (50 microM) together, the ortho- and antidromically evoked fast-IPSPs were greatly reduced. A small 'residual' IPSP remained which was best studied by depolarizing the neurone to around -50 mV. With maximum stimulation, this amounted to 26.3 +/- 15.4% (mean +/- S.E.M., n = 15) of the control IPSP evoked by orthodromic stimulation and 41 +/- 14.6% of the control IPSP evoked by antidromic stimulation. The following statements apply equally to the ortho- and antidromically activated residual IPSPs. 5. The residual IPSP was completely blocked by low concentrations of bicuculline, indicating that it is mediated by GABAA receptors. When compared with a control IPSP of similar amplitude, the residual IPSP was found to have a faster rise time and time-to-peak, but a similar decay time. 6. Neither the muscarinic cholinergic antagonist, atropine nor the presynaptic glutamate agonist, L-2-amino-4-phosphonobutyric acid (L-APB) had any effect on the residual IPSP. 7. The residual IPSP was completely blocked by the adrenergic beta-receptor antagonist, L-propranolol (50-100 microM).(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1990

Synaptic excitation of inhibitory cells by single CA3 hippocampal pyramidal cells of the guinea-pig in vitro.

1. In simultaneous recordings from pairs of neurones in hippocampal slices from guinea-pigs, single action potentials fired by CA3 pyramidal cells could initiate inhibitory postsynaptic potentials (IPSPs) in nearby pyramidal cells. 2. The latencies of these IPSPs could be as short as 3 ms. However, they were mediated disynaptically via chemical, excitatory synapses, since inhibitory coupling was suppressed by an excitatory amino acid antagonist. 3. The properties of excitatory synapses made onto inhibitory cells were examined to assess the basis for this strong coupling. Inhibitory cells were identified either by showing that they inhibited another cell or by their characteristic firing pattern. 4. Excitatory postsynaptic potentials (EPSPs) elicited by single pyramidal cell action potentials had a mean amplitude of 1-4 mV and a time to peak of 1.5-4 ms. In most cases they decayed with a time constant similar to that of the inhibitory cell membrane. 5. EPSP amplitude increased with hyperpolarization of the postsynaptic membrane. Membrane polarization had little effect on EPSP shape. 6. EPSPs fluctuated in amplitude and transmission sometimes failed, suggesting transmission was quantal and that few quanta were released. 7. When presynaptic cells were made to fire bursts of action potentials, EPSPs in inhibitory cells were initially potentiated. 8. EPSPs could cause inhibitory cells to fire. The interval between pre- and postsynaptic spikes could be as short as 2.5 ms and the probability of spike transmission could be as high as 0.6. Some inhibitory cells which received feedback excitation were also excited in feedforward fashion by mossy fibre stimuli. 9. One pyramidal cell could activate several disynaptic inhibitory pathways terminating on another pyramidal cell. This suggests that excitatory synapses made by pyramidal cell axon collaterals onto inhibitory cells are divergent. 10. This strong, divergent excitation of inhibitory cells ensures recurrent inhibition is sufficiently widespread, rapid and potent to control the spread of activity by recurrent excitatory connections between CA3 pyramidal cells.

Action Potentials↗

PubMed2000

Presynaptic control of transmission along the pathway mediating disynaptic reciprocal inhibition in the cat.

In cat lumbar motoneurones, disynaptic inhibitory postsynaptic potentials (IPSPs) evoked by stimulation of antagonist motor nerves were depressed for at least 150 ms following conditioning stimulation of flexor (1.7-2 times threshold (T)) and ankle extensor (5T) nerves. The aim of the present study was to investigate the possibility that this depression is caused by presynaptic inhibitory mechanisms acting at the terminals of group I afferent fibres projecting to the Ia inhibitory interneurones and/or the terminals of these interneurones to the target motoneurones. Conditioning stimulation of flexor, but not ankle extensor, nerves evoked a depression of the monosynaptic Ia excitatory postsynaptic potentials (EPSPs) recorded intracellularly in Ia inhibitory interneurones. This depression lasted between 200 and 700 ms and was not accompanied by a depression of the monosynaptic EPSPs evoked by stimulation of descending pathways. These results suggest that flexor, but not ankle extensor, group I afferent fibres can modulate sensory transmission at the synapse between Ia afferent fibres and Ia inhibitory interneurones. Conditioning stimulation of flexor muscle nerves, extensor muscle nerves and cutaneous nerves produced a long-lasting increase in excitability of the terminals of the Ia inhibitory interneurones. The increase in the excitability of the terminals was not secondary to an electrotonic spread of synaptic excitation at the soma. Indeed, concomitant with the excitability increase of the terminals there were signs of synaptic inhibition in the soma. The unitary IPSPs induced in target motoneurones following the spike activity of single Ia inhibitory interneurones were depressed by conditioning stimulation of muscle and cutaneous nerves. Since the conditioning stimulation also evoked compound IPSPs in those motoneurones, a firm conclusion as to whether unitary IPSP depression involved presynaptic inhibitory mechanism of the terminals of the interneurones could not be reached. The possibility that the changes in excitability of the Ia interneuronal terminals reflect the presence of a presynaptic inhibitory mechanism similar to that operating at the terminals of the afferent fibres (presynaptic inhibition) is discussed.1. In cat lumbar motoneurones, disynaptic inhibitory postsynaptic potentials (IPSPs) evoked by stimulation of antagonist motor nerves were depressed for at least 150 ms following conditioning stimulation of flexor (1.7-2 times threshold (T)) and ankle extensor (5T) nerves. The aim of the present study was to investigate the possibility that this depression is caused by presynaptic inhibitory mechanisms acting at the terminals of group I afferent fibres projecting to the Ia inhibitory interneurones and/or the terminals of these interneurones to the target motoneurones. Conditioning stimulation of flexor, but not ankle extensor, nerves evoked a depression of the monosynaptic Ia excitatory postsynaptic potentials (EPSPs) recorded intracellularly in Ia inhibitory interneurones. This depression lasted between 200 and 700 ms and was not accompanied by a depression of the monosynaptic EPSPs evoked by stimulation of descending pathways. These results suggest that flexor, but not ankle extensor, group I afferent fibres can modulate sensory transmission at the synapse between Ia afferent fibres and Ia inhibitory interneurones. Conditioning stimulation of flexor muscle nerves, extensor muscle nerves and cutaneous nerves produced a long-lasting increase in excitability of the terminals of the Ia inhibitory interneurones. The increase in the excitability of the terminals was not secondary to an electrotonic spread of synaptic excitation at the soma. Indeed, concomitant with the excitability increase of the terminals there were signs of synaptic inhibition in the soma. The unitary IPSPs induced in target motoneurones following the spike activity of single Ia inhibitory interneurones were depressed by conditioning stimulation

Action Potentials↗

PubMed1999

Local disinhibition of neocortical neuronal circuits causes augmentation of glutamatergic and GABAergic synaptic transmission in the rat neostriatum in vitro.

Intra- and extracellular recordings were performed to investigate the influence of local disinhibition of neocortical circuits on corticostriatal synaptic transmission. In rat brain slices with preserved corticostriatal connections, electrical stimulation of the neocortex elicited composed postsynaptic responses in neostriatal neurons consisting of glutamatergic excitatory postsynaptic potentials (EPSPs) and weakly expressed GABAA receptor-mediated inhibitory postsynaptic potentials (IPSPs). Following local application of the GABAA receptor antagonist bicuculline to the neocortex, neocortical neurons responded to intracortical stimulation with transient paroxysmal depolarizations. Simultaneously, the amplitude of neocortically evoked EPSPs recorded from neostriatal neurons was found to be enhanced without changes in duration. Similarly, the amplitude of IPSPs increased following disinhibition of neocortical circuits. In addition and in contrast to EPSPs, the duration of the IPSPs was found to be markedly prolonged. The results demonstrate that local disinhibition of neocortical neuronal circuits potentiates both excitatory and inhibitory synaptic transmission in striatal neurons. However, compared to AMPA receptor-mediated excitation, GABAA receptor-mediated inhibition becomes more efficient due to a marked prolongation of IPSPs. The pronounced augmentation of inhibition can be attributed to a strong activation of inhibitory interneurons within the striatum.

Animals↗

PubMed1999

Tectal afferents monosynaptically activate neurons in the pigeon isthmo-optic nucleus.

Postsynaptic responses of 105 neurons in brain slices were intracellularly recorded from the isthmo-optic nucleus (ION) in pigeons, and 18 of these neurons were labeled with Lucifer yellow. Excitatory postsynaptic potentials (EPSPs) or spikes were produced in 93 cells, inhibitory postsynaptic potentials (IPSPs) in 10 cells, and EPSPs followed by IPSPs in two cells following electrical stimulation of the tecto-isthmooptic tract. The EPSPs occurred in an all-or-none fashion, with short latencies (1.3 +/- 0.6 ms). Repetitive stimulation increased their amplitude and duration, demonstrating that temporal summation was involved. Neurons producing excitatory responses were distributed throughout cellular layers of the nucleus. Pure IPSPs had a latency of 3.9 +/- 2.3 ms, and cells that responded in this manner were only distributed in the rostral portion of the nucleus. In the remaining two cells with EPSP-IPSP responses, the latency of excitatory responses was 1.5 ms in one cell and 1.4 ms in the other, and that of inhibitory responses was, respectively, 5.1 and 4.1 ms. Thus, it appeared that excitation was monosynaptic, whereas inhibition may be polysynaptic. Four single injections resulted in dye-coupled labeling, and two pairs of closely apposed cells fired spikes, probably resulting from spatial summation of their excitatory responses. The present study suggests that tectal cells directly activate ION neurons and that tectal fibers contact isthmo-optic neurons in a one-to-one fashion. Taken together with previous studies, it appears that the entire tecto-ION-retinal pathway is excitatory.

Animals↗

PubMed1996

Pyloric motor pattern modification by a newly identified projection neuron in the crab stomatogastric nervous system.

1. We have used multiple, simultaneous intra- and extracellular recordings as well as Lucifer yellow dye-fills to identify modulatory commissural neuron 5 (MCN5) and characterize its effects in the stomatogastric nervous system (STNS) of the crab, Cancer borealis. MCN5 has a soma and neuropilar arborization in the commissural ganglion (CoG; Figs. 1 and 2), and it projects through the inferior esophageal nerve (ion) and stomatogastric nerve (stn) to the stomatogastric ganglion (STG; Figs. 1-3). 2. Within the CoGs, MCN5 receives esophageal rhythm-timed excitation and pyloric rhythm-timed inhibition (Fig. 4). Additionally, during the lateral teeth protractor phase of the gastric mill rhythm, the pyloric-timed inhibition of MCN5 is reduced or eliminated. 3. Intracellular stimulation of MCN5 excites the pyloric pacemaker ensemble, including the anterior burster (AB), pyloric dilator (PD), and lateral posterior gastric (LPG) neurons. This produces a faster pyloric rhythm. MCN5 stimulation also inhibits all nonpacemaker pyloric neurons, reducing or eliminating their activity (Figs. 5 and 6A; Tables 1 and 2). After MCN5 stimulation, bursting is enhanced for several cycles in some pyloric neurons when compared with their prestimulus activity (Figs. 5 and 6A; Tables 1 and 2). 4. MCN5 evokes distinct responses from each pyloric pacemaker neuron (Figs. 6-8). The AB and LPG neurons respond with increased activity. The AB response includes the presence of large amplitude excitatory postsynaptic potentials (EPSPs) that contribute to a depolarization of the trough of its rhythmic oscillations (Fig. 6). LPG responds by exhibiting increased activity that prolongs the duration of its burst beyond that of AB and PD (Fig. 7). In contrast, MCN5 stimulation initially produces decreased PD neuron activity, followed by a slight enhancement of each PD burst (Figs. 7 and 8). PD activity is further enhanced after MCN5 stimulation (Figs. 7 and 8). 5. MCN5-elicited action potentials evoke discrete, constant latency inhibitory postsynaptic potentials (IPSPs) in all nonpacemaker pyloric neurons, including the inferior cardiac (IC), lateral pyloric (LP), pyloric (PY), and ventricular dilator (VD) neurons (Fig. 9). MCN5 activity also inhibits these neurons indirectly, via its excitation of the pacemaker neurons. The pyloric pacemaker neurons synaptically inhibit all four nonpacemaker neurons. 6. The increased activity in the VD neuron, after MCN5 stimulation, is not mimicked by either direct hyperpolarization or by synaptically inhibiting VD via another pathway (Fig. 10). The poststimulation increase in IC neuron activity is stronger than that after hyperpolarizing current injection but is comparable with that resulting from stimulation of another inhibitory pathway (Fig. 10). The enhanced PY neuron activity is comparable with that resulting from either direct current injection or synaptic inhibition from another pathway (Fig. 10). 7. MCN5 activity increases the pyloric cycle frequency of both slow (< 1 Hz) and fast (1-2 Hz) rhythms (Fig. 11), and it significantly alters the phase relationships that define this motor pattern (Fig. 12). These phase relationships change again after MCN5 stimulation (Fig. 12). 8. MCN5 acts in concert with the pyloric pacemaker ensemble to elicit a pyloric rhythm that exhibits enhanced pacemaker neuron activity and reduced activity in all nonpacemaker neurons. Additionally, despite their electrical coupling, the three types of pacemaker neurons exhibit distinct responses to MCN5 stimulation. This partially uncouples their normally coactive bursts. The resulting motor pattern is distinct from all previously characterized pyloric rhythms.

Animals↗

PubMed1991

Frequency potentiation in granule cells in vivo at theta frequency perforant path stimulation.

The effect of frequency potentiation on the postsynaptic potential in granule cells was studied stimulating the perforant path in curarized and urethanized rats. At stimulation frequencies between 2.0-5.0 Hz, synaptic efficacy in eliciting an orthodromic action potential increased despite the hyperpolarization of the transmembrane potential. The excitatory postsynaptic potential (EPSP) slope and duration also increased while the inhibitory postsynaptic potential (IPSP) was reduced. Stimulation frequencies greater than 5.0 Hz produced similar changes in the transmembrane potential and EPSP-IPSP sequence, but they did not increase synaptic efficacy. The frequency potentiation at frequencies into the theta band suggest that this potentiation participates in theta rhythm genesis in this structure which, in turn, suggests that the fascia dentata could work as a band-pass filter. In 12.5% of cases postpotentiation was also observed.

Action Potentials↗

PubMed1996

Synaptic mechanisms and calcium binding proteins in the aged rat brain.

Synaptic mechanisms were studied ex vivo in the aged rat hippocampus, using a slice preparation and intracellular electrophysiological recordings of the CA1 pyramidal neurons. A dramatic depression of the slow cholinergic excitatory postsynaptic potential (EPSP) and of the slow, GABAB-mediated inhibitory postsynaptic potential (IPSP) were observed. These age-related changes were consistently found in three different strains of rats. The mechanisms involve 1) changes in the properties of the postsynaptic muscarinic receptors, and possibly in acetylcholine release (for the postsynaptic muscarinic receptors, and possbily in acetylcholine release (for the cholinergic EPSP), and 2) alterations in the presynaptic GABAergic interneurons, as shown by a loss in calbindin immunoreactivity (for the GABAergic IPSP). The immunoreactivity for three calcium binding proteins (calbindin, parvalbumin and calretinin) was studied in the aged rat brain. Immunoreactivity for calbindin was dramatically reduced in the pyramidal neurons of the CA1 field and in a subpopulation of interneurons in the hippocampus. Immunoreactivity for parvalbumin was reduced in the medial septal area, and in the cingulate cortex, whereas no change was observed for calretinin. These age-related alterations could 1) modify the functions of the hippocampal networks, and possibly contribute to the age-related cognitive deficits, and 2) compromise intraneuronal calcium buffering, and thus make neurons more vulnerable to toxic insults.

Animals↗

PubMed2001

Modulation of synaptic transmission in hippocampal CA1 neurons by a novel neurotoxin (beta-pompilidotoxin) derived from wasp venom.

We examined the effects of beta-pompilidotoxin (beta-PMTX), a neurotoxin derived from wasp venom, on synaptic transmission in the mammalian central nervous system (CNS). Using hippocampal slice preparations of rodents, we made both extracellular and intracellular recordings from the CA1 pyramidal neurons in response to stimulation of the Schaffer collateral/commissural fibers. Application of 5-10 microM beta-PMTX enhanced excitatory postsynaptic potentials (EPSPs) but suppressed the fast component of the inhibitory postsynaptic potentials (IPSPs). In the presence of 10 microM bicuculline, beta-PMTX potentiated EPSPs that were composed of both non-NMDA and NMDA receptor-mediated potentials. Potentiation of EPSPs was originated by repetitive firings of the presynaptic axons, causing summation of EPSPs. In the presence of 10 microM CNQX and 50 microM APV, beta-PMTX suppressed GABA(A) receptor-mediated fast IPSPs but retained GABA(B) receptor-mediated slow IPSPs. Our results suggest that beta-PMTX facilitates excitatory synaptic transmission by a presynaptic mechanism and that it causes overexcitation followed by block of the activity of some population of interneurons which regulate the activity of GABA(A) receptors.

2-Amino-5-phosphonovalerate↗