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PubMed1985

Inhibitory processes of hippocampal CA1 pyramidal neurons following kindling-induced epilepsy in the rat.

To determine the alterations in cellular function which may contribute to the chronic predisposition of neuronal tissue to epileptiform activity, the membrane properties and inhibitory processes of hippocampal CA1 pyramidal cells were investigated using in vitro slices prepared from commissural-kindled rats. No changes were observed in resting membrane potential, input resistance, spike amplitude, and membrane time constant of "kindled" CA1 pyramidal neurons when compared with controls. There were also no differences between control and kindled preparations in the amplitude of recurrent inhibitory postsynaptic potentials (IPSP) and in the duration of inhibition produced by either alvear (Alv) or stratum radiatum (SR) stimulation. Irrespective of group, repetitive stimulation of the Alv reduced the amplitude of the recurrent IPSP but failed to induce seizurelike activity. On the other hand, repetitive stimulation of SR frequently produced a neuronal burst discharge even though the duration and to some extent the amplitude of orthodromic inhibition was increased. On the basis of these data, it may be suggested that chronic changes in CA1 pyramidal cell membrane properties and transient reductions of inhibitory processes do not underlie the enhanced sensitivity of these neurons to seizure activity associated with kindling.

Animals↗

PubMed1985

Local stimulation induced GABAergic response in rat striatal slice preparations: intracellular recordings on QX-314 injected neurons.

Gamma-aminobutyric acid (GABA)ergic responses evoked by electrical stimulation in the neostriatal slice preparation were studied in neurons injected intracellularly with Na-conductance blocker QX-314. Local stimulation elicited depolarizing postsynaptic potentials (DPSPs) in the QX-314-injected neurons when the membrane potential was more negative than -60 mV. When DPSPs were minimized by depolarizing current injection in the QX-314-injected neuron, hyperpolarization was clearly observed following local stimulation. The maximum duration of the hyperpolarizing response to strong local stimulation was about 130 ms. The hyperpolarizing response was blocked by the addition of bicuculline or picrotoxin to the Ringer solution. Intracellular Cl- injections produced changes in the pattern of the local stimulation-induced responses; the initial depolarizing response was followed by a relatively large amplitude long duration depolarization. The polarity of the long duration depolarizing response could not be reversed by depolarizing currents which were normally sufficient to reverse the polarity of DPSPs in the neurons without Cl- injection. The application of pentobarbital enhanced the amplitude and the duration of the hyperpolarizing responses. The reversal potential of the pentobarbital-enhanced response was estimated to be -60 mV. On the basis of their reversal potential, sensitivity to injected Cl-, sensitivity to GABA blockers picrotoxin and bicuculline, and the effect of pentobarbital, these hyperpolarizing responses are shown to be GABAergic Cl-mediated inhibitory postsynaptic potentials (IPSPs).

Animals↗

PubMed1998

Synaptic activation of plateaus in hindlimb motoneurons of decerebrate cats.

Intracellular recordings were made from hindlimb motoneurons in decerebrate cats to study how synaptic inputs could affect the threshold at which plateau potentials are activated with current injections through the recording microelectrode in the cell body. This study was prompted by recent evidence that the noninactivating inward currents that regeneratively produce the plateau potentials arise (partly) from dendritic conductances, which may be relatively more accessible to synaptic input than to current injected into the soma. Initially, cells were studied by injecting a slow triangular current ramp intracellularly to determine the threshold for activation of the plateau. In cells where the sodium spikes were blocked with intracellular QX314, plateau activation was readily seen as a sudden jump in membrane potential, which was not directly reversed as the current was decreased. With normal spiking, the plateau activation (the noninactivating inward current) was reflected by a steep and sustained jump in firing rate that was not directly reversed as the current was decreased. Importantly, the threshold for plateau activation (at 34 Hz on average) was significantly above the recruitment level (13 Hz on average). When tonic synaptic excitation [excitatory postsynaptic potentials (EPSPs)] was provided either by stretching the triceps surae muscle or by stimulating its nerve at a high frequency, the threshold for plateau activation by intracellular current injection was significantly lowered (by 12 Hz or 5.8 mV on average, without and with QX314, respectively). Conversely, tonic synaptic inhibition [inhibitory postsynaptic potentials (IPSPs)], provided by appropriate nerve stimulation, significantly raised the plateau threshold (by 19 Hz or 7.6 mV on average). These effects were graded with the intensity of tonic EPSPs and IPSPs. Strong enough EPSPs brought the plateau threshold down sufficiently that it was activated by the intracellular current soon after recruitment. A further increase in tonic EPSPs recruited the cell directly, and in this case the plateau was activated at or before recruitment. The finding that synaptic excitation can produce plateau activation below the recruitment level is of importance for the interpretation of its function. With this low-threshold activation, the plateau potentials are likely important in securing an effective recruitment to frequencies that produce significant force generation and would subsequently have no further affect on the frequency modulation, other than to provide a steady depolarizing bias that would help to sustain firing (cf. self-sustained firing). Additional jumps in frequency after recruitment (i.e., bistable firing) would not be expected.

Action Potentials↗

PubMed2005

Inputs to nucleus pontis caudalis from adjacent trigeminal areas.

Recent studies suggest that the nucleus pontis caudalis (nPontc) plays a role in patterning mastication through interactions with the adjacent lateral tegmentum. In this study, we used in vitro intracellular recording and staining to describe the basic membrane properties and morphology of nPontc neurones and to further explore interactions with adjacent structures, using coronal sections of the brainstem of 78 rats, aged 9-28 days. Neurones were large, with dendrites that spread in all directions, and about 64% fired tonically even in the absence of synaptic inputs. Tonic neurones were predominant in the centre of the nucleus. Electrical stimulation of all regions of the nPontc produced mixed excitatory and inhibitory effects on interneurones of lateral tegmental nuclei. Focal inactivation of the dorsal nPontc with injections of tetrodotoxin also had mixed effects on the spontaneous firing of both interneurones and motoneurones but similar injections in the ventral nPontc produced mostly increases of firing. Sixty-five percent of nPontc neurones received synaptic inputs from the lateral tegmental areas and most of these (68%) were excitatory and mediated by glutamatergic receptors. Inhibitory postsynaptic potentials were mediated by GABA(A) or glycinergic receptors. Although most responses occurred at relatively long latencies (> 2 ms), they could follow relatively high-frequency stimulation (> 50 Hz). Excitatory and inhibitory connections between ipsi- and contralateral nPontc neurones were also documented, which could contribute to bilateral coordination of jaw movements. This study provides evidence that the nPontc exerts both tonic and phasic influences on the premotor components of the masticatory central pattern generator.

Action Potentials↗

PubMed1999

Saccular and utricular inputs to sternocleidomastoid motoneurons of decerebrate cats.

Connections from the otolithic organs to sternocleidomastoid (SCM) motoneurons were studied in 20 decerebrate cats. The electrical stimulation was selective for the saccular or the utricular nerves. Postsynaptic potentials were recorded from antidromically identified SCM motoneurons; these muscles participate mainly in neck rotation and flexion. Partial transections of the brainstem at the level of the obex were performed to identify the possible pathway from the otolithic organs to the SCM motoneurons. Saccular or utricular nerve stimulation mainly evoked inhibitory postsynaptic potentials (IPSPs) in the ipsilateral SCM motoneurons. Some of the sacculus-induced IPSPs were preceded by small-amplitude excitatory PSPs (EPSPs). The latencies of the PSPs ranged from 1.8 to 3.1 ms after saccular nerve stimulation and from 1.7 to 2.8 ms after utricular nerve stimulation, indicating that most of the ipsilateral connections were disynaptic. In the contralateral SCM motoneurons, saccular nerve stimulation had no or faint effects, whereas utricular nerve stimulation evoked EPSPs in about two-thirds of neurons, and no visible PSPs in about one-third of neurons. The latencies of the EPSPs ranged from 1.5 to 2.0 ms, indicating the disynaptic connection. Thus, the results suggest a difference between the two otolithic innervating patterns of SCM motoneurons. After transection of the medial vestibulospinal tract (MVST), saccular nerve stimulation did not evoke IPSPs at all in ipsilateral SCM motoneurons, but some (11/40) neurons showed small-amplitude EPSPs. Most (24/33) of the utricular-activated IPSPs disappeared after transection, whereas the other 9 neurons still indicated IPSPs. In the contralateral SCM motoneurons, no utricular-activated EPSPs were recorded after transection. These MVST transection results suggest that most of the otolith-SCM pathways are located in the MVST at the obex level. However, the results also suggest the possibility that other otolith-SCM pathways exist at the obex level.

Afferent Pathways↗

PubMed1987

Electrical membrane properties of rat subthalamic neurons in an in vitro slice preparation.

The electrical membrane properties of subthalamic (STH) neurons and their response characteristics to stimulation of the internal capsule (IC) were studied in an in vitro slice preparation. Most STH neurons recorded exhibited spontaneous repetitive firing. The input resistance of STH neurons was 146 +/- 48 M omega and showed both an anomalous and a delayed rectification when the membrane was hyperpolarized or depolarized by current injections. In neurons with the membrane potential less negative than 65 mV, depolarizing current pulses generated repetitive firing with the maximum frequency of up to 500 Hz. Two types of tetrodotoxin (TTX)-resistant cobalt-sensitive potentials, slow depolarizing potential and slow action potential, were observed in STH neurons. The slow depolarizing potential had a long duration (over 500 ms in some cases) and was able to trigger repetitive firing. The slow action potential had a duration of about 30 ms and triggered a burst of firing. The slow action potential was seen only when the neurons were hyperpolarized to more negative than 65 mV by a current injection. Electrical stimulation of IC evoked monosynaptic inhibitory postsynaptic potentials (IPSPs) in most of the neurons examined. The polarity of IPSPs was reversed in the depolarizing direction by intracellular injection of Cl-. Bath application of bicuculline markedly suppressed IPSPs and unmasked monosynaptic excitatory postsynaptic potentials (EPSPs). The EPSP was able to trigger a slow depolarization with repetitive firing or a slow action potential with burst of firing when the neuron was hyperpolarized by a continuous current injection. The results demonstrated that STH neurons in an in vitro preparation have spontaneous discharges, high input resistance, capability to generate high-frequency firing, and Ca potentials. The pattern of responses of STH neurons to synaptic inputs is dependent on their membrane potentials.

Action Potentials↗

PubMed1988

Responses of rat lateral hypothalamic neurons to periaqueductal gray stimulation and nociceptive stimuli.

The effects of dorsal periaqueductal gray (D-PAG) stimulation and noxious stimuli on neural activity in the lateral hypothalamic area (LHA) were investigated in 56 adult male anesthetized rats. Strong tail pinch was used as noxious stimulation. We examined 234 extracellular and 75 intracellular recordings of LHA responses to electrical stimulation of D-PAG. To determine neurotransmitter candidates, the effects of the opioid agonist, morphine, and its antagonist, naloxone were investigated by systemic administration and microelectrophoresis. Of 234 spontaneously firing LHA neurons, 70 (30%) were inhibited by D-PAG stimulation. Of these 70 neurons, 26/40 tested (65%) were glucose-sensitive, 16/19 (84%) were inhibited by morphine and 12/18 (67%) were inhibited by tail pinch. Glucose-sensitive neurons were selectively inhibited by morphine and tail pinch. Naloxone attenuated inhibitory responses to D-PAG stimulation, tail pinch and electrophoretic morphine. From intracellular recordings these polysynaptic inhibitory responses to D-PAG stimulation were considered to be inhibitory postsynaptic potentials (IPSPs) with 6.1 +/- 3.2 ms (mean +/- S.D.) latency and reversal membrane potential of about -78 mV. Since LHA glucose-sensitive neurons receive, selectively, both inhibitory opioid inputs from the D-PAG and inhibitory inputs through noxious stimulation, we suggest that D-PAG might be an intermediate site for transmission of noxious stimuli to the LHA.

Animals↗

PubMed1996

Excitation of rat sympathetic preganglionic neurones by selective activation of the NK1 receptor.

Whole-cell current clamp recordings were made from 32 identified sympathetic preganglionic neurones (SPN) in neonatal rat thoracolumbar spinal cord slices. Perfusion of substance P (SP; 0.1-10 microM) depolarised 7 out of 15 neurones tested and the selective NK1 receptor agonist GR73632 (0.075-5 microM) depolarised 14 out of 24 neurones. The response to GR73632 could be maintained in the presence of tetrodotoxin (0.25-0.5 microM; n = 3) and was irreversibly reduced or abolished by the selective NK1-receptor antagonist CP-99,994 (1-3 microM; n = 3). In 3 neurones, GR73632 evoked both a depolarising response and inhibitory postsynaptic potentials (IPSPs) and in the one neurone tested, the IPSPs were blocked by strychnine (20 microM), suggesting that NK1 receptors may also be found upon inhibitory glycinergic interneurones. The application of either GR73632 or SP to a subpopulation of previously quiescent SPN evoked rhythmical oscillations in membrane potential (n = 6). These results indicate that the NK1 receptor may play an important role in the regulation of both SPN and of inhibitory interneurones presynaptic to SPN.

Animals↗

PubMed2005

Modulation of available vesicles and release kinetics at the inhibitor of the crayfish neuromuscular junction.

We have investigated the effect of serotonin (5-HT) and okadaic acid (OA) on presynaptic processes at the crayfish inhibitory neuromuscular junction. Two different physiological parameters of transmitter release were examined: release kinetics and the size of the readily releasable pool of vesicles (RRP). Using a paired pulse stimulus and high frequency trains, we established that a single broad action potential, recorded in 20 mM tetraethylammonium and 1 mM 4-amino-pyridine, released the RRP in its entirety. Thus, by measuring the amplitude of inhibitory postsynaptic potential (IPSC) we were able to directly assess the effects of 5-HT and OA on the RRP. Serotonin at 200 nM and OA at 2.5 microM each significantly increased IPSC above control levels and the effects of these two modulators were comparable. Both modulators also induced a leftward shift in the rising phase of IPSC, i.e. an apparent acceleration in release kinetics. The shift caused by OA was significantly more pronounced than that induced by 5-HT. This apparent acceleration in release was not associated with a corresponding change in the presynaptic Ca2+ transient measured at a 2 kHz resolution, suggesting that modulation was not due to an acceleration in Ca2+ channel kinetics. In view of the comparable increase in the size of the RRP by the modulators, the differential modulation of release kinetics suggests that these two parameters may be modulated by separate biochemical processes.

4-Aminopyridine↗

PubMed1987

Models of synchronized hippocampal bursts in the presence of inhibition. II. Ongoing spontaneous population events.

1. We extended our computer model of the CA3 region of the hippocampal slice in order to study spontaneous activity occurring in the presence and absence of synaptic inhibition. This was done by providing a steady inward current to the excitatory neurons, whose value was randomly chosen for each cell. With the parameters used, many of the excitatory cells would, if synaptically isolated, remain quiescent, whereas others would burst periodically with periods as brief as 750 ms. Simulations were run for as long as 10 s of neural activity. 2. In the presence of synaptic inhibition, neural activity became organized into recurring, partially synchronized events: clusters of neurons (6% to 12% of the population) would discharge together, with a period averaging 340 ms, shorter than the burst period of any individual neuron. A consequence of periodic clusters of cellular bursts was the widespread occurrence of periodic synchronized synaptic potentials, as have been observed in hippocampal slices and human temporal neocortical slices. The periods between these synaptic potentials are similar in the model to those observed experimentally. 3. The period could be slowed by either increasing the time constant of the slow inhibitory postsynaptic potential (IPSP), or by making the excitatory synapses more powerful. The period seems to be generated in part as follows. Consider those cells with rapid spontaneous discharge rates. An upper bound for the period corresponds to the interval between 1) such a cell's becoming responsive enough to an excitatory synaptic input to burst, and 2) such a cell's bursting spontaneously (i.e., in response to its own intrinsic inward current). For cells with rapid spontaneous discharge rates, the interval defined in this way is approximately 350 ms. 4. Different cells participated in each cluster. A given cluster was initiated by one cell or by two cells bursting together, and spread via excitatory synapses. Excitatory synaptic paths could be traced from the initiating cell(s), directly or through other participants, to all cells participating in a cluster. Spread of activity was limited by two mechanisms, so that not all cells synaptically excited by a participating cell would themselves participate. First, cells might be refractory from having participated in a recent cluster (since the intercluster period was less than the refractory time from a cellular burst to its responsiveness to a synaptic stimulus). Second, some cells might be synaptically inhibited. Synaptic inhibition in this model did not act rapidly enough to suppress the cluster totally.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1997

Change of transmitter release kinetics during facilitation revealed by prolonged test pulses at the inhibitor of the crayfish opener muscle.

A presynaptic voltage-control method was used to study synaptic facilitation at the inhibitory neuromuscular synapse of the crayfish opener muscle. The expression of the F2 component of facilitation, monitored 150 ms after a conditioning stimulus, was examined by systematically changing the duration of the presynaptic test pulse. (Test pulses in all experiments were depolarized to 0 mV.) Control and facilitated inhibitory postsynaptic potentials (IPSPs) exhibited identical time courses when test pulse duration was brief (approximately 2 ms). When the duration of the test pulse was increased beyond 2 ms, the transmitter release time course shifted to an earlier point in time during facilitation. Meanwhile, the increase in total transmitter release, measured from inhibitory postsynaptic conductance (IPSG) area (total release), became less pronounced with increasing duration of the test pulse. With a 20-ms test pulse, facilitation did not cause any detectable change in total release but the half-maximal point of the facilitated IPSG shifted by 3 ms (release shift). This change in release kinetics was not associated with a decrease in minimal synaptic delay. Furthermore, the relationship between total release and presynaptic pulse duration suggested that the transmitter release activated by a 20-ms pulse can be defined as a distinct component of continuous transmitter release (early component). The facilitation process accelerated the release kinetics of the early component but did not modify its total transmitter content. To test the hypothesis that the release shift is indeed mediated by the same mechanism that increases IPSP amplitude during facilitation, we investigated the correlation between the release shift and IPSP amplitude change. The two parameters were significantly correlated when the magnitude of facilitation was changed 1) during the decay of facilitation and 2) by varying the strength of the conditioning stimulus. The experimental approach reported here provides two new physiological parameters, release shift and total release, for the analysis of synaptic facilitation.

Animals↗

PubMed1989

Evidence for glycine as an inhibitory neurotransmitter of vestibular, reticular, and prepositus hypoglossi neurons that project to the cat abducens nucleus.

The localization and distribution of brain-stem afferent neurons to the cat abducens nucleus has been examined by high-affinity uptake and retrograde transport of 3H-glycine. Injections of 3H-glycine selectively labeled (by autoradiography) only neurons located predominantly in the ipsilateral medial vestibular and contralateral prepositus hypoglossi nuclei, and in the contralateral dorsomedial reticular formation, the latter corresponding to the location of inhibitory burst neurons. The specificity of uptake and retrograde transport of 3H-glycine was indicated by the absence of labeling of the dorsomedial medullary reticular neurons ipsilateral and in close proximity to the injection site, where local uptake by diffusion could have occurred. The selectivity of uptake and transport was demonstrated by the absence of retrograde labeling following injections of 3H-GABA or 3H-leucine into the abducens nucleus. The immunohistochemical localization of glycine and GABA revealed a differential distribution of the 2 inhibitory neurotransmitter candidates in the extraocular motor nuclei. Glycine-immunoreactive staining of synaptic endings in the abducens nucleus was dense with a widespread soma-dendritic distribution but was sparse in the trochlear and oculomotor nuclei. By contrast, GABA-immunoreactive staining within the oculomotor and trochlear nuclei was associated with synaptic endings that were particularly prominent on the somata of motoneurons. GABA-immunoreactive staining in the abducens nucleus, however, was sparse. These differences between glycine- and GABA-immunoreactive staining in the extraocular motor nuclei were correlated with differences in the immunoreactivity of axons in the descending (glycine) and ascending (GABA) limbs of the medial longitudinal fasciculus. Glycine-immunoreactive neurons, furthermore, were observed in the same locations as neurons that were labeled autoradiographically by retrograde transport of 3H-glycine from the abducens nucleus. Electrophysiological recordings from abducens motoneurons and internuclear neurons revealed a marked reduction in the slow positivity of the orthodromic extracellular potential elicited by ipsilateral vestibular nerve stimulation following systemic administration of strychnine, an antagonist of glycine. Intracellular recordings demonstrated that the vestibular-evoked disynaptic inhibitory postsynaptic potentials in abducens neurons were effectively blocked by strychnine but were unaffected by picrotoxin, an antagonist of GABA.(ABSTRACT TRUNCATED AT 400 WORDS)

Abducens Nerve↗

PubMed1998

Tetanic stimulation induces short-term potentiation of inhibitory synaptic activity in the rostral nucleus of the solitary tract.

Whole cell recordings from neurons in the rostral nucleus of the solitary tract (rNST) were made to explore the effect of high-frequency tetanic stimulation on inhibitory postsynaptic potentials (IPSPs). IPSPs were elicited in the rNST by local electrical stimulation after pharmacological blockade of excitatory synaptic transmission. Tetanic stimulation at frequencies of 10-30 Hz resulted in sustained hyperpolarizing IPSPs that had a mean amplitude of -68 mV. The hyperpolarization resulted in a decrease in neuronal input resistance and was blocked by the gamma-aminobutyric acid-A (GABAA) antagonist bicuculline. For most of the neurons (n = 87/102), tetanic stimulation resulted in a maximum hyperpolarization immediately after initiation of the tetanic stimulation, but for some neurons the maximum was achieved after three or more consecutive shock stimuli in the tetanic train of stimuli. When the extracellular Ca2+ concentration was reduced, the maximum IPSP amplitude was reached after several consecutive shock stimuli in the tetanic train for all neurons. Tetanic stimulation at frequencies of 30 Hz and higher resulted in IPSPs that were not sustained but decayed to a more positive level of hyperpolarization. In some neurons the decay was sufficient to become depolarizing and resulted in a biphasic IPSP. It was possible to evoke this biphasic IPSP in all the neurons tested if the cells were hyperpolarized to -75 to -85 mV. The ionic mechanism of the depolarizing IPSPs was examined and was found to be due to an elevation of the extracellular K+ concentration and accumulation of intracellular Cl-. Tetanic stimulation increased the mean 80-ms decay time constant of a single shock-evoked IPSP up to 8 s. The length of the IPSP decay time constant was dependent on the duration and frequency of the tetanic stimulation as well as the extracellular Ca2+ concentration. Afferent sensory input to the rNST consists of trains of relatively high-frequency spike discharges similar to the tetanic stimulation frequencies used to elicit the IPSPs in the brain slices. Thus the short-term changes in inhibitory synaptic activity in the slice preparation probably occur in vivo and may play a key role in taste processing by facilitating synaptic integration.

2-Amino-5-phosphonovalerate↗

PubMed1988

Electrophysiological evidence from glutamate microapplications for local excitatory circuits in the CA1 area of rat hippocampal slices.

1. Evidence for local excitatory synaptic connections in CA1 of the rat hippocampus was obtained by recording excitatory postsynaptic potentials (EPSPs) intracellularly from pyramidal cells during local microapplications of glutamate. 2. Experiments were performed in hippocampal slices cut parallel to (transverse slice) or perpendicular to (longitudinal slice) alvear fibers. In normal solutions, glutamate microdrops (10-20 mM, 10-20 micron diam) applied in CA1 within 400 micron of recorded cells sometimes increased the frequency of inhibitory postsynaptic potentials for 5-10 s in both transverse and longitudinal slices. Increases in EPSP frequency were also occasionally observed, but only in transverse slices. Tetrodotoxin (1 microgram/ml) blocked glutamate-induced increases in PSP frequency, thus indicating that they were not caused by subthreshold effects on presynaptic terminals. Increases in PSP frequency were interpreted to result from glutamate activation of hippocampal neurons with inhibitory and excitatory connections to recorded neurons. 3. In both slice orientations, local excitatory circuits were studied in more isolated conditions by surgically separating CA1 from CA3 (transverse slices) and by blocking GABAergic inhibitory synapses with picrotoxin (5-10 microM). Microdrops were systematically applied at 200 and 400 micron on each side of the recording site. Significant glutamate-induced increases in EPSP frequency were observed in neurons from both slice orientations to microdrops in at least one of the locations. This provided evidence that excitatory synapses are present in both transverse and longitudinal slices. 4. Substantial increases in EPSP frequency only occurred in neurons from longitudinal slices when glutamate was microapplied 200 micron or less from the recording site. In transverse slices, however, large increases in EPSP frequency were observed to glutamate microapplications at 200 or 400 micron. These data suggest that CA1 local excitatory connections project for longer distances in the transverse than in the longitudinal plane of section. 5. Increases in EPSP frequency, averaged across cells, did not differ significantly in the four microapplication sites in either transverse or longitudinal slices. Thus local excitation in CA1 does not appear to be asymmetrically arranged in the way suggested for CA3. 6. The densities of local excitatory circuits in CA1 versus CA3 were studied by quantitatively comparing glutamate-induced increases in EPSP frequency.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

EPSPs in rat neocortical neurons in vitro. II. Involvement of N-methyl-D-aspartate receptors in the generation of EPSPs.

1. Intracellular recordings were obtained from neurons in layer II/III of rat frontal cortex. Single-electrode current- and voltage-clamp techniques were employed to compare the sensitivity of excitatory postsynaptic potentials (EPSPs) and iontophoretically evoked responses to N-methyl-D-aspartate (NMDA) to the selective NMDA antagonist D-2-amino-5-phosphonovaleric acid (D-2-APV). The voltage dependence of the amplitudes of the EPSPs before and after pharmacologic changes in the neuron's current-voltage relationship was also examined. 2. NMDA depolarized the membrane potential, increased the neuron's apparent input resistance (RN), and evoked bursts of action potentials. The NMDA-induced membrane current (INMDA) gradually increased with depolarization from -80 to -40 mV. The relationship between INMDA and membrane potential displayed a region of negative slope conductance in the potential range between -70 and -40 mV which was sufficient to explain the apparent increase in RN and the burst discharges during the NMDA-induced depolarization. 3. Short-latency EPSPs (eEPSPs) were evoked by low-intensity electrical stimulation of cortical layer IV. Changes in the eEPSP waveform following membrane depolarization and hyperpolarization resembled those of NMDA-mediated responses. However, the eEPSP was insensitive to D-2-APV applied at concentrations (up to 20 microM) that blocked NMDA responses. 4. EPSPs with latencies between 10 and 40 ms [late EPSPs (lEPSPs)] were evoked by electrical stimulation using intensities just subthreshold to the activation of IPSPs. The amplitude of the lEPSP increased with hyperpolarization and decreased with depolarization. 5. The lidocaine derivative QX-314, injected intracellularly, suppressed sodium-dependent action potentials and depolarizing inward rectification. Simultaneously, the amplitude of the eEPSP significantly decreased with depolarization. Neither the amplitude of a long-latency EPSP nor the amplitude of inhibitory postsynaptic potentials (IPSPs) was significantly affected by QX-314. 6. Cesium ions (0.5-2.0 mM) added to the bathing solution reduced or blocked hyperpolarizing inward rectification. Under these conditions, the amplitude of the eEPSP increased with hyperpolarization. The amplitude of the lEPSP was unaltered or enhanced. 7. The lEPSP was reversibly blocked by D-2-APV (5-20 microM), although the voltage-dependence of its amplitude did not resemble the action of NMDA on neocortical neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1992

5-Hydroxytryptamine increases excitability of CA1 hippocampal pyramidal cells.

In the presence of spiperone to block the 5-HT1A-mediated inhibition of pyramidal cell activity, 5-hydroxytryptamine (serotonin, 5-HT) produces a rapid transient increase in amplitude of the extracellularly recorded population spike from area CA1 of the hippocampus. Intracellular recording techniques in area CA1 of rat hippocampal slices were used to identify the ionic mechanism and to characterize the 5-HT receptor mediating this excitatory response to 5-HT. Most of the experiments were conducted in the presence of spiperone to block the 5HT1A hyperpolarization. Since spiperone also has high affinity for 5-HT2 receptors, any response mediated by 5-HT2 receptors would also be blocked. Bath perfusion of the slice with 5-HT increased the rectification of pyramidal cells in the subthreshold region, increased the resistance, and increased the amplitude of subthreshold excitatory postsynaptic potentials (EPSPs) to initiate spike firing. The 5-HT2,1C-selective agonist DOI mimicked this effect of 5-HT, and the 5-HT2,1C antagonist ketanserin (1 microM) blocked the effect of DOI. There was no change in the amplitude of the slow afterhyperpolarization (sAHP) or the amplitude of evoked inhibitory postsynaptic potentials (IPSPs). The increase in rectification and EPSP amplitude by 5-HT occurred even in the presence of the 5-HT4-selective antagonist BRL 24924 to prevent the decrease in amplitude of the sAHP by 5-HT. We conclude that 5-HT produces a fast excitatory response by increasing subthreshold conductance in CA1 hippocampal pyramidal cells. The identity of the receptor mediating this response was not conclusively identified, but resembled the 5-HT1C receptor.

Action Potentials↗

PubMed1987

The differential organization of medullary post-inspiratory activities.

Membrane potential trajectories of 68 bulbar respiratory neurones from the peri-solitary and peri-ambigual areas of the brain-stem were recorded in anaesthetized cats to explore the synaptic influences of post-inspiratory neurones upon the medullary inspiratory network. A declining wave of inhibitory postsynaptic potentials resembling the discharge of post-inspiratory neurones was seen in both bulbospinal and non-bulbospinal inspiratory neurones, including alpha- and beta-inspiratory, early-inspiratory, late-inspiratory and ramp-inspiratory neurones. Activation of laryngeal and high-threshold pulmonary receptor afferents excited bulbar post-inspiratory neurones, whilst in the case of inspiratory neurones such stimulation produced enhanced postsynaptic inhibition during the same period of the cycle. Activation of post-inspiratory neurones and enhanced post-inspiratory inhibition of inspiratory bulbospinal neurones was accompanied by suppression of the after-discharge of phrenic motoneurones. These results suggest that a population of post-inspiratory neurones exerts a widespread inhibitory function at the lower brain-stem level. Implications of such an inhibitory function for the organization of the respiratory network are discussed in relation to the generation of the respiratory rhythm.

Animals↗

PubMed1988

Electrophysiological properties of rostral medullary respiratory neurones in the cat: an intracellular study.

1. We recorded the membrane potentials of sixty-three respiratory neurones in the rostral, ventral medulla of decerebrate vagotomized cats. Stable recordings were obtained in thirty-eight expiratory and twenty-five inspiratory neurones. Axonal projections were identified by antidromic invasion after electrical stimulation of the region of the dorsal respiratory group (DRG), spinal cord, and the cervical vagus, superior laryngeal and pharyngeal nerves. 2. Two types of expiratory neurones were encountered: those in which the membrane potential progressively depolarized (augmenting neurons, n = 22) and those in which the membrane potential repolarized (decrementing or post-inspiratory neurones, n = 16) during the interval between phrenic bursts. Both types were hyperpolarized during inspiration by chloride-dependent, inhibitory postsynaptic potentials (IPSPs) which decreased membrane resistance. In augmenting neurones two waves of IPSPs appeared, one early and one late in inspiration. 3. Five out of seventeen augmenting expiratory neurones tested were antidromically activated by contralateral stimulation of the spinal cord (n = 3) or the DRG (n = 2). Spinal axons were not detected in any of the sixteen decrementing expiratory neurones tested. Of thirteen expiratory neurones tested with pharyngeal nerve stimulation, one (an augmenting type) was antidromically activated. Superior laryngeal or vagal axons could not be demonstrated for any expiratory neurones. 4. Two types of inspiratory neurones were also encountered: those displaying progressive depolarization throughout inspiration (n = 5) and those which gradually repolarized after maximal depolarization at the onset of inspiration (n = 10). None of the former had identifiable spinal or medullary axons, but superior laryngeal axons were demonstrated in three and pharyngeal axons were found in three. None of the latter was antidromically activated from any of the sites stimulated. 5. Stimulation of the superior laryngeal or pharyngeal nerves evoked excitatory postsynaptic potentials (EPSPs) in all neurones except in post-inspiratory neurones. In these, stimulation of the superior laryngeal or pharyngeal nerves evoked IPSPs in five of twelve neurones tested. 6. We conclude that a spectrum of respiratory neurones lie within or ventral to the retrofacial nucleus. These neurones may control upper-airway muscles or may play a role in chemoreception.

Action Potentials↗