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PubMed2000

An intracellular study of pudendal afferent inputs onto tail motoneurons in the spinalized cat.

Postsynaptic potentials, elicited by stimulation of the sensory pudendal (SPud) and superficial perineal nerves (SPeri) on both sides, were recorded from motoneurons innervating tail muscles in the non-anaesthetized and spinalized cat. The stimulation of SPud and SPeri on both sides predominantly produced excitatory postsynaptic potentials (EPSPs) in all kinds of tail motoneurons (70-95%). The inhibitory postsynaptic potentials (IPSPs) were often observed in motoneurons innervating ventral tail muscles (30-33%). The means of averaged central latencies of EPSPs and IPSPs ranged from 4.3 to 7.3 ms, and from 4.6 to 8.4 ms, respectively. The findings suggests that polysynaptic neuronal pathways from pudendal nerve to tail motoneurons produce tonic activities of all tail muscles to raise the tail in micturation, defecation and sexual movements which are induced by stimulation of pudendal nerves.

Animals↗

PubMed1988

Intracellular recordings from cells in the myenteric plexus of the rat duodenum.

Intracellular recordings were made in vitro from neurons in the myenteric plexus of freshly dissected preparations of the duodenum of the rat. Nearly one-quarter of neurons (18 out of 77) had long after-hyperpolarizations following their action potentials. Over 60% of neurons (20 out of 32) which were tested exhaustively by focal stimulation at seven points around the recording site were seen to receive fast excitatory synaptic inputs. These were of very short duration (10-30 ms) and were reversibly blocked by the nicotinic antagonist hexamethonium. Only four out of 18 after-hyperpolarization cells (22%) had visible fast synaptic inputs. Seven out of 32 neurons tested received slow excitatory synaptic inputs lasting up to 60 s that were associated with a decrease in conductance and an increase in excitability. No evidence for muscarinic synaptic potentials was seen; only four cells out of 30 with fast excitatory postsynaptic potentials had slow excitatory synaptic potentials visible after a single-shot stimulus; in none of these were the slow excitatory postsynaptic potentials blocked by atropine (up to 1 x 10(-5) M). No inhibitory postsynaptic potentials were recorded in any of the 77 neurons recorded in this study. The effects of five neurotransmitter candidates (acetylcholine, GABA noradrenaline, 5-hydroxytryptamine and substance P) applied by pressure microejection were studied. It is concluded that most of the neurophysiological features reported in the extensively studied guinea-pig small bowel myenteric plexus are present in the rat duodenum. However, the apparent lack of muscarinic synaptic potentials and inhibitory synaptic potentials suggests that there may be some differences between the two species. Our recordings also differ slightly from recently reported studies of rat myenteric neurons grown in cell culture.

Acetylcholine↗

PubMed1959

The electrophysiology and pharmacology of lobster neuromuscular synapses.

Effects of drugs on resting potential, membrane resistance, and excitatory and inhibitory postsynaptic potentials (e.p.s.p.'s and i.p.s.p.'s) of lobster muscle fibers were studied using intracellular microelectrodes Acetylcholine, d-tubocurarine, strychnine, and other drugs of respectively related actions on vertebrate synapses were without effects even in 1 per cent solutions (10(-)w/v). Gamma-aminobutyric acid (GABA) acted powerfully and nearly maximally at 10(-7) to 10(-6)w/v. Membrane resistance fell two- to tenfold, the resting potential usually increasing slightly. This combination of effects, which indicates activation of inhibitory synaptic membrane, was also produced by other short chain omega-amino acids and related compounds that inactivate depolarizing axodendritic synapses of cat. The conductance change, involving increased permeability to Cl(-), by its clamping action on membrane potential shortened as well as decreased individual e.p.s.p.'s. Picrotoxin in low concentration (ca. 10(-7)w/v) and guanidine in higher (ca. 10(-3)w/v) specifically inactivate inhibitory synapses. GABA and picrotoxin are competitive antagonists. The longer chain omega-amino acids which inactivate hyperpolarizing axodendritic synapses of cat are without effect on lobster neuromuscular synapse. However, one member of this group, carnitine (beta-OH-GABA betaine), activated the excitatory synapses, a decreased membrane resistance being associated with depolarzation. The pharmacological properties of lobster neuromuscular synapses and probably also of other crustacean inhibitory synapses appear to stand in a doubly inverted relation to axodendritic synapses of cat.

Acetylcholine↗

PubMed2003

Inhibitory cotransmission or after-hyperpolarizing potentials can regulate firing in recurrent networks with excitatory metabotropic transmission.

Recurrent networks of neurons communicating via excitatory connections are common in the nervous system. In the absence of mechanisms to control firing (collectively termed negative feedback), these networks are likely to be bistable and unable to meaningfully encode input signals. In most recurrent circuits, negative feedback is provided by a specialized subpopulation of interneurons, but such neurons are absent from some systems, which therefore require other forms of negative feedback. One such circuit is found within the enteric nervous system of the intestine, where AH/Dogiel type II neurons are interconnected via excitatory synapses acting through metabotropic receptors to produce slow excitatory postsynaptic potentials (slow EPSPs). Negative feedback in this recurrent network may come from either inhibitory postsynaptic potentials arising from the terminals that produce slow EPSPs or from the after hyperpolarizing potentials (AHPs) characteristic of these neurons. We have examined these possibilities using mathematical analysis, based on the Wilson-Cowan model, and computer simulations. Analysis of steady states showed that, under appropriate conditions, both types of negative feedback can provide robust regulation of firing allowing the networks to encode input signals. Numerical simulations were performed using large, anatomically realistic networks with realistic models for metabotropic transmission and suppression of the AHP. In the presence of constant exogenous input, parameters controlling aspects of synaptic events were varied, confirming the analytical results for static stimuli. The simulated networks also responded to time varying inputs in a manner consistent with known physiology. In addition, simulation revealed that neurons in networks with inhibitory contransmission fired in erratic bursts, a phenomenon observed in neurons in unparalysed tissue. Thus, either inhibitory contransmission or AHPs, or both, can allow recurrent networks of AH/Dogiel type II neurons to encode ongoing inputs in a biologically useful way. These neurons appear to be intrinsic primary afferent neurons (IPANs), which implies that the IPANs in a region act in a coordinated fashion.

Action Potentials↗

PubMed1988

Electrophysiological properties of the isolated vestibulocerebellar complex of the frog in vitro.

Parameters of the electrical activity of the isolated vestibulocerebellar complex of the frog were studied under in vitro conditions. In the region of the vestibular nucleus (nc. VIII), in the presence of stimulation of the stato-acoustic nerve (n. VIII), responses from efferent vestibular neurones and from unidentified (probably vestibulospinal) neurones were recorded. The latent periods of their excitatory postsynaptic potentials (EPSPs, 1.4-2.2 ms) were indicative of mono- and disynaptic connection. Inhibitory postsynaptic potentials (IPSPs) were also observed. Stimulation of the auricular lobe of the cerebellum evoked monosynaptic IPSPs, an EPSP-IPSP complex or pure EPSPs in nc. VIII, the latter probably by way of collaterals to the cerebellum. The inhibitory character of the effect of efferents from the cerebellum to the neurones of nc. VIII was demonstrated in the focal synaptic potential and in spontaneous and evoked unit activity. If n. VIII was stimulated, both focal and unit extra- and intracellular responses characteristic of activation of the Purkinje cells by mossy (MF) or climbing (CF) afferent fibres were recorded in the cerebellar cortex. The electrophysiological picture indicates that both synaptic transmission and the functional manifestations of the individual neurones are preserved in the tested preparation.

Animals↗

PubMed1995

NMDA-dependent GABAA-mediated polysynaptic potentials in the neonatal rat hippocampal CA3 region.

Evoked inhibitory postsynaptic potentials (IPSPs) were studied in CA3 hippocampal neurons from brain slice preparations of rats ranging from 5 to 18 days of age (P5-18) using intracellular recording techniques. With KMeSO4-filled electrodes the evoked inhibitory response consisted of fast and slow IPSPs mediated by GABAA and GABAB receptors respectively. In recordings obtained with electrodes filled with 2-(triethylamino)-N-(2,6-dimethylphenyl) acetamide and KMeSO4, electrical stimulation evoked monophasic IPSPs in mature slices (P10-18) and biphasic IPSPs with an early and a late phase in neonatal slices (P4-7). In neonates both the early and late phases of the IPSP were mediated by GABAA receptors. Pharmacological investigation revealed that the early phase arose from both direct and feedforward activation of GABAergic interneurons involving non-NMDA receptors, while the late phase resulted from polysynaptic activation of GABAergic interneurons mediated by NMDA receptors.

Animals↗

PubMed1991

An intracellular recording study of stimulus-specific response properties in cat area 17.

Stimulus-specific response properties, such as direction or orientation selectivity, were studied intracellularly in cells recorded from area 17 of the cat. In all 5 direction selective complex cells and one orientation selective simple cell successfully studied, visually evoked excitatory postsynaptic potentials (EPSPs) were tuned to the preferred direction or orientation. Visually evoked inhibitory postsynaptic potentials (IPSPs) were also tuned to the preferred direction/orientation of stimulus. IPSPs evoked by the non-preferred stimulus when present were smaller than those evoked by the preferred stimulus. IPSPs were undetected in two of the 5 cells tested. These results suggest that directionally/orientationally tuned EPSPs make a major contribution to stimulus specificity in visual cortical neurons but IPSPs evoked by a stimulus with null-direction/orientation may sharpen the stimulus specificity.

Animals↗

PubMed1981

Adenosine depression of hippocampal neurons in vitro: an intracellular study of dose-dependent actions on synaptic and membrane potentials.

In CA1 pyramidal neurons, 5 micrometer adenosine had no measurable effect on resting membrane potential or resistance, while excitatory and inhibitory postsynaptic potentials generated by orthodromic stimulation of the stratum radiatum were reduced by 20--60%. However, 10--20 micrometers adenosine not only markedly reduced (by 20--80%) the synaptic potentials, but also clearly hyperpolarized most pyramidal neurons. This effect was accompanied by a reduction in input resistance in about one-half of the cells and no measurable change in resistance in the rest. Monobutyryl cyclic AMP in concentrations of 50 micrometer or more also hyperpolarized neurons, usually no change in input resistance.

Adenosine↗

PubMed1974

Effects of lithium ions on electrical activity in sympathetic ganglia of the bullfrog.

1 The mode of action of lithium on electrical activity in the sympathetic ganglia of the bullfrog has been studied by recording extracellular and intracellular potential changes. Changes in nerve conduction and various types of synaptic transmission were studied when sodium ions in the external solution were totally replaced by equimolar concentrations of lithium ions and also when lithium ions were added to the external Ringer solution.2 Nerve conduction and nicotinic transmission in sympathetic ganglia were completely blocked in sodium-free sucrose solution, but were restored when the preparations were transferred to a sodium-free lithium solution.3 In the sodium-free lithium solution, the slow excitatory postsynaptic potential (e.p.s.p.) and muscarinic acetylcholine-depolarization were restored while the slow inhibitory postsynaptic potential (i.p.s.p.) and the muscarinic acetylcholine-hyperpolarization were not restored. Furthermore, the early after-discharges were accelerated and the inhibition of after-discharges was eliminated. These results support the hypothetical concept that the slow i.p.s.p. is generated by an activation of the electrogenic sodium pump.4 In the sodium-free lithium solution, restoration of nerve conduction and synaptic transmission were transient phenomena; both conduction and transmission were gradually blocked when preparations were soaked in the solution for long periods. The blockade appeared to be due to membrane depolarization.5 When lithium ions (20 mM) were added to the Ringer solution, nicotinic transmission was depressed. The slow e.p.s.p. was also depressed, but less so than the slow i.p.s.p. The early after-discharge was, however, accelerated; presumably due to the marked depression of the slow i.p.s.p. in this solution.6 Changes in synaptic transmission in Ringer solution containing lithium ions could be explained by membrane depolarization, a reduction of acetylcholine release and a depression of the electrogenic sodium pump.7 All results obtained in the present experiments could be explained by supposing that lithium ions are able to substitute for sodium ions in passive ionic membrane transport dependent on electrochemical energy but not in active ionic membrane transport dependent on metabolic energy.

Action Potentials↗

PubMed1989

Effects of low concentrations of 4-aminopyridine on CA1 pyramidal cells of the hippocampus.

1. Intracellular and extracellular recording techniques were used to study the effects of bath application of 4-aminopyridine (4-AP) on pyramidal cells of the CA1 subfield of rat hippocampal slices maintained in vitro. The concentration of 4-AP used in most experiments was 50 microM. However, similar results were obtained with a concentration ranging from 5 to 100 microM. 2. Following 4-AP application, cells impaled with K-acetate-filled microelectrodes hyperpolarized by an average of 2.6 mV (from -68.7 to -71.3 mV, P less than or equal to 0.01). This change was accompanied by the appearance of high-frequency spontaneous hyperpolarizations. Conversely, when KCl-filled microelectrodes were used, an average depolarization of 5.8 mV [from -73.1 to -67.3 mV, not significant (NS)] associated with the occurrence of repetitive depolarizing potentials was observed. In both cases, these changes were concomitant with a small decrease in membrane input resistance, which was statistically significant only for cells impaled with K-acetate-filled microelectrodes. When synaptic transmission was blocked by tetrodotoxin (TTX), 4-AP induced in cells studied with K-acetate microelectrodes an average depolarization of 2.4 mV (from -62.8 to -60.4 mV, P less than or equal to 0.01) accompanied by a small increase in input resistance (from 32.0 to 35.8 M omega, P less than or equal to 0.05). High-frequency spontaneous potentials failed to occur under these conditions. During 4-AP application, the threshold and the latency of action potentials elicited by a depolarizing current pulse increased in 36% of the neurons studied (n = 14). 3. The amplitude of the stratum (s.) radiatum-induced excitatory postsynaptic potential (EPSP) was augmented by 4-AP. Both the early and late inhibitory postsynaptic potentials (IPSPs) evoked by orthodromic stimuli were also increased in amplitude and duration. In addition, a late (peak latency, 150-600 ms) and long-lasting (duration, 600-1,500 ms) depolarizing potential appeared between the early and the late IPSPs and progressively increased until it partially masked these hyperpolarizations. This long-lasting depolarization (LLD) could also be induced by antidromic stimulation, although in this case it was preceded by an additional, fast-rising, brief depolarization. 4. A similar brief depolarization preceded the orthodromically induced LLD in 69% of the neurons bathed in the presence of 4-AP. The average value of the peak latency of this potential was 62 +/- 27 (SD) ms for orthodromic and 110 +/- 70 ms for antidromic responses.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗

PubMed1997

Direct and indirect corticospinal control of arm and hand motoneurons in the squirrel monkey (Saimiri sciureus).

Anatomic evidence suggests that direct corticomotoneuronal (CM) projections to hand motoneurons in the New World squirrel monkey (Saimiri sciureus) are weak or absent, but electrophysiological evidence is lacking. The nature of the corticospinal linkage to these motoneurons was therefore investigated first with the use of transcranial magnetic stimulation (TMS) of the motor cortex under ketamine sedation in five monkeys. TMS produced early responses in hand muscle electromyogram, but thresholds were high (compared with macaque monkey) and the onset latency was variable. Second, stimulation of the pyramidal tract (PT) was carried out with the use of chronically implanted electrodes in ketamine-sedated monkeys; this produced more robust responses that were markedly facilitated by repetitive stimulation, with little decrease in latency on the third compared with the first shock. Finally, postsynaptic potentials were recorded intracellularly from 93 arm and hand motoneurons in five monkeys under general chloralose anesthesia. After a single PT stimulus, the most common response was a small, slowly rising excitatory postsynaptic potential (EPSP), either alone (35 of 93 motoneurons) or followed by an inhibitory postsynaptic potential (39 of 93). The segmental delay of the early EPSPs was within the monosynaptic range (mean 0.85 ms); however, the rise time of these EPSPs was slow (mean 1.3 ms) and their amplitude was small (mean 0.74 mV). These values are significantly slower and smaller than EPSPs in a comparable sample of Old World macaque monkey motoneurons. The results show that CM connections do exist in the squirrel monkey but that they are weak and possibly located on the remote dendrites of the motoneurons. The findings are consistent with earlier anatomic studies. Repetitive PT stimulation produced large, late EPSPs in some motoneurons, suggesting that, in this species, there are relatively strong nonmonosynaptic pathways linking the corticospinal tract to hand motoneurons.

Animals↗

PubMed1985

Temperature dependence of intrinsic membrane properties and synaptic potentials in hippocampal CA1 neurons in vitro.

The temperature dependence of intrinsic membrane conductances and synaptic potentials in guinea pig hippocampal CA1 pyramidal neurons were examined in vitro as they were cooled from 37 degrees C to between 33 and 27 degrees C. Cooling reversibly increased resting input resistance in a voltage-independent manner (Q10 = 0.58 to 0.75). The amplitude and duration of orthodromically evoked action potentials were increased by cooling (Q10 = 0.87 and 0.52 to 0.53, respectively), whereas the maximum rates of rise and fall were reduced (Q10 = 1.27 to 1.49 and 2.19 to 2.44, respectively). The amplitude and duration of the afterhyperpolarization which follows a directly evoked train of action potentials were substantially increased at low temperatures. It is possible to attribute this increase to an augmentation of Ca2+ influx during the train and also to a slowing of Ca2+ removal from the cytoplasm. Spike frequency adaptation during prolonged depolarizing pulses was enhanced at low temperatures. In addition, there was a decrement in spike amplitude during the train of action potentials. These observations all suggest an increase in Ca2+-activated K+ conductance at low temperature. A late, slow, hyperpolarizing synaptic potential in response to orthodromic stimulation became apparent at low temperature. This potential had an apparent reversal potential more negative than the early inhibitory postsynaptic potential, suggesting that it was mediated by a K+ conductance, possibly activated by Ca2+ influx. We conclude that reductions in temperature of as little as 5 to 10 degrees C from normal can significantly alter the intrinsic and synaptic physiology of hippocampal neurons and should, therefore, be considered an important variable in in vitro brain slice experiments.

Action Potentials↗

PubMed1989

Intracellular analysis of trigeminal motoneuron rhythmical activity during stimulation of pontomedullary reticular formation in anesthetized guinea pig.

1. The effects of repetitive stimulation of the nucleus pontis caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation on jaw opener and closer motoneurons were examined. The PnC-Gi was stimulated at 75 Hz at current intensities less than 90 microA. 2. Rhythmically occurring, long-duration, depolarizing membrane potentials in jaw opener motoneurons [excitatory masticatory drive potential (E-MDP)] and long-duration hyperpolarizing membrane potentials [inhibitory masticatory drive potentials (I-MDP)] in jaw closer motoneurons were evoked by 40-Hz repetitive masticatory cortex stimulation. These potentials were completely suppressed by PnC-Gi stimulation. PnC-Gi stimulation also suppressed the short-duration, stimulus-locked depolarizations [excitatory postsynaptic potentials (EPSPs)] in jaw opener motoneurons and short-duration, stimulus-locked hyperpolarizations [inhibitory postsynaptic potentials (IPSPs)] in jaw closer motoneurons, evoked by the same repetitive cortical stimulation. 3. Short pulse train (3 pulses; 500 Hz) stimulation of the masticatory area of the cortex in the absence of rhythmical jaw movements activated the short-latency paucisynaptic corticotrigeminal pathways and evoked short-duration EPSPs and IPSPs in jaw opener and closer motoneurons, respectively. The same PnC-Gi stimulation that completely suppressed rhythmical MDPs, and stimulus-locked PSPs evoked by repetitive stimulation to the masticatory area of the cortex, produced an average reduction in PSP amplitude of 22 and 17% in jaw closer and opener motoneurons, respectively. 4. PnC-Gi stimulation produced minimal effects on the amplitude of the antidromic digastric field potential or on the intracellularly recorded antidromic digastric action potential. Moreover, PnC-Gi stimulation had little effect on jaw opener or jaw closer motoneuron membrane resting potentials in the absence of rhythmical jaw movements (RJMs). PnC-Gi stimulation produced variable effects on conductance pulses elicited in jaw opener and closer motoneurons in the absence of RJMs. 5. These results indicate that the powerful suppression of cortically evoked MDPs in opener and closer motoneurons during PnC-Gi stimulation is most likely not a result of postsynaptic inhibition of trigeminal motoneurons. It is proposed that this suppression is a result of suppression of activity in neurons responsible for masticatory rhythm generation.

Action Potentials↗

PubMed2005

Correlations between granule cell physiology and bioenergetics in human temporal lobe epilepsy.

Human temporal lobe epilepsy (TLE) is associated with bioenergetic abnormalities including decreased phosphocreatine (PCr) normalized to ATP. The physiological consequences of these metabolic alterations have not been established. We hypothesized that impaired bioenergetics would correlate with alterations in physiological functions under conditions that strongly activate neural metabolism. We correlated several physiological variables obtained from epileptic human dentate granule cells studied in slices with hippocampal PCr/ATP measured using in vivo magnetic resonance spectroscopy. The physiological variables included: the ability to fire multiple action potentials in response to single stimuli, the inhibitory postsynaptic potential (IPSP) conductance and the responses to a 10 Hz, 10 s stimulus train. We noted a significant negative correlation between the ability to fire multiple spikes in response to single synaptic stimulation and PCr/ATP (P < 0.03) and a positive correlation between the IPSP conductance and PCr/ATP (P < 0.05). Finally, there was a strong correlation between PCr/ATP and the recovery of the membrane potential following a stimulus train (P < 0.01), with low PCr/ATP being associated with prolonged recovery times. These data suggest that the bioenergetic impairment seen in this tissue is associated with specific changes in excitatory and inhibitory neuronal responses to synchronized synaptic inputs.

Adenosine Triphosphate↗

PubMed2000

Aberrant neuronal physiology in the basal nucleus of the amygdala in a model of chronic limbic epilepsy.

Limbic epilepsy is a chronic condition associated with a broad zone of seizure onset and pathology. Studies have focused mainly on the hippocampus, but there are indications that changes occur in other regions of the limbic system. This study used in vitro intracellular recording and histology to examine alterations to the physiology and anatomy of the basal nucleus of the amygdala in a rat model of chronic limbic epilepsy characterized by spontaneously recurring seizures. Epileptic pyramidal neuron responses evoked by stria terminalis stimulation revealed hyperexcitability characterized by multiple action potential bursts and no evident inhibitory potentials. In contrast, no hyperexcitability was observed in amygdalar neurons from kindled (included as a control for seizure activity) or control rats. Blockade of ionotropic glutamate receptors unmasked inhibitory postsynaptic potentials in epileptic pyramidal neurons. Control, kindled and epileptic inhibitory potentials were predominantly biphasic, with fast and slow components, but a few cells exhibited only the fast component (2/12 in controls, 0/3 in kindled, 3/10 in epileptic). Epileptic fast inhibitory potentials had a more rapid onset and shorter duration than control and kindled. Approximately 40% of control neurons exhibited spontaneous inhibitory potentials; no spontaneous inhibitory potentials were observed in neurons from kindled or epileptic rats. A preliminary histological examination revealed no gross alterations in the basal amygdala from epileptic animals. These results extend previous findings from this laboratory that hyperexcitability is found in multiple epileptic limbic regions and may be secondary to multiple alterations in excitatory and inhibitory efficacy. Because there were no differences between control and kindled animals, the changes observed in the epileptic animals are unlikely to be secondary to recurrent seizures.

Action Potentials↗

PubMed1991

Synaptic responses of guinea pig cingulate cortical neurons in vitro.

1. Intracellular recordings were made from layer V/VI neurons of the guinea pig anterior cingulate cortex to investigate postsynaptic potentials (PSPs) evoked by electrical stimulation of the subcortical white matter (forceps minor). 2. Four distinct types of PSPs were recorded (at the resting potential) under normal physiological conditions; 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)-sensitive excitatory postsynaptic potentials (EPSPs) were followed by bicuculline- or picrotoxin-sensitive depolarizing or hyperpolarizing inhibitory postsynaptic potentials (IPSPs), which were further followed by phaclofen-sensitive, long-lasting hyperpolarizing postsynaptic potentials (LPSPs). The average times-to-peak for the EPSP, depolarizing and hyperpolarizing IPSPs, and LPSP were 10, 22, 28, and 146 ms, respectively. 3. In the presence of CNQX and bicuculline, high-intensity electrical stimulation elicited a longer lasting EPSP with a time-to-peak of 21 ms. The amplitude and duration of the EPSP decreased with membrane hyperpolarization and increased with membrane depolarization. The EPSP was reversibly abolished by D,L-2-amino-5-phosphonovaleric acid (D,L-APV). 4. The bicuculline- or picrotoxin-sensitive depolarizing and hyperpolarizing IPSPs and the phaclofen-sensitive LPSP were markedly suppressed by CNQX, suggesting that glutamate (Glu) and/or aspartate nerve terminals project to GABAergic interneurons, and that the GABAergic interneurons are activated mainly by non-N-methyl-D-aspartate (non-NMDA) receptors. 5. In the presence of picrotoxin, the average reversal potential for the compound EPSP was 0 mV, which was similar to that (-6 mV) for the Glu-induced depolarization. In a solution containing D,L-APV at low concentrations, the average reversal potentials for the depolarizing and hyperpolarizing IPSPs and for the early and late components of the gamma-aminobutyric acid (GABA)-induced responses were -62, -72, -70, and -61 mV, respectively. Thus the value for the depolarizing IPSP was similar to that for the late response to GABA, whereas the value for the hyperpolarizing IPSP was almost the same as that for the early response to GABA. The average reversal potential of -90 mV for the LPSP was similar to -93 mV for the baclofen-induced hyperpolarization and to -94 mV for the spike afterhyperpolarization. 6. Application of phaclofen decreased the interspike interval of the spontaneous firing and reversed the increase in the interspike interval after subcortical stimulation. This result indicates that, even in a slice preparation, the anterior cingulate neurons are under tonic inhibitory control exerted by spontaneously active GABAergic interneurons.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1996

Intracellular characterization of neurons in the locust brain signaling impending collision.

1. In response to a rapidly approaching object, intracellular recordings show that excitation in the locust lobula giant movement detecting (LGMD) neuron builds up exponentially, particularly during the final stages of object approach. After the cessation of object motion, inhibitory potentials in the LGMD then help to terminate this excitation. Excitation in the LGMD follows object recession with a short, constant latency but is cut back rapidly by hyperpolarizing potentials. The timing of these hyperpolarizing potentials in the LGMD is variable, and their latency following object recession is shortest with the highest velocities of motion simulated. The hyperpolarizing potentials last from 50-300 ms and are often followed by re-excitation. The observed hyperpolarizations of the LGMD can occur without any preceding excitation and are accompanied by a measurable conductance increase. The hyperpolarizations are likely to be inhibitory postsynaptic potentials (PSPs). The behavior of the intracellularly recorded inhibitory PSPs (IPSPs) closely parallels that of the feed forward inhibitory loop in the neural network described by Rind and Bramwell. 2. The preference of the LGMD for approaching versus receding objects remains over a wide range of starting and finishing distances. The response to object approach, measured both as membrane potential and spike rate, remains single peaked with starting distances of between 200 and 2,100 mm, and approach speeds of 0.5-2 m/s. These results confirm the behavior predicted by the neural network described by Rind and Bramwell but contradicts the findings of Rind and Simmons, forcing a re-evaluation of the suitability of some of the mechanical visual stimuli used in that study. 3. For depolarization of the LGMD neuron to be maintained or increased throughout the motion of image edges, the edges must move with increasing velocity over the eye. Membrane potential declines before the end of edge motion with constant velocities of edge motion. 4. A second identified neuron, the LGMD2 also is shown to respond directionally to approaching objects. In both the LGMD and LGMD2 neurons, postsynaptic inhibition shapes the directional response to object motion.

Animals↗

PubMed2003

Long-term depression of synaptic inhibition is expressed postsynaptically in the developing auditory system.

Inhibitory transmission is critically involved in the functional maturation of neural circuits within the brain. However, the mechanisms involved in its plasticity and development remain poorly understood. At an inhibitory synapse of the developing auditory brain stem, we used whole cell recordings to determine the site of induction and expression of long-term depression (LTD), a robust activity-dependent phenomenon that decreases inhibitory synaptic gain and is postulated to underlie synapse elimination. Recordings were obtained from lateral superior olivary (LSO) neurons, and hyperpolarizing inhibitory potentials were evoked by stimulation of the medial nucleus of the trapezoid body (MNTB). Both postsynaptic glycine and GABAA receptors could independently display LTD when isolated pharmacologically. Focal application of GABA, but not glycine, on the postsynaptic LSO neuron was sufficient to induce depression of the amino acid-evoked response, or MNTB-evoked inhibitory postsynaptic potentials. This GABA-mediated depression, in the absence of MNTB stimulation, was blocked by a GABAB receptor antagonist. To assess whether a change in neurotransmitter release is associated with the LTD, the polyvalent cation, ruthenium red, was used to increase the frequency of miniature inhibitory synaptic events. Consistent with a postsynaptic locus of expression, we found that the mean amplitude of miniature events decreased after LTD with no change in their frequency of occurrence. Furthermore, there was no change in the paired-pulse ratio or release kinetics of evoked inhibitory responses. Together, these results provide direct evidence that activity-dependent LTD of inhibition has a postsynaptic locus of induction and alteration, and that GABA but not glycine plays a pivotal role.

Animals↗