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PubMed2005

Modulation of synaptic transmission in neocortex by network activities.

Neocortical neurons integrate inputs from thousands of presynaptic neurons that fire in vivo with frequencies that can reach 20 Hz. An important issue in understanding cortical integration is to determine the actual impact of presynaptic firing on postsynaptic neuron in the context of an active network. We used dual intracellular recordings from synaptically connected neurons or microstimulation to study the properties of spontaneous and evoked single-axon excitatory postsynaptic potentials (EPSPs) in vivo, in barbiturate or ketamine-xylazine anaesthetized cats. We found that active states of the cortical network were associated with higher variability and decrease in amplitude and duration of the EPSPs owing to a shunting effect. Moreover, the number of apparent failures markedly increased during active states as compared with silent states. Single-axon EPSPs in vivo showed mainly paired-pulse facilitation, and the paired-pulse ratio increased during active states as compare to silent states, suggesting a decrease in release probability during active states. Raising extracellular Ca(2+) concentration to 2.5-3.0 mm by reverse microdialysis reduced the number of apparent failures and significantly increased the mean amplitude of individual synaptic potentials. Quantitative analysis of spontaneous synaptic activity suggested that the proportion of presynaptic activity that impact at the soma of a cortical neuron in vivo was low because of a high failure rate, a shunting effect and probably dendritic filtering. We conclude that during active states of cortical network, the efficacy of synaptic transmission in individual synapses is low, thus safe transmission of information requires synchronized activity of a large population of presynaptic neurons.

Action Potentials↗
PubMed1993

Nucleus basalis stimulation facilitates thalamocortical synaptic transmission in the rat auditory cortex.

Nucleus basalis (NB) neurons are a primary source of neocortical acetylcholine (ACh) and likely contribute to mechanisms of neocortical activation. However, the functions of neocortical activation and its cholinergic component remain unclear. To identify functional consequences of NB activity, we have studied the effects of NB stimulation on thalamocortical transmission. Here we report that tetanic NB stimulation facilitated field potentials, single neuron discharges, and monosynaptic excitatory postsynaptic potentials (EPSPs) elicited in middle to deep cortical layers of the rat auditory cortex following stimulation of the auditory thalamus (medial geniculate, MG). NB stimulation produced a twofold increase in the slope and amplitude of the evoked short-latency (onset 3.0 +/- 0.13 ms, peak 6.3 +/- 0.21 ms), negative-polarity cortical field potential and increased the probability and synchrony of MG-evoked unit discharge, without altering the preceding fiber volley. Intracortical application of atropine blocked the NB-mediated facilitation of field potentials, indicating action of ACh at cortical muscarinic receptors. Intracellular recordings revealed that the short-latency cortical field potential coincided with a short-latency EPSP (onset 3.3 +/- 0.20 ms, peak 5.6 +/- 0.47 ms). NB stimulation decreased the onset and peak latencies of the EPSP by about 20% and increased its amplitude by 26%. NB stimulation also produced slow membrane depolarization and sometimes reduced a long-lasting IPSP that followed the EPSP. The combined effects of NB stimulation served to increase cortical excitability and facilitate the ability of the EPSP to elicit action potentials. Taken together, these data indicate that NB cholinergic neurons can modify neocortical functions by facilitating thalamocortical synaptic transmission.

Animals↗
PubMed1993

Parallel processing of proprioceptive information in the terminal abdominal ganglion of the crayfish.

The processing of proprioceptive information from the exopodite-endopodite chordotonal organ in the tailfan of the crayfish Procambarus clarkii (Girard) is described. The chordotonal organ monitors relative movements of the exopodite about the endopodite. Displacement of the chordotonal strand elicits a burst of sensory spikes in root 3 of the terminal ganglion which are followed at a short and constant latency by excitatory postsynaptic potentials in interneurones. The afferents make excitatory monosynaptic connections with spiking and nonspiking local interneurones and intersegmental interneurones. No direct connections with motor neurones were found. Individual afferents make divergent patterns of connection onto different classes of interneurone. In turn, interneurones receive convergent inputs from some, but not all, chordotonal afferents. Ascending and spiking local interneurones receive inputs from afferents with velocity thresholds from 2-400 degrees/s, while nonspiking interneurones receive inputs only from afferents with high velocity thresholds (200-400 degrees/s). The reflex effects of chordotonal organ stimulation upon a number of uropod motor neurones are weak. Repetitive stimulation of the chordotonal organ at 850 degrees/s produces a small reduction in the firing frequency of the reductor motor neurone. Injecting depolarizing current into ascending or non-spiking local interneurones that receive direct chordotonal input produces a similar inhibition.

Animals↗
PubMed1993

Changes in evoked potentials and amino acid content during fluorocitrate action studied in rat hippocampal cortex.

Fluorocitrate inhibits the glial tricarboxylic acid cycle and thereby the synthesis of glutamine, which is the main precursor for transmitter glutamate. We investigated the possibility that there is a functional correlate to fluorocitrate action by recording evoked field potentials in rat hippocampal slices. The excitatory postsynaptic potential (field-EPSP) was markedly depressed after 7-8 h of fluorocitrate action. The population spike was also reduced, but a major part of the reduction may be the result of weaker synaptic activation rather than reduced excitability of the postsynaptic cells. The activity of thin unmyelinated fibres was only slightly affected. Preceding the changes in the field-EPSP there was a decrease in the glutamine content in the fluorocitrate treated slices relative to controls. Only a small decrease in tissue glutamate was seen concomitantly with the synaptic failure, probably because the transmitter pool of glutamate in those fibres stimulated makes little contribution to the total tissue glutamate.

Adenosine Triphosphate↗
PubMed1993

Adenosine, L-AP4, and baclofen modulation of paired-pulse potentiation in the dentate gyrus: interstimulus interval-dependent pharmacology.

Paired-pulse potentiation of the glutamate-mediated excitatory postsynaptic potential (EPSP) recorded in the dentate gyrus molecular layer is thought to be mediated presynaptically. It is known that the activation of adenosine (A1) and GABAB receptors results in the reduction of glutamate release in the dentate molecular layer via presynaptic mechanisms. To examine possible modulatory roles of these receptors on paired-pulse potentiation, we examined the effects of adenosine and baclofen (a GABAB agonist) on paired-pulse potentiation using extracellular recording from the lateral perforant path in rat hippocampal slices maintained in vitro. We compared these effects with those of L-alpha-amino-4-phosphonobutyric acid (L-AP4) over a wide range of interstimulus intervals (ISIs). L-AP4 enhanced paired-pulse potentiation over the full range of ISIs tested (40-800 ms), whereas adenosine enhanced paired-pulse potentiation only at ISIs of 40-100 ms. In contrast, baclofen reduced paired-pulse potentiation only at ISIs of 400-800 ms. Furthermore, baclofen increased the amplitude of lateral perforant path field potentials, previously reported to be baclofen-insensitive. These results suggest that paired-pulse potentiation can be modulated through the activation of adenosine and baclofen receptors, indicate that this modulation is dependent on ISI, and show that there are at least two pharmacologically separable components of paired-pulse potentiation in the dentate gyrus.

Adenosine↗
PubMed1981

Dendritic spikes induced in fast pyramidal tract neurons by thalamic stimulation.

In deeply anesthetized cats the synaptic events induced in fast pyramidal tract cells (Pt cells) by ventrolateral (VL) stimulation were analyzed with intracellular recordings. In 40% of the fastest conducting Pt neurons it was found that VL stimulation induced fast depolarizing potentials (FPPs) with or without underlying excitatory postsynaptic potentials (EPSPs). These FPPs were all or non fast rising events lasting about 2 ms. They could be induced by brachium conjunctivum stimulation or they could also occur spontaneously. Those occurring spontaneously had amplitude and time course similar to those evoked by VL stimulation suggesting that they were of thalamic origin. On the basis of their amplitude and lack of collision with antidromic action potentials FPPs were neither axonal nor IS events. Passage of hyperpolarizing currents could block them in an all or none manner. It is concluded that FPPs represent electronically attenuated dendritic spikes generated in small side branches (oblique ascending dendrites) or fast Pt neurons where VL terminals most probably establish their synaptic contacts.

Animals↗
PubMedDate not supplied

Spontaneous potentiation of focal potentials of the CA1 field in long-surviving hippocampal slices of the rat in the absence of electrical stimulation.

The changes in the efficiency of the synaptic transmission in the Schaffer collaterals-field CA1 neurons pathways following prolonged deprivation of afferentation, the cessation (up to four hours) of stimulation of the tested input with brief series of tests every hour (the control afferent inputs, were stimulated throughout the entire experiment at a frequency of 0.05/sec), were investigated in surviving slices of the hippocampus of rats. The evoked focal potentials, population spikes (PS) and population excitatory postsynaptic potentials (pEPSP) were recorded. The prolonged cessation of stimulation led to a significant (p < 0.001) increase in the amplitude of the PS (up to 208% in relation to the baseline level). This phenomenon of potentiation was specific in relation to input and exhibited the properties of "E-S potentiation". A hypothesis is advanced regarding the association of mechanisms responsible for the development of "deprivational" potentiation and of the late phase of long-term posttetanic potentiation.

Animals↗
PubMed1983

Effects of lithium on electrical activity and potassium ion distribution in the vertebrate central nervous system.

Three different regions of the vertebrate central nervous system maintained in vitro (frog spinal cord, guinea pig olfactory cortex and hippocampus) have been used to investigate how Li+ influences membrane potential, membrane resistance, action potentials, synaptic potentials and the transmembrane K+-distribution of neurons and glial cells. In view of the therapeutic action of Li+ in manic-depressive disease, a special effort was made to determine the threshold concentration for the actions of Li+ on the parameters described above. It was observed that Li+ induced a membrane depolarization of both neurons and glial cells, a decrease of action potential amplitudes, a facilitation of monosynaptic excitatory postsynaptic potentials and a depression of polysynaptic reflexes. The membrane resistance of neurons was not altered. Li+ also induced an elevation of the free extracellular potassium concentration and a decrease of the free intracellular potassium concentration. Furthermore, in the presence of Li+ a slowing of the recovery of the membrane potential of neurons and glial cells, and of the extracellular potassium concentration after repetitive synaptic stimulation was observed. The threshold concentrations for the effects of Li+ were below 5 mmol/l in the frog spinal cord and below 2 mmol/l in the guinea pig olfactory cortex and hippocampus. The basic mechanism underlying the action of Li+ may be an interaction with the transport-function of the Na+/K+ pump.

Animals↗
PubMed1985

The action of norepinephrine in the dentate gyrus: beta-mediated facilitation of evoked potentials in vitro.

The effects of superfusion of norepinephrine (NE) on perforant path (PP) evoked potentials in the dentate gyrus were evaluated in the rat hippocampal slice preparation. Superfusion of NE (10 microM) produced a facilitation of the PP evoked responses. Facilitation of the synaptically-evoked responses was expressed in the field potential as an increase in extracellular excitatory postsynaptic potential (EPSP) (117% of control), a decrease in population spike onset latency (94% of control) and an increase in population spike amplitude (131% of control). In 24% of the slices the facilitation of the population spike amplitude lasted longer than 30 min. Isoproterenol, a beta-agonist, mimicked NE effects while timolol, a beta-antagonist, blocked them. Facilitation of the population spike amplitude by NE could not be accounted for solely by the increase in EPSP slope also produced by NE. Superfusion of NE did not produce facilitation of the antidromically evoked field potentials, but in 4 of 8 slices produced a small decrease. NE effects were activity-independent, since the subsequently evoked PP responses were facilitated even when the PP was not concurrently stimulated during superfusion with NE.

Animals↗
PubMed1987

Long-lasting potentiation of synaptic potentials in the motor cortex produced by stimulation of the sensory cortex in the cat: a basis of motor learning.

A long-lasting increase in the efficiency of synaptic transmission in the central nervous system has been thought to be one of the bases of learning and memory. To explore the possibility that the motor cortex (area 4 gamma) itself is involved in motor learning, the existence of long-term potentiation (LTP) was examined by recording excitatory postsynaptic potentials (EPSPs) from motor cortical neurons. Short tetanic intracortical microstimulation (ICMS) of the somatic sensory cortex produced a marked potentiation of the EPSPs in a small group of motor cortical neurons. The results raised the possibility that the input from the sensory cortex participates in motor learning and retention of the learned motor skills.

Animals↗
PubMed1992

Studies on long-term potentiation of the population spike component of hippocampal field potential by the tetanic stimulation of the perforant path rats: effects of a dopamine agonist, SKF-38393.

Long-term potentiation of the field potentials recorded in the dentate gyrus of the hippocampus was observed in freely-moving rats by delivering a brief tetanic stimulation to the perforant path, and the effects of the D1 agonist, SKF-38393, on it was investigated. The field potential was divided into two components; excitatory postsynaptic potential (EPSP) and population spike. In Expt. I, synaptic stimulus-response (S-R) relationship, spike S-R relationship, and EPSP-spike (E-S) relationship were plotted. The estimated slope of the regression line in the spike S-R relationship was enhanced after delivery of the tetanic stimulation (10 pulse at 400 Hz), where that in synaptic S-R relationship was not enhanced. The estimated slope of the regression line in the E-S relationship was also enhanced by the tetanic stimulation. In Expt. II, time-dependent change of the field potential after tetanic stimulation was investigated. The population spike was enhanced significantly for about 2 h following tetanic stimulation, while pEPSP did not change significantly. These changes following tetanic stimulation in Expt. I and II were significantly inhibited by previous administration of SKF-38393 (10 mg/kg, i.p.), and the effect of this drug was dose-dependently antagonized by the D1 antagonist, SCH-23390 (0.1, 0.2 and 0.5 mg/kg, i.p.). These results suggest that a brief tetanic stimulation of the perforant path induces long-term potentiation of the population spike without potentiating the synaptic input in the perforant path-dentate synapses, and that potentiation of the population spike is inhibited by the dopaminergic D1 mechanism.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

AF102B, a muscarinic M1 receptor agonist, mimics some effects of acetylcholine on neurons of rat hippocampus slices.

The putative muscarinic M1 receptor agonist, AF102B, was applied to rat hippocampal slices and the responses of intracellularly recorded pyramidal cells were examined. AF102B mimicked some effects of acetylcholine on these cells as follows: at low concentration, AF102B attenuated a slow after-hyperpolarization in response to a long depolarizing current pulse. This effect was blocked by the M1 antagonist, pirenzepine. At higher concentrations, AF102B also depolarized the cells and caused an increase in their input resistance. AF102B did not affect local excitatory postsynaptic potentials or reactivity to topically applied excitatory amino acid substances. These experiments indicate that AF102B acts as an agonist at some muscarinic M1 receptor subtypes in mammalian brain.

Acetylcholine↗
PubMed1992

SDZ ENS 163, a selective muscarinic M1 receptor agonist, facilitates the induction of long-term potentiation in rat hippocampal slices.

The effect of SDZ ENS 163; (+)-(3S,cis)-3-ethyldihydro-4-[(1-methyl-1H-imidazol-5-yl)methyl-2 (3H)- thiphenonedihydrogenphosphate], a selective muscarinic M1 agonist, on long-term potentiation (LTP) was studied in a rat hippocampal slice preparation. LTP was induced by theta-burst stimulation (TBS) delivered to the Schaffer/commissural fibers. In untreated slices delivery of 8 or 10 trains at 100 Hz induced a 27 +/- 8.3 and 54 +/- 7.2% potentiation of the amplitude of the excitatory postsynaptic potential (epsp), respectively (calculated as percentage of the pre-LTP amplitude). In slices pretreated with SDZ ENS 163 (2 x 10(-6) M, -30 min) delivery of 8 or 10 trains at 100 Hz induced a 62 +/- 8.4 and 54 +/- 7.1% potentiation of the epsp amplitude, respectively. In addition, treatment with SDZ ENS 163 (2 x 10(-6) M) increased the N-methyl-D-aspartate receptor-induced component of the epsp response to TBS from 21 +/- 3 (control) to 33 +/- 2%. Pretreatment with the muscarinic antagonist, scopolamine (6 x 10(-8) M), or with the M1 selective muscarinic receptor antagonist, pirenzepine (6 x 10(-8) M), did not affect LTP in untreated slices but inhibited the enhancement of LTP by SDZ ENS 163 (2 x 10(-6) M) completely. AF-DX 116 (10(-6) M, -60 min), a selective muscarinic M2 receptor antagonist did not affect LTP in control slices nor in slices treated with SDZ ENS 163 (2 x 10(-6) M). These data suggest that activation of muscarinic M1 receptors by SDZ ENS 163 facilitates the induction of LTP.

Animals↗
PubMed1992

Compound 48/80 blocks transmission and increases the excitability of ganglion neurons.

Compound 48/80 (5.0-50 micrograms/ml) significantly and reversibly decreased (1) the amplitude, but not the shape of the compound action potential, (2) the amplitude and duration of the acetylcholine potential and (3) the residual fast excitatory postsynaptic potential recorded from neurons of the 9th and 10th paravertebral ganglia of the bullfrog Rana catesbeiana. The excitability of B-type ganglion neurons in the presence of nicotinic and muscarinic receptor antagonists was increased by compound 48/80 without altering the input resistance or membrane potential. In addition, compound 48/80 (10-50 micrograms/ml) significantly decreased the duration of the spike afterhyperpolarization (AHP). The amplitude but not the decay rate of the current underlying the slow component of the spike AHP was decreased by compound 48/80. Compound 48/80 did not, however, alter either the amplitude or the duration of calcium-dependent spikes. Intracellular recordings from dissociated sympathetic neurons also demonstrated a compound 48/80-induced increase in neuronal excitability. These results suggest that compound 48/80 interacts with the nicotinic receptor/channel complex to decrease ganglionic transmission, and also has a direct action to increase neuronal excitability by blocking potassium channels mediating the duration of the spike AHP.

Acetylcholine↗
PubMed1989

Comparative aspects of hippocampal and neocortical long-term potentiation.

Long-term potentiation (LTP) is a candidate for the synaptic alternations underlying memory storage in the mammalian CNS. In this chapter LTP in hippocampus and in visual neocortex are compared. Comparisons of the optimal tetanus parameters revealed that 2-3 trains of high-frequency stimulation (100-400 Hz) delivered within a brief period of time (minutes) results in maximal potentiation in hippocampal synapses. In contrast, the parameters most effective in neocortex were either low-frequency (2 Hz for 60 min) or high-frequency bursts (100 Hz, 100 ms train at 1/5 s for 10 min), both of which deliver at least an order of magnitude more afferent activation than that required for hippocampus. Hippocampal population spike potentiation averages 250% and the population excitatory postsynaptic potential (EPSP) potentiation averages 50%. Neocortical LTP also averages about 50%. The expression of LTP requires about 5 min in CA1 hippocampus, whereas about 30 min are required for expression of neocortical potentiation. Both hippocampus and visual neocortex display an enhanced potentiation early in development, with a later stabilization at lower adult levels. Centering at postnatal day 15, hippocampal CA1 displays an LTP magnitude that is over twice that seen at day 60. Neocortical responses display a similar peak at postnatal day 15 and a subsequent adult stabilization at approximately half of the day 15 maximum. Both tissues first display LTP during the early stages of synapse formation between postnatal days 6-10. The role of the NMDA receptor is implicated in aspects of both hippocampal and neocortical LTP.

Action Potentials↗
PubMed1985

Synaptic activity of myenteric neurons in tissue culture.

Intracellular recordings were made from myenteric neurons of the guinea-pig caecum grown in tissue culture. The experiments were carried out on cultures older than 15 days, in which the neurons formed ganglion-like aggregates with many interconnecting nerve fibres. Intracellular injection of horseradish peroxidase demonstrated that the neurons project processes both within and outside the aggregates. Spontaneous activity was recorded in about 50% of the cells. This activity was composed of depolarizing potentials 2-20 mV in amplitude, and in most cases 10-20 ms in duration. In some instances, the potentials occurred in short bursts. The spontaneous potentials appear to be nicotinic cholinergic excitatory postsynaptic potentials (EPSPs). Electrical stimulation of the connecting fibers elicited in the neurons nicotinic cholinergic EPSPs, since they were blocked by hexamethonium. By varying the stimulus intensity and by stimulating several fibers, it was shown that the neurons are multiple-innervated. During repetitive presynaptic stimulation at frequencies above 10 Hz, there was a progressive reduction of the EPSP amplitude. It is concluded that the cultured myenteric neurons retain many of the characteristics found in the freshly isolated preparation and may be useful for studying the synaptic properties of these cells.

Animals↗
PubMed1991

Intracellular recording of spontaneous activity of canine intracardiac ganglion cells.

Intracellular recordings were made from 302 canine intracardiac ganglion cells with intact synaptic connections. Fifty-two % of these cells exhibited spontaneous membrane potential changes consisting primarily of miniature excitatory postsynaptic potential (EPSP)-like depolarizations upon which an action potential or burst of action potentials was sometimes evoked. Most of the spontaneous potential changes are presumed to be synaptically mediated involving nicotinic mechanisms because they were blocked by low Ca2+/high Mg2+ and hexamethonium solutions.

Action Potentials↗
PubMed1983

An electrophysiological study of the accessory olfactory bulb in the rabbit--II. Input-output relations as assessed from analysis of intra- and extracellular unit recordings.

The input-output relations of the rabbit accessory olfactory bulb were studied by intra- and extracellular single unit recordings following electrical stimulation of the vomeronasal nerves, the lateral olfactory tract and the corticomedial amygdala. Cellular activity of accessory bulb mitral cells evoked by stimulation of the vomeronasal nerves consisted of a brief excitation with a latency of 16 ms. This initial response was followed by a period of reduced firing probability which was due to an inhibitory postsynaptic potential. In many cases this secondary response was followed by a second excitatory postsynaptic potential on which action potentials were generated at higher stimulus intensities. Deeper cells in the granule cell layer responded with a long latency, long duration, excitation, often consisting of bursts of 2-3 spikes. The majority of mitral cells were antidromically invaded by amygdala stimulation. The latencies of the antidromic spikes showed a wide range of variation (12-80 ms). Due to this great variation in antidromic latency the inhibitory postsynaptic potential following the antidromic action potential was rather modest but prolonged in duration. In many cases the onset of the inhibitory postsynaptic potential preceded the antidromic response. The majority of cells did not respond to lateral olfactory tract stimulation. Only 10% of the tested cells were invaded antidromically by stimulation at this site. These neurons were also driven antidromically by amygdala stimulation. We conclude that, although the physiological characteristics of mitral cells of the main and accessory olfactory bulb are very similar, there are important differences. The efferent fibres of the accessory bulb conduct at very slow and variable rates and project directly to the corticomedial amygdala.

Amygdala↗