Distributions of spike bursts in cat duodenum.

The histograms of spike bursts over short distances were examined in the isolated cat duodenum with multiple electrodes arranged circumferentially and longitudinally. At a single cross section of the duodenum, spike bursts occurred simultaneously in any single slow-wave cycle, but all eight monitored sites in the circumference participated simulatenously only in a bout 25% of the spike-burst cycles. There also were wide variations in the incidence of spike bursts at different locations in a planar cross section. In a longitudinal section, net level of activity over short distances varied widely. Also, spike bursts were out of phase in the longitudinal axis, appearing to spread caudad; 80% of spike burst groups involved less than an average of 5.5 consecutive electrode sites (spaced at 5-mm intervals). Since spike bursts seem to be correlated with ring contractions of the circular muscle, the fact that they appear sequentially in time along the duodenum indicates that such contractions must always be peristaltic. An estimated 80% of such contractions sweep less than about 3 cm. Records of spike bursts from a single electrode do not accurately reflect activity beyond that one point site.     

Influence of alpha-cellulose on myoelectric activity of proximal canine colon

The relations between dietary fiber intake and myoelectric activity of the proximal canine colon were examined in four normal beagles fed four diets of varying fiber content in a randomized block design. The basal diet was a canned, meat-based product to which 3, 6, and 9% by weight of alpha-cellulose was added. Colonic motility was monitored using four bipolar Ag-AgCl electrodes. Two slow-wave frequencies were observed: 1) 18.4 +/- 0.1 cycles/min (cpm) and 2) 5.6 +/- 0.03 cpm. Fiber had no effect on either frequency. Spike activity showed three distinct patterns: 1) short bursts phase locked to slow waves of the 18.4 cpm frequency, 2) short bursts phase locked to slow waves of the 5.6 cpm frequency, and 3) prolonged sequences unrelated to slow waves, lasting from 5 to greater than 60 s and grouped in distinct aborally conducted bursts that occurred at a frequency of 2.9 +/- 0.1/h (SE). Fiber had no effect on the frequency of these bursts, but as fiber intake increased there was a linear decrease in burst duration from 11.4 +/- 0.6 min for the basal diet to 8.2 +/- 0.4 min for the high-fiber diet (P less than 0.001). We conclude that luminal factors influence spike burst activity in the proximal colon, because increments of undigestible fiber reduce burst duration on a dose-related basis.     

cAMP and calcium in generation of slow waves in cat colon

Rhythmic oscillations in interactions between cAMP and calcium have been proposed to account for a variety of rhythmic phenomena in cells. This idea was investigated in relation to the rhythmic signals (electrical slow waves) found in the electromyogram of the cat colon. A longitudinal strip of muscularis propria from cat colon was studied in a superfusion bath that allowed recording of the electromyogram from eight sites that were 2 cm apart. The effect of increasing cAMP (by exposure of the tissue to cAMP, dibutyryl cAMP, isobutylmethylxanthine, theophylline, caffeine, and papaverine) was to reduce frequency and amplitude of slow waves and duration of migrating spike bursts. All these maneuvers raised tissue cAMP levels. Dibutyryl cGMP and cGMP had no effect. THe changes in slow waves, but not migrating spike bursts, seen with raised cAMP levels were partly reversed by raising the calcium concentration in the extracellular fluid. Raising the extracellular sodium and potassium concentrations had no effect. The results are consistent with the hypothesis that interactions between cAMP and calcium are involved in slow-wave generation in colon muscle.     

Oscillations of the spontaneous slow-wave sleep rhythm in lateral geniculate nucleus relay neurons of behaving cats

Intracellular recordings of 31 lateral geniculate nucleus relay neurons were performed in darkness in behaving cats in order to analyse electrical postsynaptic events which appeared during slow-wave sleep. A specific pattern characterized slow-wave sleep: a rapid depolarizing potential arising from baseline initiated a slow depolarization lasting for 40-60 ms which in turn most often elicited delayed fast spikes. This pattern recurred at a frequency of 6-12/s. The slow depolarizations were voltage dependent, usually not separated by any obvious phasic hyperpolarization and showed refractoriness. Other rapid depolarizing potentials occurring during the time course or at the end of a slow depolarization could have generated spike(s) but were followed by a rapid decay. Slow depolarizations were not observed during arousal or paradoxical sleep when the neurons tonically depolarized and displayed either rapid depolarizing potentials with a fast decay or repetitive firing and long high frequency bursts. In five of the studied neurons, decreases in frequency of the spontaneous rapid depolarizing potentials occurred during slow-wave sleep for 3-30 s oscillatory periods without any change in the behavioural state. During these periods all of the few remaining rapid depolarizing potentials arose from a flat baseline, had a higher amplitude and initiated a slow depolarization which always elicited a spike or burst of spikes after a brief delay. The slow-wave sleep rhythm decreased to 1-5/s. Simultaneously the baseline membrane potential hyperpolarized by a few millivolts and reached a level for reversal of inhibitory postsynaptic potentials. Imposed hyperpolarization of the membrane during wakefulness did not reveal any slow depolarization. But strong synaptic excitatory inputs and direct excitation (a break of the current pulse) from a hyperpolarized membrane did evoke the slow depolarization and eventually the fast spike(s) in both control and oscillatory neurons. A rhythm similar to that of slow-wave sleep was elicited during wakefulness by optic tract stimulation and was enhanced by membrane hyperpolarization. But under these conditions the rhythm was initiated by a phasic hyperpolarization and was composed of an alternating hyperpolarization-depolarization. Spontaneously and synaptically evoked rapid depolarizing potentials arising from baseline had a similar rising slope. The spontaneous ones initiated a slow depolarization leading to fast spike(s) during slow-wave sleep and could directly generate fast spike(s) during wakefulness.(ABSTRACT TRUNCATED AT 400 WORDS)     

Analogue automated analysis of small intestinal electromyogram

The recording of intestinal electrical activity is used to study digestive motility. This activity consists of slow waves occurring at a frequency of 13–20 cycles per minute. The slow waves are sometimes superimposed with spike potentials. Different patterns of distribution of spike potentials on the slow waves have been shown to occur in physiological and pathological conditions, so that longlasting recording sessions are increasingly required. This presents the problem of analysis of large amounts of data that has not yet been resolved satisfactorily. We present herein an analogue automated system of analysis of the intestinal electrical activityin dogs. This system works in real time and provides online data recorded on a graphic recorder. A microcomputer controlled printer and tape recorder were also used. Slow waves are characterised both by the amplitude and the timing of occurrence of relative minima. The spike bursts are detected on the slow waves; their distribution on the slow waves is given, and their energy is measured. Thus, our system allows an easy analysis of long duration chronic recordings, qualitatively (distribution of the spike bursts on the slow waves) as well as quantitatively (time of occurrence of slow waves and number and energy of the spike bursts).     

Influence of intrinsic nerves on electromyogram of cat colon in vitro

The electromyogram of the circular muscle layer of the cat colon was studied in vitro in superfused strips of muscle. Records exhibited electrical slow waves and migrating spike bursts, as described previously. Both the neurotoxin, tetrodotoxin, and the local anesthetic lidocaine, (P less than 0.05) prolonged the duration of migrating spike bursts, but migrating spike bursts were not affected by the adrenergic alpha-antagonist, phenoxybenzamine, nor by the adrenergic beta-antagonist, propranolol. Also, physostigmine and atropine did not affect them. Large concentrations of catecholamines did abolish them. This suggests that the migrating spike burst represents periodic release of the muscle from the tonic influence of nonadrenergic inhibitory nerves in the intramural plexuses. Slow-wave frequency and the congruence of slow waves were not affected (P greater than 0.05) by the antagonists listed above, nor by cholinergic and adrenergic agonists. This suggests that the slow waves are not importantly controlled by intrinsic nerves.     

A study of pace-maker activity in intestinal smooth muscle

1. Electrical activity of longitudinal muscle from cat intestine was recorded in the double sucrose gap.2. Approximately 20% of the preparations demonstrated slow, spontaneous fluctuations of membrane voltage, slow waves. This activity, although quite uniform in a given preparation, showed considerable inter-preparation variation with respect to amplitude, frequency and wave form.3. Application of steady hyperpolarizing current decreased slow-wave frequency and increased slow-wave amplitude while depolarizing currents increased frequency and decreased amplitude.4. Some preparations with no spontaneous slow-wave activity developed slow waves when the membrane was hyperpolarized into a given range which, depending on the preparation, varied in size from 10 to 40 mV. Step or ramp depolarization of the membrane from hyperpolarized levels triggered slow waves in some preparations.5. When the membrane potential of a slow-wave generating preparation was clamped at the resting potential, spontaneous inward-directed current transients were observed.6. No changes in membrane conductance were observed during the course of a slow wave.7. The slow-wave pattern was simulated for individual preparations by applying the membrane current measured under voltage clamp to the passive membrane resistance and capacitance measured independently under current clamp.8. In addition to the defined slow-wave activity, voltage-dependent oscillations in membrane potential were sometimes observed.9. Application of 10(-5)M ouabain irreversibly blocked slow waves and produced a membrane depolarization equal to or slightly greater than the slow wave crest. Repolarization of the membrane to the resting potential, or hyperpolarization, failed to restore slow-wave activity.10. Removal of external potassium produced a reversible sequence of events almost identical to those following ouabain application.11. Replacement of 50% of the external sodium chloride with sucrose produced no changes in slow-wave activity with respect to rates of rise or fall, maximum amplitude or frequency. Sucrose replacement of all external sodium chloride eliminated slow waves after 5 min; however, activity could be restored by a slight hyperpolarization. Longer exposures to the modified bath abolished activity.12. Following a conditioning exposure to potassium-free Krebs solution, readmission of potassium at normal concentration produced a mean hyperpolarization of 20.5 mV and in spontaneous preparations an arrest of activity.13. Pump current in sodium-loaded, non-spontaneously active preparations was measured by voltage clamp and was observed to be voltage-dependent.14. The results of this study indicate that an electrogenic pump is present in longitudinal muscle of cat duodenum, and that oscillations in the level of pump current produce slow waves.     

Effect of bethanechol, gastrin I, or cholecystokinin on myoelectrical activity.

The purpose of this study was to determine the effect of bethanechol, gastrin I, or the octapeptide of cholecystokinin (CCK-OP) on the smooth muscle of the isolated cat colon. Myoelectrical activity was recorded with monopolar glass-pore electrodes. Slow-wave frequency was 5.9 +/- 0.2 cycles/min during the basal period. Slow waves were generally coupled during the control period and the apparent propagation velocity was predominantly aborad at a velocity of 3.8 +/- 0.4 mm/s. Spike activity was superimposed on 11.9 +/- 1.5% of the slow waves during the control period. Bethanechol stimulated a dose-dependent increase in colonic spike activity, with a threshold concentration of 10(-7) M. Bethanechol did not alter the congruence of the colonic slow-wave frequency at any concentration. Gastrin I or CCK-OP increased colonic spike activity. The threshold concentrations for gastrin I and CCK-OP were 2 X 10(-11) M and 4 x 10(-11) M, respectively. Unlike bethanechol, gastrin I (2 X 10(-9) M - 2 X 10(-8) M) and CCK-OP (4 X 10(-9) - 4 X 10(-8) M) altered slow-wave frequency and decreased slow-wave congruence. These studies suggest that 1) bethanechol, gastrin I, or CCK-OP increases colonic spike activity, and 2) only gastrin I or CCK-OP alters the slow-wave frequency of colonic muscle. Thus neurohumoral substances may act independently on colonic spike activity and colonic slow-wave frequency.     

EEG sharp waves and sparse ensemble unit activity in the macaque hippocampus

Neural unit activity and EEGs were recorded from inferior temporal regions of three rhesus macaques chronically implanted with "hyperdrives" holding 12 individually movable tetrodes. Recordings were made from each monkey over a period of approximately 3 mo, while the electrodes were moved by small increments through the hippocampus and neighboring structures. After recording, the monkeys were necropsied, and the brains were sectioned and Nissl-stained, permitting identification of individual electrode tracks. The results establish that hippocampal pyramidal cells are "complex spike cells," firing at overall average rates of approximately 0.3 Hz, with spike trains consisting of long periods of silence interspersed with bursts of activity. The results also establish that the monkey hippocampal EEG shows "sharp wave" events consisting of a high-frequency "ripple" oscillation ( approximately 110 Hz) together with a large slow-wave EEG deflection lasting several hundred milliseconds. The evidence suggests that monkey sharp waves are probably generated mainly in the CA1 region and that sharp waves are associated with an inactive/drowsy-or-sleeping behavioral state, which is also associated with increased hippocampal pyramidal cell activity and increased hippocampal EEG amplitude. The results of this initial study of ensembles of primate hippocampal neurons are consistent with previous studies in rodents and consistent with the hypothesis that theories and models of hippocampal memory function developed on the basis of rat data may be applicable to a wide range of mammalian species.     

Fractal properties of sympathetic nerve discharge

Fano factor analysis and dispersional analysis were used to characterize time series of single and multifiber spikes recorded from the preganglionic cervical sympathetic nerve and cardiac-related slow-wave activity of the whole postganglionic sympathetic vertebral nerve (VN) in anesthetized cats. Fluctuations in spike counts and interspike intervals for single preganglionic fibers proved to be fractal (i.e., time-scale invariant), as reflected by a power law relationship between indices of the variance of these properties and the window size used to make the measurements. Importantly, random shuffling of the data eliminated the power law relationships. Fluctuations in spike counts in preganglionic multifiber activity also were fractal, as were fluctuations in the height and of the area of cardiac-related slow waves recorded from the whole postganglionic VN. These fractal fluctuations were persistent (i.e., positively correlated), as reflected by a Hurst exponent significantly >0.5. Although fluctuations in the interval between cardiac-related VN slow waves were random, those in the interval between heart beats were fractal and persistent. These results demonstrate for the first time that apparently random fluctuations in sympathetic nerve discharge are, in fact, dictated by a complex deterministic process that imparts "long-term" memory to the system. Whether such time-scale invariant behavior plays a role in generating the fractal component of heart rate variability remains to be determined.     

Relation between slow-wave frequency and spiking activity during the migrating myoelectric complex in dogs

The quantitative relation between slow-wave periods and spiking activity was evaluated in vivo in canine small intestine during the fasted state. Experiments were performed in three conscious dogs with three bipolar electrodes, implanted respectively 10, 25 and 40cm beyond the ligament of Treitz. Digitized electrical recordings were automatically processed for the individual slow-wave periods and spike-burst intensities using a set of computer programs developed in our laboratory. A linear correlation existed between the degree of spiking activity and the average length of the preceding slow-wave period. The slopes of the regression lines were less steep for more distal electrodes. A second series of experiments showed that an increase in the slow-wave period precedes the onset of phase 3 of the migrating myoelectric complex and that a fall in slow-wave period precedes the end of phase 3. These data show that a low slow-wave frequency is accompanied by a facilitation of spiking activity, whereas shortening of the slow-wave period is accompanied by a decrease in spike burst intensity. This relation between slow-wave period and spiking activity shows an aboral trend that may be related to intrinsic slow-wave frequency.     

On the nature of the oscillations of the membrane potential (slow waves) produced by acetylcholine or carbachol in intestinal smooth muscle

1. Intracellular recording was made with glass micro-electrodes from cells of the longitudinal muscle of the guinea-pig ileum in isotonic and in hypertonic solution.2. In isotonic solution spontaneous bursts of electrical activity occurred; these consisted of a slow potential component which carried a burst of spike action potentials. Acetylcholine increased the size (and the frequency) of the slow potential component. This had the effect of first reducing and then abolishing the spike potentials; continuous slow wave activity was thus produced. Slow waves were about 1 sec in duration and up to 50 mV in size in isotonic solution.3. In hypertonic solution the membrane potential was stable. There were no spontaneous spikes and no slow potentials. However, spikes, but not slow potentials, were elicited by depolarizing current. Carbachol (or acetylcholine) reduced the membrane potential and initiated spikes and oscillations of the membrane potential (slow waves). Slow waves were 2-5 sec in duration and 10-40 mV in size in hypertonic solution.4. The response to carbachol in hypertonic solution was unaffected by surgical denervation of the tissue, by tetrodotoxin, or by ganglion blocking agents, indicating that muscarinic stimulants produced their effects by acting directly on the smooth muscle cell.5. In hypertonic solution slow waves occurred only in the presence of a muscarinic stimulant and could not be elicited with depolarizing current (unless carbachol was present) nor by increasing the external potassium concentration.6. In hypertonic solution slow waves were abolished by hyperpolarizing the membrane and their rate of rise was proportional to the level of the membrane potential from which they arose. The membrane resistance was reduced at the peak of the slow wave. Slow waves were rapidly abolished by sodium-deficient solutions but spikes were not.7. It is suggested that slow waves represent an inward current through a slow, sodium-sensitive and voltage-dependent ion channel, and that acetylcholine or carbachol increase, while hypertonic solution decreases, the current carried by this channel.     

Sleep homeostasis and cortical synchronization: II. A local field potential study of sleep slow waves in the rat

STUDY OBJECTIVE: Sleep slow-wave activity (SWA, EEG power between 0.5 and 4.0 Hz) decreases homeostatically in the course of non-rapid eye movement sleep (NREM) sleep. According to a recent hypothesis, the homeostatic decrease of sleep SWA is due to a progressive decrease in the strength of corticocortical connections. This hypothesis was evaluated in a large-scale thalamocortical model, which showed that a decrease in synaptic strength, implemented through a reduction of postsynaptic currents, resulted in lower sleep SWA in simulated local field potentials (LFP). The decrease in SWA was associated with a decreased proportion of high-amplitude slow waves, a decreased slope of the slow waves, and an increase in the number of multipeak waves. Here we tested the model predictions by obtaining LFP recordings from the rat cerebral cortex and comparing conditions of high homeostatic sleep pressure (early sleep) and low homeostatic sleep pressure (late sleep). DESIGN: Intracortical LFP recordings during baseline sleep and after 6 hours of sleep deprivation. SETTING: Basic sleep research laboratory. PATIENTS OR PARTICIPANTS: WKY adult male rats. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Early sleep (sleep at the beginning of the major sleep phase, sleep immediately after sleep deprivation) was associated with (1) high SWA, (2) many large slow waves, (3) steep slope of slow waves, and (4) rare occurrence of multipeak waves. By contrast, late sleep (sleep at the end of the major sleep phase, sleep several hours after the end of sleep deprivation) was associated with (1) low SWA, (2) few high-amplitude slow waves, (3) reduced slope of slow waves, and (4) more frequent multipeak waves. CONCLUSION: In rats, changes in sleep SWA are associated with changes in the amplitude and slope of slow waves, and in the number of multi-peak waves. Such changes in slow-wave parameters are compatible with the hypothesis that average synaptic strength decreases in the course of sleep.     

Bursts and recurrences of bursts in the spike trains of spontaneously active striate cortex neurons

Simultaneous recordings were made from small collections (2-7) of spontaneously active single units in the striate cortex of unanesthetized cats, by means of chronically implanted electrodes. The recorded spike trains were computer scanned for bursts of spikes, and the bursts were catalogued and studied. The firing rates of the neurons ranged from 0.16 to 32 spikes/s; the mean was 8.9 spikes/s, the standard deviation 7.0 spikes/s. Bursts of spikes were assigned a quantitative measure, termed Poisson surprise (S), defined as the negative logarithm of their probability in a random (Poisson) spike train. Only bursts having S greater than 10, corresponding to an occurrence rate of about 0.01 bursts/1,000 spikes in a random spike train, were considered to be of interest. Bursts having S greater than 10 occurred at a rate of about 5-15 bursts/1,000 spikes, or about 1-5 bursts/min. The rate slightly increased with spike rate; averaging about 2 bursts/min for neurons having 3 spikes/s and about 4.5 bursts/min for neurons having 30 spikes/s. About 21% of the recorded units emitted significantly fewer bursts than the rest (below 1 burst/1,000 spikes). The percentage of these neurons was independent of spike rate. The spike rate during bursts was found to be about 3-6 times the average spike rate; about the same for longer as for shorter bursts. Bursts typically contained 10-50 spikes and lasted 0.5-2.0 s. When the number of spikes in the successively emitted bursts was listed, it was found that in some neurons these numbers were not distributed at random but were clustered around one or more preferred values. In this sense, bursts occasionally "recurred" a few times in a few minutes. The finding suggests that neurons are highly reliable. When bursts of two or more simultaneously recorded neurons were compared, the bursts often appeared to be temporally close, especially between pairs of neurons recorded by the same electrode; but bursts seldom started and ended simultaneously on two channels. Recurring bursts emitted by one neuron were occasionally accompanied by time-locked recurring bursts by other neurons.     

Excitation-contraction coupling without Ca2+ action potentials in small intestine

Sensitive mechanical and intracellular electrical recordings showed that phasic contractions occurred in response to electrical slow waves in the absence of Ca2+ action potentials. Drugs that either enhanced or depressed slow waves were used to study the relationship between slow-wave amplitude and the amplitude of the phasic contractions. Acetylcholine (Ach) (10(-8) to 3 X 10(-7) M) increased slow waves and contractions without causing action potentials. When ACh was raised to 10(-6) M, action potentials were elicited and accompanying contractions increased in amplitude by at least a factor of five. The Ca2+ channel blocker, Mn2+ (0.5 mM), decreased slow-wave amplitude and the associated phasic contractions. These data agree with a previous study (12), suggesting that an oscillation in intracellular Ca2+ occurs during each slow-wave cycle. The present study suggests that the increase in intracellular Ca2+ during the slow wave is sufficient to activate the contractile apparatus.     

The activity of thalamus and cerebral cortex neurons in rabbits during “slow wave-spindle” EEG complexes

“Slow wave-spindle” complexes were studied during slow wave sleep in rabbits at the thalamic (medial thalamus) and cortical (upper and lower layers of the sensorimotor cortex) levels. Slow wave complexes are biphasic positive-negative complexes or triphasic complexes with a predominantly negative component. Spindles have characteristics close to those of spontaneous sleep spindles. Complexes arise singly, as though inserted into the rhythm of spontaneous sleep spindles, or in series with periods similar to the spindle rhythm. Medial thalamus neurons and some cortical neurons had the same activity during waves as during spindles: if the neuron decreased (increased) its spike frequency in a spindle, then decreases (increases) in frequency were also seen in slow waves; if the neuron produced trains of discharges during spindles, then trains of activity were also seen from the slow-wave part of “slow wave-spindle” complexes. The membrane potential changed in a similar fashion: on a background of hyperpolarization which started at the slow wave, individual depolarization oscillations appeared in the EEG wave rhythm; these oscillations were not always accompanied by spike trains. The slow wave mechanisms, the rhythms of isolated complexes and simultaneous complexes and spontaneous sleep spindles may share a common underlying mechanism: slow, cyclical variations in excitability in thalamocortical neuronal networks, which have previously been demonstrated for spindle-likes activity. The possibility that there are common mechanisms for slow waves in complexes and other EEG slow waves, particularly δ activity, remains hypothetical. Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 84, No. 3, pp. 182–190, March, 1998.     

Physiological role of the transient potassium current in the pyloric circuit of the lobster stomatogastric ganglion.

1. Our experiments were performed to assess the quantitative role of the transient potassium current, IA, in determining the cycle frequency and phasing of neurons in the network generating the pyloric motor rhythm in the stomatogastric ganglion of the spiny lobster, Panulirus interruptus. We used 4-aminopyridine (4-AP) to reduce IA and recorded the effects of this treatment on cell activity. 2. In the intact circuit with an actively cycling pyloric rhythm, 4-AP had three major effects on the rhythm. First, the cycle period was decreased approximately 20%. Second, 4-AP enhanced the activity of all cells, causing increases in spikes/burst and spike frequency within bursts. Third, 4-AP altered the phasing of follower cells relative to the onset of the pacemaker (AB/PD) bursts. The lateral pyloric (LP) and pylorics (PYs) were phase advanced by 4-AP, whereas the ventral dilator (VD) was phase delayed. 3. Voltage-clamp studies indicated that pyloric cells differed in the amount of IA they expressed on or near the soma. IA was largest in pyloric dilator (PD) and PY cells, smaller in the anterior burster (AB), LP, and inferior cardiac (IC) cells, and undetectable in the VD cell. When cells were isolated from synaptic input, however, all were excited by 4-AP, suggesting that all possess functionally significant IA. In VD cells, IA-like currents probably occur primarily in nonsomatic cell regions. 4. We measured postinhibitory rebound by determining the delay to the first spike after a series of 200-ms hyperpolarizing prepulses in the PD, PY, LP, VD, and IC cells. In all five cell types, the delay was progressively increased as the potential of the hyperpolarizing prepulse became more negative. This increased delay reflected the removal of IA inactivation. The delay was greatest in the PY cell and least in the IC. In four cells (the PD, PY, LP, and VD) 4-AP decreased the delay to the first spike at all prepulse potentials. In the IC the delay to the first spike was unaffected by 4-AP, suggesting that IA was not responsible for the relatively short delay after hyperpolarizing prepulses. 5. In all five cell types, 4-AP increased the spike frequency for the duration of a 1-s depolarization. The 4-AP-sensitive current responsible for this behavior appears to have very rapid kinetics and may represent a distinct channel subtype. Functionally, this current may act to dampen cell excitability and to reduce spike frequency during bursts.     

Membrane properties of the smooth-muscle fibres of the guinea-pig portal vein

The membrane activities and the various characteristic constants of the smooth-muscle membrane of the guinea-pig portal vein were investigated with the micro-electrode technique.1. The mean membrane potential was -37 mV. Spontaneous discharges appeared as regular bursts of short trains of spikes alternating with silent periods, as a mixture of single spikes and bursts of spikes appearing continuously, or as regular spikes with low frequency.2. Spontaneous spikes with overshoot were frequently observed. The maximum rate of rise of the spike was 3.7 V/sec. The shapes of the spikes were classified into three different types, i.e. pace-maker type of spike, monophasic spike and spike with a hump during the falling phase.3. Tetrodotoxin (10(-5) g/ml.) did not influence the patterns of the spontaneous train discharges nor the shape of the spike.4. Extracellularly applied outward current elicited spikes which were either monophasic or had a hump on the falling phase. Inward current elicited break excitation of the spike.5. Current-voltage relations, produced by application of inward current pulses to the tissue and measured at various distances from the stimulating partition, were linear.6. The smooth-muscle membrane of portal vein showed cable-like properties. The mean space constant of the membrane was 0.52 mm; the mean time constant of the membrane calculated from the electrotonic potential was 330 msec.7. Conduction velocity of the spike measured by insertion of two micro-electrodes was 0.58 cm/sec.8. The time constant of the foot of the propagated spike was 27 msec. The time constant of the membrane calculated from the time constant of the foot of the spike and the conduction velocity was 310 msec.9. The membrane properties of longitudinal smooth muscle of the portal vein were discussed in comparison with other veins and various visceral smooth muscles.     

Heterogeneity in spontaneous and tetraethylammonium induced intracellular electrical activity in colonic circular muscle

Marked differences were observed in the intracellular electrical activities (spontaneous and TEA-induced) comparing the submucosal and myenteric plexus surfaces of the circular muscle of the dog colon. Distinct characteristics of the cells at the myenteric plexus surface were: a less (10 mV) polarized membrane, a lower amplitude slow wave, and the occurrence of burst type spiking activity. However, slow waves with a high upstroke amplitude (2.5 times higher than the plateau) were observed in 40% of the preparations. This high upstroke amplitude was dependent on the occurrence of a regenerative membrane potential change (a spike) during the slow wave propagation into the myenteric plexus surface. Such a spike was mediated by Ca²⁺-influx and could be evoked or enhanced by electrical pulses or by blocking a TEA-sensitive potassium conductance. In the presence of TEA, spikes occurred in bursts. Both slow waves and spiking activities generated contraction. In conclusion, at least two types of cells exist in the circular muscle layer with marked differences in electrophysiological properties. Slow waves are generated at the submucosal surface, passively propagated to the outermost circular muscle where they induce regenerative membrane potential changes.     

Sleep homeostasis and cortical synchronization: III. A high-density EEG study of sleep slow waves in humans

STUDY OBJECTIVES: The mechanisms responsible for the homeostatic decrease of slow-wave activity (SWA, defined in this study as electroencephalogram [EEG] power between 0.5 and 4.0 Hz) during sleep are unknown. In agreement with a recent hypothesis, in the first of 3 companion papers, large-scale computer simulations of the sleeping thalamocortical system showed that a decrease in cortical synaptic strength is sufficient to account for the decline in SWA. In the model, the reduction in SWA was accompanied by decreased incidence of high-amplitude slow waves, decreased wave slopes, and increased number of waves with multiple peaks. In a second companion paper in the rat, local field potential recordings during early and late sleep confirmed the predictions of the model. Here, we investigated the model's predictions in humans by using all-night high-density (hd)-EEG recordings to explore slow-wave parameters over the entire cortical mantle. DESIGN: 256-channel EEG recordings in humans over the course of an entire night's sleep. SETTING: Sound-attenuated sleep research room PATIENTS OR PARTICIPANTS: Seven healthy male subjects INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: During late sleep (non-rapid eye movement [NREM] episodes 3 and 4, toward morning), when compared with early sleep (NREM sleep episodes 1 and 2, at the beginning of the night), the analysis revealed (1) reduced SWA, (2) fewer large-amplitude slow waves, (3) decreased wave slopes, (4) more frequent multipeak waves. The decrease in slope between early and late sleep was present even when waves were directly matched by wave amplitude and slow-wave power in the background EEG. Finally, hd-EEG showed that multipeak waves have multiple cortical origins. CONCLUSIONS: In the human EEG, the decline of SWA during sleep is accompanied by changes in slow-wave parameters that were predicted by a computer model simulating a homeostatic reduction of cortical synaptic strength.