Short Latency Depolarizations Research Articles

Commissural and lemniscal synaptic input to the gerbil inferior colliculus.

The central nucleus of the inferior colliculus (ICC) receives direct inputs, bilaterally, from all auditory brain stem nuclear groups. To evaluate the contribution made to gerbil ICC neuron physiology by two major afferent pathways, we examined the synaptic responses evoked by direct stimulation of the commissure of the inferior colliculus (CIC) and the ipsilateral lateral lemniscus (LL). Frontal midbrain slices were obtained from postnatal day (P) 9-P19 gerbils, and whole cell recordings were made under current- (n = 22) or voltage-clamp (n = 52) conditions. Excitatory and inhibitory synaptic responses were characterized by sequentially exposing the slice to ionotropic glutamate receptor antagonists [6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) + aminophosphonpentanoic acid (AP-5), or kynurenic acid)], a gamma-aminobutryic acid type A receptor antagonist (bicuculline), and a glycine receptor antagonist (strychnine). In current clamp, LL stimulation typically produced a short latency depolarization followed by a longer duration hyperpolarization. The depolarization was abolished by AP-5 + CNQX, and the remaining inhibitory potential displayed either bicuculline or strychnine sensitivity. In voltage clamp, 79% of ICC neurons displayed synaptic currents after stimulation of each pathway. The synaptic currents were typically complex waveforms, and ionotropic glutamate receptor antagonists reduced inward currents at a holding potential of -80 mV in the majority of neurons. In addition, this treatment reduced outward synaptic currents at a holding potential of -20 mV, indicating that inhibitory interneuronal input was often activated by LL or CIC afferents. A minority of neurons had synaptic currents that were unaffected by glutamate receptor antagonists, but it was more common for CIC-evoked currents to be unaffected (38%) rather than LL-evoked currents (22%). The CIC provided a strong inhibitory input that was almost exclusively GABAergic, whereas the LL inhibition often included a glycinergic component. These experiments have shown that the CIC provides a major glutamatergic and GABAergic input to most ICC neurons. However, much of the inhibitory input from both the CIC and the LL appears to be mediated by interneuronal connections.

1621 A model study of hierarchical networks for the emergence of simple and complex cells

Small transient all-or-none depolarization (also termed in the literature fast prepotentials, spikelets, pseudospikes, d-spikes, or short latency depolarizations) and their association with lucifer yellow (LY) dye-coupling were analyzed in CA1–CA3 hippocampal pyramidal cells in urethane anesthetized rats. It was found that (a) 15 of the 24 LY-injected pyramidal neurons (63%) showed dye-coupling; (b) spontaneous, anti-and orthodromically evoked spikelets (3–7 ms in duration; 3- to 12-mV peak) were recorded in 40 of 95 cells (42%); (c) there was a significantly higher probability of dye-coupled neurons with spikelets and of uncoupled ones without spikelets; (d) spikelet waveform and amplitude were unaffected by spontaneous or imposed polarizations; (e) large hyperpolarizations could reduce the rate and even prevent spikelets; and (f) spikelets could precede or follow spikes, the latter were more frequent with large depolarizations. Electrophysiological findings, and the association of dye-coupling and spikelets, suggest strongly that at least some spikelets are coupling potentials. This implies that pyramidal cells may be electrotonically coupled under physiological conditions.

Electrotonic coupling between rat sympathetic preganglionic neurones in vitro.

1. Using the whole-cell recording technique in rat spinal cord slices we have shown that 26% of sympathetic preganglionic neurones (SPNs) show spontaneous membrane potential oscillations. These oscillations consist of trains of biphasic waves, which we have termed spikelets because of their similarity to truncated action potentials. 2. The spikelets were inhibited by TTX and anaesthetics such as alpha-chloralose but not by the intracellular application of lidocaine N-ethyl bromide (QX-314). 3. By stimulating the ventral roots we have demonstrated the presence of short-latency depolarizations (SLDs) in oscillating neurones. These SLDs have a similar waveform to the spontaneous spikelets, and also show the ability to override the frequency of occurrence of the spontaneous spikelets. These observations suggest that the spikelets result from electrotonic coupling between the oscillating SPNs. 4. SLDs were also observed in a population of non-oscillating, electrotonically coupled, quiescent SPNs. It was possible to induce oscillations in these neurones by the injection of depolarizing current (in the presence of QX-314), suggesting that these neurones are also gap-junction coupled. 5. Simultaneous whole-cell recordings were obtained from twenty-three pairs of SPNs. Two pairs displayed both spontaneous, synchronized oscillations and action potentials. Electrotonic coupling was confirmed by the detection of membrane polarization in both neurones in response to current injected into one neurone. In a further two pairs of quiescent SPNs, injection of depolarizing current pulses into one neurone induced action potential discharge in that neurone and a depolarization and oscillations in the other neurone. 6. The ability of groups of electrotonically coupled SPNs to generate spontaneous discharges within the spinal cord provides a novel mechanism for the integration and synchronization of information within the sympathetic nervous system.

Origin and function of spiral fibers projecting to the goldfish Mauthner cell.

Two neuron types contact the Mauthner cell (M cell) in the axon cap, a specialized region of high electrical resistance surrounding the initial segment of the M cell axon. One type produces a mixed electrical and chemical inhibition of the M cell. The second sends axons into the central core of the axon cap, where they spiral around the initial segment making both conventional synapses and gap junction contacts. The origin and synaptic effects of these spiral fibers have not been studied previously. When goldfish M cells were filled with Lucifer yellow, presynaptic spiral fibers were seen in the axon cap. These fibers could be traced back through the medial longitudinal fasciculus to their somata, near the contralateral fifth nerve motor nucleus. The same somata were labeled by horseradish peroxidase injected extracellularly into the axon cap. Recordings were made in the axon cap and the M cell after stimulation of hindbrain areas near the spiral fiber somata and axons. Extracellularly, a negative potential was observed close to the termination of the spiral fibers and termed the spiral fiber potential (SFP). Intracellularly, a graded, short latency depolarization of the M cell corresponded to the SFP and could cause the M cell to spike. This depolarization did not shunt the membrane, indicating that it may be produced through gap junctions. Intracellular responses to hindbrain stimulation also had a chloride-dependent, second component that shunted the membrane during paired-pulse testing. This inhibitory second component was probably evoked by cells other than the spiral fiber cells themselves.

Electrophysiological properties of neurons in the rat subiculum in vitro.

The present study determined the membrane and synaptic properties of neurons in the rat subiculum. Using the in vitro hippocampal slice preparation, intracellular recordings were obtained from 91 subicular neurons. Membrane properties and morphological characteristics were similar to those reported for hippocampal pyramidal neurons. Two categories of subicular neurons were distinguished based on their response to a depolarizing current pulse. One type of neuron showed bursting behavior and the second type was characterized as regular firing. Analysis of the charging functions during hyperpolarizing current pulses yielded a mean tau 0 and tau 1 for subicular neurons of about 13 ms and 0.60 ms, respectively. Using the model of an equivalent cylinder, the mean dendrite-to-soma conductance ratio (rho) was estimated at 6.0 and electrotonic length constant (L) at 0.7. There was no difference in these values between bursting and regular firing neurons. Tetrodotoxin-resistant potentials (presumed calcium hump/spike) were evoked from bursting subicular neurons at lower current intensities than CA1 pyramidal neurons. Calcium humps could only be evoked from about half the regular firing subicular neurons. Subicular cells showed an excitatory/inhibitory postsynaptic potential (EPSP/IPSP) sequence in response to electrical stimulation in different layers of the CA1 area. An EPSP could also be evoked from stimulation of the superficial or deep layers of the presubiculum and was attributed to activation of entorhinal fibers of passage. At high stimulation intensity, an antidromic spike was often evoked following stimulation in the presubicular area of CA1 alveus. The evoked EPSPs were blocked by addition of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) to the bathing medium. In magnesium-free, CNQX bathing solution, a longer lasting depolarization was recorded; this response was blocked by application of a N-methyl-D-aspartate (NMDA) receptor antagonist (AP5). Iontophoretic application of glutamate or quisqualate (10 mM) along the soma-dendritic axis of subicular neurons leads to either a short-latency depolarization or a burst of action potentials. Application of 10 mM GABA near the recording site usually produced a hyperpolarization, which, at times, was mixed with a depolarization. Mixed hyperpolarizing/depolarizing responses were observed when GABA was applied to the basal or apical dendritic areas. There were no significant differences in the synaptic properties or responses to drug application between bursting and regular firing neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Anatomical and electrotonic coupling in developing genioglossal motoneurons of the rat

Dye-, tracer- and electronic coupling were studied independently in genioglossal (GG) motoneurons using intracellular recordings in in vitro brainstem slices from rats postnatal ages 1–30 days. The subpopulation of GG motoneurons were retrogradely labeled after an injection of dextran-rhodamine into the posterior tongue. Dye-coupling was studied with Lucifer yellow injected into 55 motoneurons and tracer-coupling with neurobiotin injected into 89 presumptive GG motoneurons. Of the motoneurons injected with Lucifer yellow, only 6 of 41 cells (16.2%) exhibited dye-coupling; all occurred in animals less than 9 days old. In all but one instance, dye-coupling was restricted to only one other cell. No evidence of dye-coupling was found in the 14 cells injected in animals older than 8 days. Tracer-coupling (neurobiotin) was demonstrated in 12 of 30 cells (40%) from animals 1–2 days old and in 6 of 21 cells (28.6%) from animals 3–8 days old. Of the remaining 38 cells from animals 10 days of age and older, only one cell was found to be tracer-coupled. Cells injected with neurobiotin were coupled to an average of two other cells. Electrotonic coupling, as demonstrated with a short latency depolarization (SLD) in response to stimulation of hypoglossal axons, was found in developing GG motoneurons. These SLDs were revealed in 17 of 40 GG motoneurons (42.5%) examined in 1–8-day-old animals. There were no SLDs recorded in the 10 cells examined from animals of 10 days and older. The significance of coupling relative to patency of the newborn upper airways is discussed.

Ipsilateral fast corticospinal pathways do not account for recovery in stroke.

We tested the hypothesis that in adult humans, recovery from stroke results from the emergence of ipsilateral, fast-conducting corticospinal pathways. In 10 patients recovering from stroke, the unaffected hemisphere was stimulated with an electromagnet and changes in the firing probability of single biceps motor units were used to derive postsynaptic potentials in single biceps motoneurons. Stimuli sufficient to excite the neurons of the fast-conducting corticospinal pathway (as shown by short-latency facilitation of contralateral biceps motoneurons) did not produce short-latency depolarization of ipsilateral biceps motoneurons. The hypothesis is therefore not supported.

Postnatal changes in motoneurone electrotonic coupling studied in the in vitro rat lumbar spinal cord.

1. Electrotonic coupling between motoneurones innervating ankle flexor and extensor muscles, as well as between unidentified lumbar motoneurones, was studied using intracellular recordings in an in vitro spinal cord-hindlimb preparation isolated from rats between birth (P0) and 13 days (P13). 2. Graded ventral root stimulation could elicit graded, short latency depolarizations (SLD) which preceded, coincided with, or followed the antidromic action potential. These SLDs were identified as electrotonic junctional potentials by their latency, relative insensitivity to changes in membrane potential and their resistance to one or more of the following: (1) high-frequency stimulation, (2) collision with a somatofugal action potential, (3) removal of Ca2+ from the bathing solution. 3. SLDs were studied in 162 neurones and were identified in 77.2% of the cells in preparations from P0 to P3 rats (n = 57), but only in 30.8% at P8 to P13 (n = 39). 4. SLDs were largest in the youngest animals (P0 to P3), decreasing from a mean of 1.31 mV (+/- 0.17, n = 34) to 0.56 mV (+/- 0.10, n = 7) at P8 to P13. The SLDs comprised two to eight (4.3 +/- 0.36) all-or-none components as determined from twenty collision experiments. 5. Electrotonic coupling between motoneurones was specific. SLDs could be elicited in given motoneurones by stimulation of their homonymous but never of their antagonistic muscle nerves. 6. These results indicate that electrotonic coupling between lumbar motoneurones in neonatal animals exhibits a high degree of specificity and that its significance, as judged by the amplitude and frequency of occurrence of SLDs, decreases postnatally at a rate that can be correlated with the functional maturity of the motoneurones and the muscular system.

In vivo electrophysiological analysis of lucifer yellow-coupled hippocampal pyramids

Small transient all-or-none depolarization (also termed in the literature fast prepotentials, spikelets, pseudospikes, d-spikes, or short latency depolarizations) and their association with lucifer yellow (LY) dye-coupling were analyzed in CA1–CA3 hippocampal pyramidal cells in urethane anesthetized rats. It was found that (a) 15 of the 24 LY-injected pyramidal neurons (63%) showed dye-coupling; (b) spontaneous, anti-and orthodromically evoked spikelets (3–7 ms in duration; 3- to 12-mV peak) were recorded in 40 of 95 cells (42%); (c) there was a significantly higher probability of dye-coupled neurons with spikelets and of uncoupled ones without spikelets; (d) spikelet waveform and amplitude were unaffected by spontaneous or imposed polarizations; (e) large hyperpolarizations could reduce the rate and even prevent spikelets; and (f) spikelets could precede or follow spikes, the latter were more frequent with large depolarizations. Electrophysiological findings, and the association of dye-coupling and spikelets, suggest strongly that at least some spikelets are coupling potentials. This implies that pyramidal cells may be electrotonically coupled under physiological conditions.

Prolonged enhancement of anterior thalamic synaptic responsiveness by stimulation of a brain-stem cholinergic group

This study describes the effects of brain-stem cholinergic laterodorsal tegmental (LDT) stimulation on the synaptic responsiveness of anterior thalamic (AT) neurons. A sample of AT cells, physiologically identified by their short-latency (less than 6.5 msec) response to mammillary body (MB) stimulation, was recorded in unanesthetized, chronically implanted cats and in urethane-anesthetized cats. In chronic experiments, LDT stimulation evoked a short-latency (10-20 msec) excitation in most AT cells. Moreover, brief LDT trains (3 shocks at 300 Hz, every 3 sec) enhanced the responsiveness of AT cells to both MB (orthodromic) and cortical (ortho- and antidromic) stimuli. This effect did not vary as a function of the interval between LDT conditioning and MB or cortical testing shocks, but as a function of the number of trials. The effects of LDT stimuli resisted reserpine treatment (0.75 mg/kg), suggesting that they were not dependent on the coactivation of monoaminergic fibers. Finally, LDT trains did not suppress inhibitory processes in AT neurons when conditioning-testing intervals were longer than 60 msec. Intracellular recordings performed in urethane-anesthetized cats revealed that LDT stimulation induced a short-latency depolarization which increased with membrane hyperpolarization and was associated with an increase in apparent membrane conductance. Usually, isolated LDT trains did not evoke lasting changes in membrane potential or conductance. However, when LDT trains were applied every 3 sec, they gradually decreased the apparent membrane conductance without altering the membrane potential. This conductance change had a time course similar to the LDT-induced potentiation of responsiveness observed in the chronic experiments. In some neurons, LDT conditioning trains also induced a marked increase in the probability of fast prepotentials being triggered by subthreshold MB or cortical orthodromic volleys. In order to distinguish the cumulative effects of repeated LDT trains from the possibly slow time course of LDT influences, we studied the effects of a unique 1 sec LDT train (at 30 Hz) on the synaptic responsiveness of AT cells recorded extracellularly in reserpine-treated, urethane-anesthetized animals. Such LDT trains induced a 2.9-fold increase in synaptic responsiveness, reaching its peak 40-50 sec after the LDT train and lasting up to 4 min. Iontophoretic application of the muscarinic blocker scopolamine blocked these long-lasting potentiating effects of LDT stimuli. Removal of cortical and basal forebrain inputs to the AT nuclear complex by appropriate transections did not abolish the potentiating effects of LDT trains.(ABSTRACT TRUNCATED AT 400 WORDS)

Dye-coupling in the neostriatum of the rat: II. Decreased coupling between neurons during development.

Physiological and morphological evidence for coupling between neostriatal neurons was obtained from the developing rat. Intracellular injections of Lucifer Yellow-CH (LY) were made in rat neostriatal slices to study dye transfer (coupling) between neurons. The incidence of interneuronal coupling was 70% in early postnatal (P) periods and declined gradually to 10% in the adult. The number of neurons filled by a single intracellular injection also declined with age. LY injection into single neurons commonly marked aggregates of 4 to 6 cells in neonates. Single injections never produced more than one coupled pair in P20 or older rats. Neurons in which fast prepotentials (FPPs) could be evoked were consistently found to be dye-coupled. FPPs were resistant to collision with action potentials generated by intracellular current injection. When chemical synaptic transmission was blocked Mn2+, short-latency depolarizations (SLDs) could be evoked by extracellular stimulation. The SLDs were distinguished from chemical synaptic potentials by their "all or none" nature and by their insensitivity to changes in membrane potential. No SLDs were observed in adult neurons. FPPs and SLDs may be indicators of electronic transmission between coupled cells. The high incidence of coupling early in development might reflect intercellular communication that contributes to the differentiation and growth of neostriatal neurons.

Wind-activated thoracic interneurons of the cockroach: II. Patterns of connection from ventral giant interneurons.

A number of thoracic interneurons (TIs) have been found to receive inputs from ventral giant interneurons (vGIs). Each of these cells responds to wind with short latency depolarizations. The previous paper described response properties of several TIs to wind stimuli, including those excited by vGIs. The data showed a correlation between the shape of the TI's wind fields and its morphology. The presence of ventral branches located near the midline of the ganglion predicts a strong response to wind on that side. These ventral median (VM) branches are in the proper location to permit overlap with processes from vGIs. Here we describe the patterns of connections between individual vGIs and 13 of the thoracic interneurons located in the meso- and metathoracic ganglia. A correlation was found between the presence of VM branches and excitation by vGIs. TIs were only excited by vGIs on the side(s) on which VM branches exist. However, presence of a VM branch does not imply that all vGIs on that side make connections with the TI. Summation was found between various vGIs that excited each individual thoracic interneuron. In unilateral thoracic interneurons, no sign of inhibition was found from vGIs on the sides opposite that which contained excitatory vGI axons. Neither was there any evidence of inhibition from dorsal giant interneurons. In addition preliminary evidence indicated that left-right homologues do not inhibit one another. Thus, the data suggest that directional wind fields are primarily the result of selective connection from specific vGIs.

Two types of muscarinic response to acetylcholine in mammalian cortical neurons.

Applications of acetylcholine (AcCho) to pyramidal cells of guinea pig cingulate cortical slices maintained in vitro result in a short latency inhibition, followed by a prolonged increase in excitability. Cholinergic inhibition is mediated through the rapid excitation of interneurons that utilize the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). This rapid excitation of interneurons is associated with a membrane depolarization and a decrease in neuronal input resistance. In contrast, AcCho-induced excitation of pyramidal cells is due to a direct action that produces a voltage-dependent increase in input resistance. In the experiments reported here, we investigated the possibility that these two responses are mediated by different subclasses of cholinergic receptors. The inhibitory and slow excitatory responses of pyramidal neurons were blocked by muscarinic but not by nicotinic antagonists. Pirenzepine was more effective in blocking the AcCho-induced slow depolarization than in blocking the hyperpolarization of pyramidal neurons. The two responses also varied in their sensitivity to various cholinergic agonists, making it possible to selectively activate either. These data suggest that AcCho may produce two physiologically and pharmacologically distinct muscarinic responses on neocortical neurons: slowly developing voltage-dependent depolarizations associated with an increase in input resistance in pyramidal cells and short-latency depolarizations associated with a decrease in input resistance in presumed GABAergic interneurons.

Epinephrine- and norepinephrine-evoked potential changes of frog primary afferent terminals: Pharmacological characterization of α and β components

The effects of superfused epinephrine (E) and norepinephrine (NE) on the membrane potential of primary afferent fibers of the isolated frog spinal cord were studied by sucrose gap recordings from the dorsal root. In all preparations both E and NE, applied in concentrations ranging from 0.1 μM to 1.0 mM, produced a hyperpolarization of afferent terminals. In many instances this was followed by a slow depolarization and, in a small number of cords, a small depolarization preceded the increase in membrane potential. E- and NE-induced hyperpolarizations were blocked by the selective α 2-antagonists yohimbine and piperoxan, but not by the selective α 1-antagonists prazosin and corynanthine or by the ß-blockers propranolol and sotalol. The α 2-agonists clonidine, α-methylnorepinephrine and guanabenz also hyperpolarized terminals, causing a change in potential that was reduced by yohimbine and piperoxan. Taken together, these results suggest that α 2-receptors mediate the hyperpolarizing effects of E and NE. The ß-agonist isoproterenol evoked a slow depolarization similar to that produced by E and NE. The isoproterenol-depolarization was antagonized by propranolol. Sometimes, application of E and NE after superfusion with yohimbine produced only a depolarization of the dorsal root and this depolarization was sensitive to propranolol. It would appear therefore that the late depolarization seen after the application of E and NE is produced by activation of ß-receptors. In contrast, the α 1-agonist phenylephrine elicited a short latency, short duration depolarization similar to those seen preceding approximately 10% of the E- and NE-hyperpolarizations. Such short-latency depolarizations were blocked by prazosin and corynanthine. The major component of the response to both E and NE is indirectly mediated through a synaptic process: application of Mn 2+, Mg 2+, procaine or tetrodotoxin in concentrations sufficient to block synaptic transmission substantially reduced, but never eliminated, the actions of the catecholamines. Interneurons are probably involved because mephenesin, which reduces interneuronal transmission, significantly decreased the E and NE effects. Furthermore, interneurons which secrete excitatory amino acids and/or GABA may mediate the indirect effects of the catecholamines on afferent terminals because (−)baclofen and d,l-α-aminoadipate decrease, and picrotoxin and bicuculline increase, the dorsal root (DR) effects of E and NE. These results indicate that catecholamines can alter the membrane potential of afferent fibers indirectly and probably directly and' that such effects are produced by activation of both α- and ß-receptors. These results may be important in understanding the pharmacological basis of previous reports which have shown that catecholamines can affect the transmission of sensory information in the spinal cord.

Electrotonic and dye coupling in hippocampal CA1 pyramidal cells in vitro

The presence of electrotonic and dye coupling in region CA1 of the guinea-pig hippocampus was investigated in the in vitro hippocampal slice preparation. No electrotonic coupling potentials were observed in simultaneous recordings from 101 pairs of pyramidal cells. Also, no electrotonically-coupled short latency depolarizations were observed in more than 75 pyramidal cells in response to antidromic activation of the pyramidal cell population, either in normal bathing medium or in medium with lowered Ca 2+ concentration and added Mn 2+. When the fluorescent dye Lucifer Yellow was injected into pyramidal cell somas, spread of the dye to other cells (dye coupling) was often observed. Injection of Lucifer Yellow into the dendrites of these neurons resulted in many fewer cases of dye coupling. The failure to find electrophysiological evidence of electrotonic coupling among CA1 pyramidal cells suggests that such coupling is not a functionally important feature of this area of the CNS. The lack of electrophysiological evidence of coupling combined with the observation that the site of Lucifer Yellow injection influences the extent of dye coupling further suggests that at least part of the observed dye coupling may be artifactual. Electrotonic coupling may exist in a small percentage of hippocampal pyramidal cells. However, it is not clear that this small amount of coupling is either necessary or sufficient for the synchronization of neural activity as has been hypothesized to occur during epileptogenesis.

A physiological test for electrotonic coupling between CA1 pyramidal cells in rat hippocampal slices

Antidromic stimulation in slices of rat hippocampal cortex was used to test for electrotonic coupling between CA1 pyramidal neurons. The slices were incubated in low Ca 2+ medium containing Mn 2+, in order to block chemical synapses. In a small percentage of intracellular recordings, short-latency depolarizations could be observed after chemical transmission had been blocked. Preceding somatic action potential did not block the depolarizations. This indirect test provides electrophysiological evidence for coupling between some CA1 pyramidal cells.

An identifiable class of statoacoustic interneurons with bilateral projections in the goldfish medulla

Previous studies have demonstrated that some goldfish medullary neurons, inhibitory to the Mauthner cell, can be identified by a passive hyperpolarizing potential coincident with the antidromic impulse of the latter. We describe in this report a group of these interneurons that were further distinguished by their short latency responses to stimulation of the eighth nerve. Specifically, they exhibited graded short latency depolarizations following weak stimulation of the ipsilateral eighth nerve. Short latency depolarizations were followed at times by mono- or polysynaptic postsynaptic potentials. Our evidence indicated that short latency depolarizations were due to electrotonic transmission from eighth nerve afferents. Stronger stimuli evoked a shorter latency impulse which arose abruptly from the baseline. Collision tests and membrane hyperpolarizations did not reveal synaptic potentials underlying the impulses. These physiological results, therefore, suggested that the short latency impulse was a propagated response generated at an electrotonically remote site, possibly an efferent process in the eighth nerve. However, no such projection was found in morphological studies of 77 dye-injected neurons. The morphology rather indicated that these cells were statoacoustic interneurons. Thus, the short latency impulse may be due to remote, electrotonic synaptic inputs. These interneurons had their somata clustered dorsolateral and posterior to the soma of the Mauthner cell. The apparent axon projected contralaterally within the acoustic commissure and could be traced into a caudally directed tract which was lateral to the sensory division of the facial nerve. The axon ramified bilaterally and terminated in part on other statoacoustic neurons, reticular neurons and the Mauthner cells. Selective activation of these interneurons evoked unitary, inhibitory postsynaptic potentials in the Mauthner cell. Their projections suggested a widespread ipsi- and contralateral inhibitory action on other medullary areas as well. These results indicate that a re-evaluation of criteria for efferent identification and of present models for efferent function are required.

Electrical synapses between motoneurons in the spinal cord of the newborn rat.

Ventral roots of the newborn rat spinal cord were stimulated while recording intracellularly from motoneurons. In many cells, stimulation subthreshold for an antidromic action potential in the impaled cell produced a small, short-latency depolarization, which was unaffected by membrane polarization. This response (antidromic synaptic potential, a.s.p.) was also seen, in some cells, on stimulating the ventral root of an adjacent segment. Replacement of Ca2+ (2 mM) with Mn2+ (3 mM) or Mg2+ (10 mM) completely abolished orthodromic synaptic potentials, but the a.s.p. persisted. These results strongly suggest that the a.s.p. is produced by an electrical interaction between motoneurons.

An intracellular analysis of some intrinsic factors controlling neural output from inferior mesenteric ganglion of guinea pigs.

1. In vitro studies were conducted on neurons within the inferior mesenteric ganglion (IMG) of guinea pigs to investigate how intrinsic features of the spike-generating process interact with preganglionic inputs to produce the output firing patterns of these neurons. Intracellular-electrode techniques were used to monitor and control electrical activity of IMG neurons. Preganglionic inputs were activated either synchronously by stimulating an attached nerve trunk or asynchronously by leaving the ganglion attached to a segment of terminal colon and activating the colonic-IMG mechanosensory system. 2. Ninety-seven percent of the neurons studied demonstrated an afterspike hyperpolarization (ASH). The ASH process was activated only by the occurrence of a spike and did not have a synaptically induced component. Further activation of this process was produced by two or more spikes having interspike intervals less than the duration of an ASH following a single spike. An aftertrain hyperpolarization (ATH) resulted from this progressive activation. The amplitude of both the ASH and the ATH decreased when the resting membrane potential was hyperpolarized by current injection or by increasing the external potassium ion concentration. 3. Neuronal excitability was reduced during the ASH. From this observation it was concluded that when IMG neurons operate in the occasional-firing mode, the ASH process prevents output frequency from greatly exceeding the reciprocal of the ASH duration produced by a single spike. 4. Two types of synaptically induced slow depolarizations were observed: a slow, long-latency depolarization and a short-latency depolarization (SLD). These depolarizations differed in their latency, onset, and duration. Both were capable of converting synchronous, preganglionic input from subthreshold (non-spike-activating) to threshold (spike-activating) activity. 5. Neurons having resting potentials more positive than -60 mV were capable of firing in the rhythmic-firing mode; 40% of these neurons demonstrated tonic- and 60% phasic-firing behavior. Frequency-current relations for tonic-discharging neurons were linear from the rhythmic-firing threshold to current levels approximately 2.5 times the threshold value. Minimal frequency for tonic firing and the slope of the linear portion of the frequency-current relation were indirectly related to the duration of the ASH. 6. This study suggests that sympathetic, noradrenergic neurons of the IMG can operate in either the occasional- or rhythmic-firing mode. In the physiologic state in vivo, most IMG neurons probably do not produce action potentials in excess of 10-15 Hz because of their intrinsic properties which regulate firing in both modes of operation.

Electrotonic coupling between frog spinal motoneurons. An electrophysiological and morphological study

Summary In motoneurons of the isolated spinal cord of frogs ( Rana esculenta ) short latency depolarizations (‘VR-EPSPs’), produced by stimulation of different ventral roots, were investigated. During increased extracellular magnesium ion concentration, postsynaptic potentials were reversibly suppressed. In addition, the antidromic spike invasion of the somatodendritic membrane of motoneurons was blocked because of membrane hyperpolarization and the subsequent increment in threshold depolarization. Consequently, the antidromic focal potential diminished in amplitude and the VR-EPSPs disappeared to a similar extent. At the same time, the neuron input resistance increased and the extracellular concentration of potassium ions, [K + ] e , decreased below control levels. However, antidromic spikes again invaded the somatodendritic membrane of motoneurons, despite the maintained action of magnesium ions, whenever the bulk of motoneurons were depolarized by increasing [K + ] e . As a result, the VR-EPSPs reappeared, whereas all chemical PSPs remained blocked. PSPs were also blocked reversibly by application of manganese ions. No effects were seen either in [K + ] e , membrane potential, passive membrane properties, or in antidromic spike invasion of motoneurons, and VR-EPSPs remained unchanged. On the basis of these results, it was concluded that the VR-EPSP is electronically propagated between different motoneurons. Electron microscopic inspection of the membranes of frog motoneuron somata and dendrites, as exposed by freeze-fracturing, revealed numerous membrane specializations of gap junction character. As a typical feature of these gap junctions, regions of densely packed particles surrounded small particle free regions. As a consequence of these findings the term VR-EPSP, as employed by Kubota and Brookhart, should be used with some reservation. If the proposed interpretation of the signal should prove to be correct, the designation ‘ventral root electrotonic junction potential’ (VR-EJP) would, in our opinion, be more appropriate.