Soma-dendritic Spike Research Articles

Increase in antidromic excitability in presumed serotonergic dorsal raphe neurons during paradoxical sleep in the cat

Putative serotonergic dorsal raphe (DRN) neurons display a dramatic state-related change in behaviour, discharging regularly at a high rate during waking and at progressively slower rates during slow-wave sleep (SWS) and ceasing firing during paradoxical sleep (PS). Using the antidromic latency technique and extracellular recording, we have examined the change in neuronal excitability of presumed serotonergic DRN neurons during the wake–sleep cycle in freely moving cats. We found that, under normal conditions, suprathreshold stimulation of the main ascending serotonergic pathway resulted in a marked decrease in both the magnitude and variability of antidromic latency during PS, while subthreshold stimulation led to a marked increase in antidromic responsiveness during PS compared with during other behavioural states. The antidromic latency shift resulted from a change in the delay between the initial segment (IS) and soma-dendritic (SD) spikes, the antidromic latency being inversely related to the interval between the stimulus and the preceding spontaneous action potential. A marked decrease in the magnitude and variability of antidromic latency was also seen following suppression of the spontaneous discharge of DRN neurons by application of 5-HT autoreceptor agonists or muscimol, a potent GABA agonist. A marked IS–SD delay or blockage of SD spikes was, however, seen in association with the PS occurring during recovery from 5-HT autoreceptor agonist or during muscimol application. The present findings are discussed in the light of previous in vitro intracellular recording data and our recent findings of the disfacilitation mechanisms responsible for the cessation of discharge of DRN neurons during PS.

Perinatal development of action potential propagation in cat rubrospinal axons.

1. The development of action potential conduction was studied by intracellular recording of antidromic spikes in cat rubrospinal cells. 2. The distance between the C1 and L1 spinal segments increased linearly from 5.6 cm at embryonic day (E) 59 to 9.8 cm at postnatal day (P) 30. 3. The conduction time from the C1 segment to the rubrospinal neuron soma, estimated from antidromic spike latency evoked by stimulation of the C1 segment, decreased rapidly prior to birth and then slowly thereafter. This coincided with a reduction in conduction time variation between cells. 4. The conduction time from the red nucleus to the L1 segment followed a similar time course during development. The conduction time reached the adult value by P30, at which time the spinal cord is only half the adult length. 5. The conduction velocity between the C1 and L1 segments increased monotonically between E59 and P30, from a low of 1 m s-1 to a maximum of 34 m s-1. 6. The rise time of rubrospinal neuron somadendritic spikes followed a developmental time course similar to that for conduction time. 7. Myelination of rubrospinal axons, as judged by the presence of myelinated segment spikes, began to occur prior to E59. 8. These findings suggest that development of action potential propagation in rubrospinal cells can be divided into an early and a late stage: conduction time reaches the adult value during the early stage, i.e. by the first postnatal month, and is maintained during the late stage. We propose that myelination, axon diameter increase and maturation of membrane properties act to reduce conduction time to adult values during the early stage, while a proportional increase in fibre diameter with axonal length results in a constant conduction time during the late stage.

The control of jaw-opener motoneurons during active sleep

Brainstem and spinal cord motoneurons that innervate somatic musculature serving antigravity functions are postsynaptically inhibited during active sleep [3,12,22,23]. However, it has been reported that hypoglossal motoneurons (which do not innervate antigravity muscles) are not postsynaptically inhibited during active sleep, but are disfacilitated [16,17]. In the present report we describe changes, during active sleep, in the excitability and membrane potential of digastric and synergistic motoneurons of the trigeminal motor pool; these neurons do not perform antigravity functions [21]. The experiments described in the present report were performed in chronic cats that were prepared for intracellular recording. The motoneurons hyperpolarized an average of 11 mV (S.D.± 1.29, n = 8, P < 0.005) during active sleep compared to quiet sleep. Hyperpolarization was accompanied by a reduction in the excitability of the somadendritic regions of the neurons, as indicated by an increase in the delay of propagation of antidromic spikes from the initial segment to the somadendritic portion of the cell. High gain membrane potential recordings from these motoneurons revealed the occurrence of a remarkably large number of hyperpolarizing potentials during active sleep. When K-chloride-filled microelectrodes were utilized and chloride ions were injected intracellularly, the polarity of these potentials was reversed. During phasic episodes of active sleep, there was a clear increase in hyperpolarizing potential activity, a blockade of somadendritic spikes and phasic reductions in the amplitude of the initial segment spikes. Hyperpolarizing potentials occurred in conjunction with ponto-geniculo-occipital waves. These potentials were reversed in polarity when chloride ions were injected into the cells, indicating that motoneurons of the trigeminal motor pool that do not perform antigravity functions are postsynaptically inhibited during active sleep. The similarities between the inhibitory phenomena in these neurons and those observed in jaw-closer and spinal cord motoneurons lead us to conclude that the excitability of trigeminal motoneurons that innervate muscles with reciprocal functions is suppressed by a postsynaptic inhibitory process during active sleep, as are most other somatic motoneurons [3,12,22,23].

Active electrophysiological properties of spinal motoneurons in aged cats following axotomy

The present study was designed to examine the effects of the aging process on the response of motoneurons to axotomy. Accordingly, in aged cats using intracellular recording techniques, the electrophysiological properties of axotomized lumbar spinal cord motoneurons were compared with those of control (nonaxotomized) motoneurons. In motoneurons that were subjected to axotomy, there was a reduction in axonal conduction velocity compared to that exhibited by control motoneurons. In addition, there were a number of changes in the configuration of the action potential following axotomy. The amplitude of the spike and the overshoot increased as did the slope of the soma-dendritic spike, whereas the delay between the initial segment and the soma-dendritic spikes decreased. The duration of the action potential's afterhyperpolarization increased; its amplitude remained unaffected although the calculated afterhyperpolarization current decreased. Following the spike, most of the axotomized motoneurons exhibited hyperpolarization undershoots and delayed depolarizations. Axotomized motoneurons exhibited a small decrease in the membrane potential and a reduction in the rheobasic current compared to control cells. The changes in the frequency distribution of axonal conduction velocity, afterhyperpolarization duration, afterhyperpolarization current and rheobase measurements suggest that aged motoneurons dedifferentiated following axotomy. These results indicate that axotomy, in aged motoneurons, results in the disruption of a variety of electrophysiological parameters and that the specific patterns of the responses that occur in axotomized motoneurons of adult cats also emerge in axotomized motoneurons of aged animals.

Properties and ionic basis of the action potentials in the periaqueductal grey neurones of the guinea‐pig.

1. Action potentials of neurones of the ventral part of the guinea-pig periaqueductal grey (PAG) were studied by intracellular recording in a mesencephalic slice preparation maintained in vitro. 2. Fast spikes spontaneously fired last 2.8 +/- 0.6 ms (mean +/- S.D.) and have an amplitude of 72.3 +/- 5.3 mV (n = 28). The neurones could be antidromically activated from the neighbouring white matter and these spikes show an initial segment component that triggers the soma-dendritic spike. These two components were dissociated by hyperpolarization. Action potentials are Na+ dependent and a Ca2+ conductance is responsible for the hump on the falling phase. Hyperpolarization makes the hump disappear and a faster rate of rise and fall are seen. Accommodation of the firing threshold is observed in response to depolarizing ramps, which is eliminated with hyperpolarization. 3. High-threshold Ca2+ spikes are evoked in either Na(+)-free solution or in the presence of tetrodotoxin (TTX). These presumed dendritic action potentials display a fast repolarization and a large after-hyperpolarization (AHP) that prevent repetitive firing. This AHP is mainly generated by Ca(2+)-dependent K+ conductances. 4. The repolarization of fast action potentials depends on the activation of K+ conductances as well as a Na+ inactivation process. A fast-activated tetraethyl-ammonium (TEA)-sensitive K+ conductance, that could be Ca2+ dependent, and a K+ conductance blocked by apamin seem to be involved in the repolarization. 5. Each fast action potential is followed by a pronounced AHP with two components, an initial fast and a slow decaying phase. Membrane hyperpolarization around -60 mV eliminated the first component and the AHP acquired a plateau-like shape. At -90 mV the AHP was nullified. The slow phase was Ca2+ dependent and an apamin-sensitive K+ conductance is involved in its generation. This conductance may be active during the early part of the AHP, but a fast-activated TEA-sensitive K+ conductance and other voltage-dependent K+ conductances might also be present. A Ca2+ conductance is hypothesized to account for the fast depolarizing change after the AHP peak. 6. A delayed return to the baseline is observed after hyperpolarizing pulses. It is generated by the activation of a transient voltage-dependent K+ conductance that is inactive at resting membrane potential (RMP, around -50 mV). This transient hyperpolarization is abolished by Ca2+ channel blockers and insensitive to high external concentrations of 4-aminopyridine, TEA and Cs+.(ABSTRACT TRUNCATED AT 400 WORDS)

Estrogen-dependent and estrogen-independent effects of progesterone on the electrophysiological excitability of dorsal midbrain neurons in golden hamsters.

During the induction of lordosis responses in golden hamsters, the joint actions of estradiol (E) and progesterone (P) have been found to produce major changes in the activity levels, sensory responsiveness and movement-related firing of neurons in the dorsal midbrain, a region vital for lordosis in this species. The present study investigated the possibility that these effects of E and P on dorsal midbrain neurons might arise through changes in transsynaptic excitability or spike-generating processes. Single dorsal midbrain neurons were orthodromically or antidromically activated by ventromedial midbrain tegmental stimulation in ovariectomized, urethane-anesthetized hamsters before and after subcutaneous injection of P in propylene glycol vehicle. P injection produced two neurophysiological effects: (1) a strong depression of transsynaptic activation, and (2) in antidromically invaded neurons, a change in the amplitude (either an increase or decrease) of the soma-dendritic spike component. Both of these effects appeared rapidly (i.e. within 10-20 min) after P injection. The P effect on orthodromic neuronal excitability was contingent upon E priming of the hamsters, but, in contrast, the P effect on antidromic spike amplitude was not. Several features of these neurophysiological effects of P imply that the hormone may have been acting through nongenomic mechanisms, possibly involving receptors in neuronal membranes.

Sodium-dependent regenerative responses in dendrites of axotomized motoneurons in the cat.

Ten days after extradural axotomy, partial spikes are found in greater than 20% of cat L7 motoneurons, while 15-21 days after axotomy the incidence increases to 60%. These responses are produced in excitable (hot) spots in the dendrites by synaptic excitation. Intracellular injection of QX-314, a lidocaine derivative and effective blocker of Na+ channels from within neurons, results in elimination of partial spikes before blocking somadendritic spikes. The action of QX-314 does not depend on changes in passive membrane properties or on changes in synaptic properties. Injections of Cs+ and Cl- ions rule out any major role for calcium, potassium, or chloride currents in the production of partial spikes. The partial spikes represent an unusual Na+-dependent dendritic phenomenon induced by axotomy when carried out relatively near the soma. It is reasonable to postulate that the partial spikes result from a higher concentration of Na+ channels in the dendrites. This may be the consequence of a high rate of production of Na+-channel proteins that are intended for the cut end of the axon; alternatively, they may result from the reflection from the cut end of such proteins produced at either a normal or an increased rate. These aberrant channels are inserted into somatic and dendritic membranes in higher concentrations than normal and, as well as producing local dendritic regions of low safety factor responsible for the partial spikes, also produce somadendritic spikes of unusually fast rise time and lower than usual threshold, which are relatively resistant to QX-314.

Antidromic discharge property of meso-accumbens dopaminergic VTA neurons in rats

Three groups of meso-accumbens (Acc) neurons in the ventral tegmental area were differentiated by their antidromic discharge property; dopaminergic type 1 (n = 10), non-dopaminergic type 2 (n = 2) and unclassified (n = 2) neurons. During repetitive activation at 10 Hz, the latency of the initial segment (IS) spike, which was often not followed by the somadendritic (SD) spike, was gradually prolonged in type 1, but not in type 2 and unclassified neurons. The latency prolongation of type 1 neurons was reduced to about a half of the normal in rats treated with kainic acid plus haloperidol, but only slightly when treated with kainic acid or picrotoxin. The rate of SD invasion tended to increase after all kinds of chemical treatment. Stimulation of the medial forebrain bundle in type 1 neurons gave responses comparable to Acc stimulation. It is suggested that the latency prolongation of IS spike is produced mainly by axonal mechanism. But additional somatic mechanisms such as dopaminergic self-inhibition and GABAergic and non-GABAergic inputs from the Acc would make some contribution, and at the same time produce frequent suppression of the antidromic SD spike.

On re‐excitation of feline motoneurones: its mechanism and consequences.

Conditions required for re-excitation of lumbosacral motoneurones, i.e. for double impulses in the motor axons associated with a single soma-dendritic action potential, were examined in cats anaesthetized with pentobarbitone and paralysed with gallamine triethiodide. Simultaneous recording from a motoneurone (intracellular, and in some experiments also extracellular), and from its axon in a ventral root, was used to assess the relations between the soma and the double axonal action potentials. Action potentials (greater than 70 mV) evoked by brief depolarizing current pulses applied intracellularly were never observed to cause re-excitation. Re-excitation could, however, be regularly induced by procedures which increased the delay between the initial segment and soma-dendritic components of these potentials. Re-excitation could be evoked (i) when brief hyperpolarizing pulses were applied before the onset of the soma-dendritic spikes, (ii) when the depolarizing pulses were applied on a background of long hyperpolarizing pulses or (iii) when two action potentials were evoked in a quick succession (by two brief depolarizing pulses). No relationship was found between the presence of re-excitation of motor axons and the presence of the delayed depolarization which follows the soma-dendritic spikes. Neither re-excitation nor delayed depolarization were found to be dependent upon re-excitation of the initial segment. These observations are thus at variance with previous suggestions that the initial segment spikes induce the re-excitation of motor axons and that the initial segment spikes cause the delayed depolarization following soma-dendritic spikes. Since re-excitation of a motor axon occurred without any signs of a second initial segment spike, it is concluded that it is initiated at the level of the axon, most likely at the first node of Ranvier. Re-excitation of motor axons was also observed during repetitive firing induced by intracellular current injection. However, it occurred then only occasionally, and only under strong depolarizing drive. It is thus not expected to be a common phenomenon under natural conditions of repetitive firing.

Intracellular recording from pectoral fin motoneurons of the stingray Dasyatis sabina, an elasmobranch fish.

Intracellular recordings were made from antidromically identified pectoral fin motoneurons in unanesthetized, decerebrate stingrays (Dasyatis sabina). These recordings had the three all-or-none components seen in other vertebrate motoneuron recordings. About 25% of the impalements had resting membrane potentials that were greater than -80 mV, which is larger than those of motoneurons from other vertebrate species. A novel depolarizing afterpotential (DAP) is associated with the isolated action potential occurring at the first node of Ranvier of the axon (M-spike). Occlusion experiments exclude recurrent events as the source of this potential. A capacitive source for the DAP is postulated. Using morphological and passive electrical data on motoneurons from previous studies, calculations of the passive decay of the nodal spike indicate that the membrane resistance of the initial segment is low and nearly equal to that of nodal membrane. The soma-dendritic (SD) spike is followed by a prominent, humped delayed depolarization (DD). The DD is temporally associated with the onset of the action potential produced by the initial segment (IS spike). Sources of the long-lasting period of repolarization recorded with the IS spike, which may underlie the DD, are postulated. The afterhyperpolarization (AHP) of stingray motoneurons tends to be shorter and smaller in amplitude than that of other vertebrate motoneurons. A negligible conductance change was often found during the period following an SD spike. No significant correlation was found between AHP duration and axonal conduction velocity. The input conductance of stingray motoneurons ranged between 1.5 X 10(-7) and 13.3 X 10(-7) S. The relationship between input conductance and axonal conduction velocity was determined from 42 motoneurons. These data were fitted by a power function with an exponent of 1.7, indicating that, in terms of membrane conductance properties, large stingray motoneurons are simply scaled-up versions of the small motoneurons.

Afterpotentials and transduction properties in different types of central neurones.

In mammalian central neurones, the soma-dendritic spike is generally followed by afterpotentials, a brief depolarizing potential (delayed depolarization) and a more longlasting afterhyperpolarization (AHP). These afterpotentials, and in particular the AHP, have long been considered as important factors in the control of excitation-to-frequency transduction. Analysis of the afterpotential properties has been performed on various types of central neurones; spinal alpha-motoneurones, dorsal spinocerebellar tract cells, rubrospinal neurones and hippocampal CA1 pyramidal cells. These investigations have shown the afterpotentials to differ considerably in their characteristics among these types of neurones. Studies of the firing behaviour of the neurones have also shown great variations in their firing properties, the observed differences being well in accord with those expected on the basis of their different afterpotential characteristics. The results suggest that the afterpotentials play a major role in the control of excitation-to-frequency transduction in several types of central neurones.

Neural and humoral interactions between basal prechiasmatic area and median eminence

Publisher Summary This chapter provides information on the neural and humoral interactions between basal prechiasmatic area and median eminence. In the Wistar female rat during proestrus, two types of neuronal responses were recorded in the basal prechiasmatic area (PVA), a part of organum vasculosum laminae terminalis, following electrical stimulation of the arcuate nucleus (ARC)-median eminence (ME) region, namely, antidromic and orthodromic responses. In the antidromically activated units, high frequency stimuli inhibited somadendritic spikes and subsequent spontaneous activity. These results, when taken in conjunction with the observation that LH-RH affected the arcuate nucleus-median eminence ARC-ME activity, suggest that the responsiveness to Luteinizing-hormone- releasing hormone (LH-RH) might characterize these structures. It also appears likely that the inhibitory effect of the ARC-ME on the basal PVA is mediated by an inhibitory interneuron.

Studies of antidromically identified neurosecretory cells of the hypothalamus by intracellular and extracellular recordings.

1. Neurosecretory neurones in supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus of cats, anaesthetized with chloralose, and dogs, anaesthetized with Nembutal, were studied. These neurosecretory neurones were identified by action potentials evoked antidromically following stimulation of the posterior lobe of the pituitary gland. Reactions of 158 such neurones in cats and 228 in dogs were analysed.2. The latencies of antidromic potentials evoked in neurosecretory neurones by posterior lobe stimulation were between 10 and 22 msec for SON and between 14 and 28 msec for PVN cells. Approximate speed of conduction in the axons was 0.4-0.9 m/sec. The absolute refractory period for the soma-dendritic (SD) spike was 5-10 msec. These cells followed repetitive stimulation up to a rate of 100/sec.A notch was generally present on the rising phase of antidromic potentials and when the antidromically conducted signal fell in the relative refractory period of the preceding response, a complete separation between this first small A-spike and later large B-spikes, probably soma-dendritic spike, frequently occurred. Thus, two responses, a small and a large, sometimes appeared with more than 10 msec intervening. When the second antidromic response fell in the absolute refractory period of the first, the B-spike was blocked and only the A-spike appeared.3. Intracellular recordings from neurosecretory cells, mainly from SON in the dog, showed that these neurones possess resting membrane potentials of 50-80 mV, and action potentials of the same magnitude. In spontaneously firing neurosecretory cells separate A- and B-spikes also occurred and could be recorded intracellularly.4. Neurosecretory cells were excited by current injected intracellularly through a micro-electrode. The rheobase was 1-10 nA. A low intensity of stimulation only induced a small A-spike, but as the current was increased the full sized spike was evoked. Application of suprathreshold depolarizing current produced repetitive discharges. The intervals between spikes shortened with an increase in applied current intensity.5. There were a few neurones excited by stimulation of the posterior pituitary whose potentials did not meet the adopted criteria of antidromic potentials. These units were not classified as neurosecretory cells. The characteristics of cells giving the atypical ;antidromic potentials' were: the neurones discharged repetitively to antidromic stimulation, but with fluctuating and very long latencies.6. Neurosecretory cells in both SON and PVN were orthodromically excited by single pulse stimulations of the septal area, mid-brain reticular formation (RF), central gray, anterior commissure and hippocampus. The orthodromic responses generally consisted of two to three spikes with latencies of 10-30 msec. Excitation was followed by an inhibition, of ;spontaneous' discharges as well as of subsequent antidromic excitation, lasting 100-500 msec. Intracellular recordings from neurosecretory cells showed that stimulations of the septal area and RF produced action potentials or EPSPs of short duration followed by long lasting IPSPs. Hyperpolarization was always longer than the preceding EPSP, and its duration was generally 80 msec. Large IPSPs of 20 mV could be recorded occasionally.7. Antidromic excitation of neurosecretory cells by stimulation of the posterior pituitary was followed by the inhibition of ;spontaneous' discharges of the cells. This inhibition usually lasted for 100 msec. A corresponding IPSP was recorded during this inhibitory phase. These findings indicate the existence of recurrent collaterals in neurosecretory cells.8. This conclusion that recurrent collaterals exist was also supported by other evidence, namely, that certain neurones were found in the SON and PVN which responded to a single pulse antidromic stimulation of the posterior pituitary with five to seven discharges at a rate of between 500 and 800/sec. Weaker stimuli produced fewer spikes. Such cells resembled in their behaviour ;Renshaw cells' of the spinal cord. RF stimulation had an inhibitory effect on some of these neurones and an excitatory effect on others.9. Neurosecretory cells in the SON and PVN were excited by osmotic stimulation. Other neurones in close proximity were also found to be osmosensitive but they were either interneurones or neurosecretory cells whose axons ended in areas other than the posterior pituitary since they were not antidromically excitable.

Electrophysiological properties of trochlear motoneurons as revealed by IVth nerve stimulation.

Stimulation of the IVth cranial nerve evokes a triphasic field potential in the trochlear nucleus (TN) (sharp, positive-negative field succeeded by a slow positivity). This field potential was interpreted in terms of successive compartmental activation of single trochlear motoneurons (TMns) and, subsequently, it was utilized to study motoneuronal organization within the TN. Laminar field potential profiles indicate the TN to be spherical (about 1 mm in diameter) and to contain motoneurons of varying size which show, predominantly, a dorsal to ventral axo-soma-dendritic orientation. Smaller motoneurons were located in the dorso-medial part of the TN. Intracellular recordings from the TMns demonstrated an absence of ortho- and antidromically evoked synaptic potentials following stimulation of the IVth nerve or the opthalmic division of the Vth nerve. On the other hand, each somadendritic spike was followed by an after-potential sequence of “depolarization-hyperpolarization” which could produce marked excitability changes in the TN (as determined by stimulation of the IVth nerve at different condition-test intervals). Similar excitability changes (but of different magnitude) were found in the abducens nucleus (ABN). The origin of this after-potential sequence was examined in relationship to spike propagation throughout the soma-dendritic compartments. The effects of polarizing current on the antidromic spike, membrane resistance and rectification, firing frequency and depolarization-hyperpolarization sequence was also studied. Physiological implications of these findings are discussed in terms of motoneuronal response within the oculomotor system.

The differentiation of axonal and soma-dendritic spike activity.

Experiments were performed to examine the usefulness of mean spike duration measurements as a means of distinguishing between axonal and soma-dendritic activity recorded from the C.N.S. by glass insulated platinum microelectrodes. Units recorded from cat gracile and cuneate nuclei were separated into presynaptic and postsynaptic groups on the basis of: a) the maximum number of spikes evoked from a single electrical stimulus to the skin receptor area; b) the maximum frequency at which evoked spikes would follow every stimulus; c) the variability of latency at threshold stimulus intensity; d) the decrement of this variability upon increasing the intensity; e) the reduction of mean latency upon increasing stimulus intensity above threshold. Fifteen presynaptic units were recorded, all of which had short mean spike durations. Of the 41 postsynaptic units 5 exhibited short mean spike durations in the range associated with presynaptic units and were consequently classed as postsynaptic axons. The remaining postsynaptic units had long mean spike durations. On the basis of mean spike duration alone no presynaptic (i.e. primary afferent fibre) unit would have been erroneously classified as a postsynaptic (soma-dendritic) unit.

Intracellular recording from spinal motoneurones in cats with post-asphyxial rigidity.

1. Intracellular recordings were obtained from lumbar spinal motoneurones in cats with post-asphyxial rigidity of the hind limbs.2. Membrane potentials, latencies and (or) appearance of excitatory post-synaptic potentials, initial segment responses and soma-dendritic spikes were not materially different from those observed in cells of normal cords.3. Dorsal root stimulation activated all the motoneurones examined through monosynaptic pathways in contrast to cells in normal cords in which such a stimulus sometimes elicits only a post-synaptic potential. In a number of cells subsequent polysynaptic activation caused a spike about 10 msec after the monosynaptic response, notwithstanding the serious interneuronal destruction which characterized these preparations.4. In a few preparations the effects of acute asphyxiation could be examined. The soma depolarized at a rate of 3-4 mV/min. Synaptic activation was more resistant to O(2) lack than antidromic and direct excitation, in contrast to the experience with normal cells. Survival times of 8.5, 11 and 16 min were found. At certain levels of depolarization ;spontaneous' spikes were observed, which, since they were preceded by post-synaptic potentials, could be considered as the result of synaptic activation.5. To account for the enhanced reflex activity of rigid preparations, it was postulated that the substantial loss of interneurones in the cord had caused denervation supersensitivity of the motoneurones to the transmitter compound without materially changing their electrical excitability.6. It was postulated that the early presynaptic failure during asphyxiation in normal preparations was dependent on a mechanism resembling presynaptic inhibition. The prolonged asphyxial survival of reflex activity in rigid preparations may be due to the destruction of interneurones involved in this form of inhibition.

Temporal Summation of After-Hyperpolarization following a Motoneurone Spike

WHEN recorded intracellularly, the soma-dendritic spike potential of cat spinal motoneurones (SD spike1) is followed by a brief phase of depolarization which reverses to a prolonged hyperpolarization (duration, 60–250 msec.)1,2. Investigation of after-hyperpolarization has yielded three experimental results which conjointly led to the hypothesis that it is due to a prolonged increase in permeability to potassium ions3: there is an increased membrane conductance; when the membrane potential is changed by applying current intracellularly, the size of the after-hyperpolarization is increased by depolarization and decreased by hyperpolarization, being reduced to zero at about 20-mV. hyperpolarization; this equilibrium potential is shifted in the depolarizing direction by an electrophoretic injection of sodium ions into the motoneurone, which would of course result in a decrease of intracellular potassium ion concentration. In the present investigation on after-hyperpolarization, successive spike potentials of a cat motoneurone resulted in a considerable summation of after-hyperpolarizations and there was a corresponding increase in the membrane conductance.