Electrophysiological Properties of Lumbar Motoneurons in the α-Chloralose-Anesthetized Cat During Carbachol-Induced Motor Inhibition

1997 ◽  
Vol 78 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Ming-Chu Xi ◽  
Rong-Huan Liu ◽  
Jack Yamuy ◽  
Francisco R. Morales ◽  
Michael H. Chase
Keyword(s):  
Spinal Cord ◽  
Input Resistance ◽  
High Gain ◽  
Monosynaptic Reflex ◽  
Resting Membrane Potential ◽  
Motor Inhibition ◽  
Active Sleep ◽  
Electrophysiological Properties ◽  
Naturally Occurring ◽  
Anesthetized Cat

Xi, Ming-Chu, Rong-Huan Liu, Jack Yamuy, Francisco R. Morales, and Michael H. Chase. Electrophysiological properties of lumbar motoneurons in the α-chloralose-anesthetized cat during carbachol-induced motor inhibition. J. Neurophysiol. 78: 129–136, 1997. The present study was undertaken 1) to examine the neuronal mechanisms responsible for the inhibition of spinal cord motoneurons that occurs in α-chloralose-anesthetized cats following the microinjection of carbachol into the nucleus pontis oralis (NPO), and 2) to determine whether the inhibitory mechanisms are the same as those that are responsible for the postsynaptic inhibition of motoneurons that is present during naturally occurring active sleep. Accordingly, the basic electrophysiological properties of lumbar motoneurons were examined, with the use of intracellular recording techniques, in cats anesthetized with α-chloralose and compared with those present during naturally occurring active sleep. The intrapontine administration of carbachol resulted in a sustained reduction in the amplitude of the spinal cord Ia monosynaptic reflex. Discrete large-amplitude inhibitory postsynaptic potentials (IPSPs), which are only present during the state of active sleep in the chronic cat, were also observed in high-gain recordings from lumbar motoneurons after the injection of carbachol. During carbachol-induced motor inhibition, lumbar motoneurons exhibited a statistically significant decrease in input resistance, membrane time constant and a reduction in the amplitude of the action potential's afterhyperpolarization. In addition, there was a statistically significant increase in rheobase and in the delay between the initial-segment (IS) and somadendritic (SD) portions of the action potential (IS-SD delay). There was a significant increase in the mean motoneuron resting membrane potential (i.e., hyperpolarization). The preceding changes in the electrophysiological properties of motoneurons, as well as the development of discrete IPSPs, indicate that lumbar motoneurons are postsynaptically inhibited after the intrapontine administration of carbachol in cats that are anesthetized with α-chloralose. These changes in the electrophysiological properties of lumbar motoneurons were found to be comparable with those that take place during the atonia of active (rapid-eye-movement) sleep in chronic cats. The present results support the conclusion that the neural system that is responsible for motor inhibition during naturally occurring active sleep can also be activated in α-chloralose-anesthetized cats following the injection of carbachol into the NPO.

scholarly journals The Motor Inhibitory System Operating During Active Sleep Is Tonically Suppressed by GABAergic Mechanisms During Other States

2001 ◽  
Vol 86 (4) ◽  
pp. 1908-1915 ◽  
Author(s):  
Ming-Chu Xi ◽  
Francisco R. Morales ◽  
Michael H. Chase
Keyword(s):  
Spinal Cord ◽  
Large Amplitude ◽  
Input Resistance ◽  
Monosynaptic Reflex ◽  
Motor Inhibition ◽  
Active Sleep ◽  
Quiet Sleep ◽  
Inhibitory System ◽  
Electrophysiological Properties ◽  
Naturally Occurring

The present study was undertaken to explore the neuronal mechanisms responsible for muscle atonia that occurs after the microinjection of bicuculline into the nucleus pontis oralis (NPO). Specifically, we wished to test the hypothesis that motoneurons are postsynaptically inhibited after the microinjection of bicuculline into the NPO and determine whether the inhibitory mechanisms are the same as those that are utilized during naturally occurring active (rapid eye movement) sleep. Accordingly, intracellular records were obtained from lumbar motoneurons in cats anesthetized with α-chloralose before and during bicuculline-induced motor inhibition. The microinjection of bicuculline into the NPO resulted in a sustained reduction in the amplitude of the spinal cord Ia-monosynaptic reflex. In addition, lumbar motoneurons exhibited significant changes in their electrophysiological properties [i.e., a decrease in input resistance and membrane time constant, a reduction in the amplitude of the action potential's afterhyperpolarization (AHP) and an increase in rheobase]. Discrete, large-amplitude inhibitory postsynaptic potentials (IPSPs) were also observed in high-gain recordings from lumbar motoneurons. These potentials were comparable to those that are only present during the state of naturally occurring active sleep. Furthermore, stimulation of the medullary nucleus reticularis gigantocellularis evoked a large-amplitude IPSP in lumbar motoneurons after, but never prior to, the injection of bicuculline; this reflects the pattern of motor responses that occur in conjunction with the phenomenon of “reticular response-reversal.” The preceding changes in the electrophysiological properties of motoneurons, as well as the development of active sleep-specific IPSPs, indicate that lumbar motoneurons are postsynaptically inhibited following the intrapontine administration of bicuculline in a manner that is comparable to that which occurs spontaneously during the atonia of active sleep. The present results support the conclusion that the brain stem-spinal cord inhibitory system, which is responsible for motor inhibition during active sleep, can be activated by the injection of bicuculline into the NPO. These data suggest that the active sleep-dependent motor inhibitory system is under constant GABAergic inhibitory control, which is centered in the NPO. Thus during wakefulness and quiet sleep, the glycinergically mediated postsynaptic inhibition of motoneurons is prevented from occurring due to GABAergic mechanisms.

Motoneuron properties during motor inhibition produced by microinjection of carbachol into the pontine reticular formation of the decerebrate cat

1987 ◽  
Vol 57 (4) ◽  
pp. 1118-1129 ◽  
Author(s):  
F. R. Morales ◽  
J. K. Engelhardt ◽  
P. J. Soja ◽  
A. E. Pereda ◽  
M. H. Chase
Keyword(s):  
Spinal Cord ◽  
Motor Activity ◽  
Reticular Formation ◽  
Input Resistance ◽  
Ventral Root ◽  
Monosynaptic Reflex ◽  
Pontine Reticular Formation ◽  
Active Sleep ◽  
Decerebrate Cat ◽  
Inhibitory Postsynaptic Potentials

It is well established that cholinergic agonists, when injected into the pontine reticular formation in cats, produce a generalized suppression of motor activity (1, 3, 6, 14, 18, 27, 33, 50). The responsible neuronal mechanisms were explored by measuring ventral root activity, the amplitude of the Ia-monosynaptic reflex, and the basic electrophysiological properties of hindlimb motoneurons before and after carbachol was microinjected into the pontine reticular formation of decerebrate cats. Intrapontine microinjections of carbachol (0.25-1.0 microliter, 16 mg/ml) resulted in the tonic suppression of ventral root activity and a decrease in the amplitude of the Ia-monosynaptic reflex. An analysis of intracellular records from lumbar motoneurons during the suppression of motor activity induced by carbachol revealed a considerable decrease in input resistance and membrane time constant as well as a reduction in motoneuron excitability, as evidenced by a nearly twofold increase in rheobase. Discrete inhibitory postsynaptic potentials were also observed following carbachol administration. The changes in motoneuron properties (rheobase, input resistance, and membrane time constant), as well as the development of discrete inhibitory postsynaptic potentials, indicate that spinal cord motoneurons were postsynaptically inhibited following the pontine administration of carbachol. In addition, the inhibitory processes that arose after carbachol administration in the decerebrate cat were remarkably similar to those that are present during active sleep in the chronic cat. These findings suggest that the microinjection of carbachol into the pontine reticular formation activates the same brain stem-spinal cord system that is responsible for the postsynaptic inhibition of alpha-motoneurons that occurs during active sleep.

scholarly journals Serotonin differentially modulates the functional properties of damaged and intact motoneurons of the frog spinal cord

2019 ◽  
Vol 484 (3) ◽  
pp. 372-376
Author(s):  
N. I. Kalinina ◽  
A. V. Zaitsev ◽  
N. P. Vesselkin
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injuries ◽  
Dendritic Tree ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Electrophysiological Properties ◽  
Frog Spinal Cord ◽  
Specific Morphology ◽  
Isolated Segment

The role of serotonin in the recovery of motor functions in spinal cord injuries is intensively studied, but the mechanism of its action remains unclear. In this work, we used the preparation of an isolated segment of the spinal cord of an adult frog to compare the electrophysiological properties of damaged and intact lumbar moto- neurons and the modulating effect of serotonin (5-HT) on them. Due to specific morphology of the motoneurons (a very branched dendritic tree), we could reliably obtain damaged (on the surface of the slice) and intact moto- neurons (in the depth of the slice). Using intracellular recording, we found significant differences between these groups of neurons in the resting membrane potential, input resistance, properties of the action potential (amplitude, duration, fast and medium phases of the afterhyperpolarization), the frequency of spikes. We found that 5-HT reduced the amplitude of the afterhyperpolarization and increased the frequency of spikes in intact neurons, whereas in damaged motoneurons, 5-HT increased the amplitude of the afterhyperpolarization and did not affect the frequency of discharges. The results of the study show that the properties of the motoneurons and the effect of neuromodulators on them, in particular, 5-HT, can change after damage.

Basic electrophysiological properties of spinal cord motoneurons during old age in the cat

1987 ◽  
Vol 58 (1) ◽  
pp. 180-194 ◽  
Author(s):  
F. R. Morales ◽  
P. A. Boxer ◽  
S. J. Fung ◽  
M. H. Chase
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Action Potential ◽  
Old Age ◽  
Conduction Velocity ◽  
Input Resistance ◽  
Action Potential Amplitude ◽  
Electrophysiological Properties ◽  
Potential Amplitude ◽  
Versus Input

1. The electrophysiological properties of alpha-motoneurons in old cats (14–15 yr) were compared with those of adult cats (1–3 yr). These properties were measured utilizing intracellular recording and stimulating techniques. 2. Unaltered in the old cat motoneurons were the membrane potential, action potential amplitude, and slopes of the initial segment (IS) and soma dendritic (SD) spikes, as well as the duration and amplitude of the action potential's afterhyperpolarization. 3. In contrast, the following changes in the electrophysiological properties of lumbar motoneurons were found in the old cats: a decrease in axonal conduction velocity, a shortening of the IS-SD delay, an increase in input resistance, and a decrease in rheobase. 4. In spite of these considerable changes in motoneuron properties in the old cat, normal correlations between different electrophysiological properties were maintained. The following key relationships, among others, were the same in adult and old cat motoneurons: membrane potential polarization versus action potential amplitude, duration of the afterhyperpolarization versus motor axon conduction velocity, and rheobase versus input conductance. 5. A review of the existing literature reveals that neither chronic spinal cord section nor deafferentation (13, 21) in adult animals produce the changes observed in old cats. Thus we consider it unlikely that a loss of synaptic contacts was responsible for the modifications in electrophysiological properties observed in old cat motoneurons. 6. We conclude that during old age there are significant changes in the soma-dendritic portion of cat motoneurons, as indicated by the modifications found in input resistance, rheobase, and IS-SD delay, as well as significant changes in their axons, as indicated by a decrease in conduction velocity.

scholarly journals Melatonin Reduces Excitability in Dorsal Root Ganglia Neurons with Inflection on the Repolarization Phase of the Action Potential

2019 ◽  
Vol 20 (11) ◽  
pp. 2611 ◽  
Author(s):  
Klausen Oliveira-Abreu ◽  
Nathalia Silva-dos-Santos ◽  
Andrelina Coelho-de-Souza ◽  
Francisco Ferreira-da-Silva ◽  
Kerly Silva-Alves ◽  
...  
Keyword(s):  
Action Potential ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Neuronal Excitability ◽  
Input Resistance ◽  
Cell Types ◽  
Neuronal Population ◽  
Resting Membrane Potential ◽  
Electrophysiological Properties ◽  
Repolarization Phase

Melatonin is a neurohormone produced and secreted at night by pineal gland. Many effects of melatonin have already been described, for example: Activation of potassium channels in the suprachiasmatic nucleus and inhibition of excitability of a sub-population of neurons of the dorsal root ganglia (DRG). The DRG is described as a structure with several neuronal populations. One classification, based on the repolarizing phase of the action potential (AP), divides DRG neurons into two types: Without (N0) and with (Ninf) inflection on the repolarization phase of the action potential. We have previously demonstrated that melatonin inhibits excitability in N0 neurons, and in the present work, we aimed to investigate the melatonin effects on the other neurons (Ninf) of the DRG neuronal population. This investigation was done using sharp microelectrode technique in the current clamp mode. Melatonin (0.01–1000.0 nM) showed inhibitory activity on neuronal excitability, which can be observed by the blockade of the AP and by the increase in rheobase. However, we observed that, while some neurons were sensitive to melatonin effect on excitability (excitability melatonin sensitive—EMS), other neurons were not sensitive to melatonin effect on excitability (excitability melatonin not sensitive—EMNS). Concerning the passive electrophysiological properties of the neurons, melatonin caused a hyperpolarization of the resting membrane potential in both cell types. Regarding the input resistance (Rin), melatonin did not change this parameter in the EMS cells, but increased its values in the EMNS cells. Melatonin also altered several AP parameters in EMS cells, the most conspicuously changed was the (dV/dt)max of AP depolarization, which is in coherence with melatonin effects on excitability. Otherwise, in EMNS cells, melatonin (0.1–1000.0 nM) induced no alteration of (dV/dt)max of AP depolarization. Thus, taking these data together, and the data of previous publication on melatonin effect on N0 neurons shows that this substance has a greater pharmacological potency on Ninf neurons. We suggest that melatonin has important physiological function related to Ninf neurons and this is likely to bear a potential relevant therapeutic use, since Ninf neurons are related to nociception.

Sciatic Chronic Constriction Injury Produces Cell-Type-Specific Changes in the Electrophysiological Properties of Rat Substantia Gelatinosa Neurons

2006 ◽  
Vol 96 (2) ◽  
pp. 579-590 ◽  
Author(s):  
Sridhar Balasubramanyan ◽  
Patrick L. Stemkowski ◽  
Martin J. Stebbing ◽  
Peter A. Smith
Keyword(s):  
Action Potential ◽  
Dorsal Horn ◽  
Chronic Constriction Injury ◽  
Input Resistance ◽  
Substantia Gelatinosa ◽  
Resting Membrane Potential ◽  
Cellular Mechanisms ◽  
Electrophysiological Properties ◽  
Putative Role ◽  
Cell Recording

Peripheral nerve injury increases spontaneous action potential discharge in spinal dorsal horn neurons and augments their response to peripheral stimulation. This “central hypersensitivity, ” which relates to the onset and persistence of neuropathic pain, reflects spontaneous activity in primary afferent fibers as well as long-term changes in the intrinsic properties of the dorsal horn (centralization). To isolate and investigate cellular mechanisms underlying “centralization,” sciatic nerves of 20-day-old rats were subjected to 13–25 days of chronic constriction injury (CCI; Mosconi-Kruger polyethylene cuff model). Spinal cord slices were then acutely prepared from sham-operated or CCI animals, and whole cell recording was used to compare the properties of five types of substantia gelatinosa neuron. These were defined as tonic, irregular, phasic, transient, or delay according to their discharge pattern in response to depolarizing current. CCI did not affect resting membrane potential, rheobase, or input resistance in any neuron type but increased the amplitude and frequency of spontaneous and miniature excitatory postsynaptic currents (EPSCs) in delay, transient, and irregular cells. These changes involved alterations in the action potential-independent neurotransmitter release machinery and possible increases in the postsynaptic effectiveness of glutamate. By contrast, in tonic cells, CCI reduced the amplitude and frequency of spontaneous and miniature EPSCs. Such changes may relate to the putative role of tonic cells as inhibitory GABAergic interneurons, whereas increased synaptic drive to delay cells may relate to their putative role as the excitatory output neurons of the substantia gelatinosa. Complementary changes in synaptic excitation of inhibitory and excitatory neurons may thus contribute to pain centralization.

Changes in Electrophysiological Properties of Lamprey Spinal Motoneurons During Fictive Swimming

2002 ◽  
Vol 88 (5) ◽  
pp. 2463-2476 ◽  
Author(s):  
Michelle M. Martin
Keyword(s):  
Spinal Cord ◽  
Input Resistance ◽  
Spike Frequency ◽  
Calcium Currents ◽  
Quiescent State ◽  
Spike Frequency Adaptation ◽  
Free Solution ◽  
Spinal Motoneurons ◽  
Electrophysiological Properties ◽  
Frequency Adaptation

Electrophysiological properties of lamprey spinal motoneurons were measured to determine whether their cellular properties change as the spinal cord goes from a quiescent state to the active state of fictive swimming. Intracellular microelectrode recordings of membrane potential were made from motoneurons in the isolated spinal cord preparation. Electrophysiological properties were first characterized in the quiescent spinal cord, and then fictive swimming was induced by perfusion with d-glutamate and the measurements were repeated. During the depolarizing excitatory phase of fictive swimming, the motoneurons had significantly reduced rheobase and significantly increased input resistance compared with the quiescent state, with no significant changes in these parameters during the repolarizing inhibitory phase of swimming. Spike threshold did not change significantly during fictive swimming compared with the quiescent state. During fictive swimming, the slope of the spike frequency versus injected current ( F-I) relationship decreased significantly as did spike-frequency adaptation and the amplitude of the slow after-spike hyperpolarization (sAHP). Serotonin is known to be released endogenously from the spinal cord during fictive swimming and is known to reduce the amplitude of the sAHP. Therefore the effects of serotonin on cellular properties were tested in the quiescent spinal cord. It was found that, in addition to reducing the sAHP amplitude, serotonin also reduced the slope of the F-I relationship and reduced spike-frequency adaptation, reproducing the changes observed in these parameters during fictive swimming. Application of spiperone, a serotonin antagonist, significantly increased the sAHP amplitude during fictive swimming but had no significant effect on F-I slope or adaptation. Because serotonin may act in part through reduction of calcium currents, the effect of calcium-free solution (cobalt substituted for calcium) was tested in the quiescent spinal cord. Similar to fictive swimming and serotonin application, the calcium-free solution significantly reduced the sAHP amplitude, the slope of the F-I relationship, and spike-frequency adaptation. These results suggest that there are significant changes in the firing properties of motoneurons during fictive swimming compared with the quiescent state, and it is possible that these changes may be attributed in part to the endogenous release of serotonin acting via reduction of calcium currents.

Changes in the electrophysiological properties of cat spinal motoneurons following the intramuscular injection of adriamycin compared with changes in the properties of motoneurons in aged cats

1995 ◽  
Vol 74 (5) ◽  
pp. 1972-1981 ◽  
Author(s):  
R. H. Liu ◽  
J. Yamuy ◽  
M. C. Xi ◽  
F. R. Morales ◽  
M. H. Chase
Keyword(s):  
Electrical Properties ◽  
Action Potential ◽  
Conduction Velocity ◽  
Time Constant ◽  
Correlation Coefficients ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Electrophysiological Properties ◽  
Axonal Conduction ◽  
Adult Cat

1. This study was undertaken to investigate the effects of adriamycin (ADM, Doxorubicin) on the basic electrophysiological properties of spinal cord motoneurons in the adult cat. ADM was injected into the biceps, gastrocnemius, semitendinosus, and semimembranosus muscles of the left hindlimb (1.2 mg per muscle). Intracellular recordings from motoneurons innervating these muscles were carried out 12, 20, or 40 days after ADM administration and from corresponding motoneurons in untreated control cats. 2. Twelve days after ADM injection, motoneurons innervating ADM-treated muscles (ADM MNs) exhibited statistically significant increases in input resistance, membrane time constant, and amplitude of the action potential's afterhyperpolarization (AHP). In addition, there was a statistically significant decrease in rheobase and in the delay between the action potential of the initial segment (IS) and that of the somadendritic (SD) portion of the motoneuron (IS-SD delay). There were no significant changes in the resting membrane potential, threshold depolarization, action potential amplitude, or axonal conduction velocity. 3. The changes in electrical properties of motoneurons at 20 and 40 days after ADM injection were qualitatively similar to those observed at 12 days. However, at 40 days after ADM injection there was a statistically significant decrease in the axonal conduction velocity of the ADM MNs. 4. The normal correlations that are present between the AHP duration and electrical properties of the control motoneurons were observed in the ADM MNs, e.g., AHP duration was positively correlated with the input resistance and time constant and negatively correlated with the axonal conduction velocity. The correlation coefficients, however, were reduced in comparison with the control data. 5. This study demonstrates that ADM exerts significant effects on the electrical properties of motoneurons when injected into their target muscles. The majority of the changes in motoneuron electrical properties caused by ADM resemble those observed in motoneurons of aged cats. Additional research is required to determine whether the specific changes induced in motoneurons by ADM and those that occur in motoneurons in old age are due to similar degradative mechanisms.

Membrane properties of rat subicular neurons in vitro

1993 ◽  
Vol 70 (3) ◽  
pp. 1244-1248 ◽  
Author(s):  
D. Mattia ◽  
G. G. Hwa ◽  
M. Avoli
Keyword(s):  
Hippocampal Slices ◽  
Rhythmic Activity ◽  
Input Resistance ◽  
Membrane Properties ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Channel Blockers ◽  
Electrophysiological Properties ◽  
Low Threshold

1. Conventional intracellular recordings were performed in rat hippocampal slices to investigate the electrophysiological properties of subicular neurons. These cells had a resting membrane potential (RMP) of -66 +/- 7.2 mV (mean +/- SD; n = 50), input resistance of 23.6 +/- 8.2 M omega (n = 51), time constant of 7.1 +/- 1.9 ms (n = 51), action potential amplitude of 85.8 +/- 13.8 mV (n = 50), and duration of 2.9 +/- 1.2 ms (n = 48). Analysis of the current-voltage relationship revealed membrane inward rectification in both depolarizing and hyperpolarizing direction. The latter type was readily abolished by Cs+ (3 mM; n = 6 cells). 2. Injection of depolarizing current pulses of threshold intensity induced in all subicular neurons (n = 51) recorded at RMP a burst of two to three fast action potentials (frequency = 212.7 +/- 90 Hz, n = 13 cells). This burst rode on a slow depolarizing envelope and was followed by an afterhyperpolarization and later by regular spiking mode once the pulse was prolonged. Similar bursts were also generated upon termination of a hyperpolarizing current pulse. 3. The slow depolarization underlying the burst resembled a low-threshold response, which in thalamic cells is caused by a Ca2+ conductance and is contributed by the Cs(+)-sensitive inward rectifier. However, bursts in subicular cells persisted in medium containing the Ca(2+)-channel blockers Co2+ (2 mM) and Cd2+ (1 mM) (n = 5 cells) but disappeared during application of TTX (1 microM; n = 3 cells). Hence they were mediated by Na+. Blockade of the hyperpolarizing inward rectification by Cs+ did not prevent the rebound response (n = 3 cells). 4. Our findings demonstrate that intrinsic bursts, presumably related to a "low-threshold" Na+ conductance are present in rat subicular neurons. Similar intrinsic characteristics have been suggested to underlie the rhythmic activity described in other neuronal networks, although in most cases the low-threshold electrogenesis was caused by Ca2+. We propose that the bursting mechanism might play a role in modulating incoming signals from the classical hippocampal circuit within the limbic system.

Structural and functional alterations in rat corticospinal neurons after axotomy

1996 ◽  
Vol 75 (1) ◽  
pp. 248-267 ◽  
Author(s):  
G. F. Tseng ◽  
D. A. Prince
Keyword(s):  
Steady State ◽  
Cervical Spinal Cord ◽  
Input Resistance ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Survival Group ◽  
Double Labeling ◽  
Postsynaptic Potentials ◽  
Electrophysiological Properties

1. The electrophysiological properties of rat corticospinal neurons (CSNs) were studied 3, 9, and 12 mo after axotomy in the cervical spinal cord, with the use of a combination of the in vitro neocortical slice technique, intracellular recordings, and a double-labeling method that allowed identification of CSNs studied in vitro. 2. CSNs retained the rhodamine-labeled microspheres employed as a retrograde marker and were functionally active in the longest survival group (1 yr). 3. The somatic area of axotomized CSNs became progressively smaller, a reduction that amounted to 37% for all cells at 1 yr. There were no obvious differences between normal and axotomized cells in terms of apical dendritic widths, numbers of apical dendritic branches, or basal dendritic arbors. Intracortical axonal arborizations of axotomized neurons were in general similar to those of normal CSNs in that most axons ended in layers V and VI with only occasional collaterals reaching supragranular layers. 4. Axotomized CSNs were grouped according to their spike firing patterns during depolarizing current pulses so that their electrophysiological behavior could be compared with that of regular spiking and adapting groups of normal CSNs. No significant differences were found in resting membrane potential, or spike parameters between axotomized neurons in any survival group and normal controls. Neurons surviving 1 yr after axotomy had a higher input resistance (RN) than normal CSNs. There was a reduction in the percentage of CSNs that generated prominent spike depolarizing afterpotentials in the axotomized group. 5. The steady-state relationship between spike frequency and applied current (f-I slope) became steeper over time and was significantly greater 9 mo after axotomy in regular spiking (RS) and adapting neurons than in normal CSNs in the same groups. The increase in steady-state f-I slope was in part related to increases in the RN of axotomized neurons. 6. There was a significant decrease in the generation of slow afterhyperpolarizations following trains of spikes in axotomized versus normal RS neurons, first detected at 3 mo and also present in 9 mo and 1 yr survival groups. 7. Biphasic inhibitory postsynaptic potentials (IPSPs) were evoked in only 1 of 11 axotomized neurons in the 3-mo group, 2 of 12 cells examined at 9 mo, and 3 of 15 neurons 1 yr after axotomy. The proportions of neurons generating IPSPs were significantly smaller than in comparable groups of control CSNs. As a consequence, longer duration evoked excitatory postsynaptic potentials were generated by axotomized CSNs. 8. Results show that axotomized CSNs undergo alterations in intrinsic membrane properties and inhibitory synaptic electrogenesis that would tend to make them more responsive to excitatory inputs.

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