Biomedical subjects

A Baranyi

Publications and source records attributed to A Baranyi.

At least 19 recordsLinked to original sources

PubMed1993

Electrophysiological characterization of different types of neurons recorded in vivo in the motor cortex of the cat. I. Patterns of firing activity and synaptic responses.

1. Patterns of firing activity and characteristics of antidromic and synaptic responses to stimulation of the pyramidal tract at peduncular level [peduncular pyramidal tract (PP)] and the ventrolateral thalamic nucleus (VL) were studied in neurons of area 4 gamma of the motor cortex of awake, chronic cats using intracellular microelectrode techniques. The results offer a new functional classification of neocortical neurons based on electrophysiological properties of the 640 recorded cells. 2. Four classes of neurons were distinguished: (class i) inactivating bursting (ib) neurons (n = 60) including fast antidromic response PP (fPP) (n = 0), slow antidromic response PP (sPP) (n = 11), and no antidromic response PP cells (nPP) (n = 49); (class ii) noninactivating bursting (nib) neurons (n = 79), including fPP (n = 23), sPP (n = 0), and nPP cells (n = 56); (class iii) fast-spiking (fsp) neurons (n = 56), including fPP (n = 0), sPP (n = 0), and nPP cells (n = 56); and (class iv) regular-spiking (rsp) neurons (n = 445), including fPP (n = 96), sPP (n = 38), and nPP cells (n = 311). (Neurons in each classification were further separated by their antidromic responses to PP stimulation: fast PP (fPP) slow PP (sPP), or nPP cells, the latter not responding antidromically to electrical stimulation of the peduncle.) 3. Recurrent monosynaptic excitatory postsynaptic potentials (EPSPs) followed antidromic spikes elicited by PP stimulation in most (96%) fPP but much fewer (24%) sPP cells. In fPP cells, it was possible to separate the PP EPSPs into two monosynaptic EPSP components that were generated by other fPP and sPP cells, respectively. VL stimulation evoked monosynaptic EPSPs in 100% of fPP cells (vs. 63% of sPP cells) and antidromic action potentials in 16% of fPP cells (vs. 12% of sPP cells). 4. Firing activity consisted of single spike discharges in most PP cells; however, noninactivating bursting was observed in 19% of fPP cells, and inactivating bursting was observed in 23% of sPP cells (see below). In 18% of ib and 11% of nib/nPP neurons, VL stimulation elicited antidromic action potentials. Other bursting neurons proved to be PP cells with characteristic differences in axonal conduction velocity (see above). All PP cells among the nib cells were fPP, and all PP cells among the ib cells were sPP cells. All fsp neurons were found to be nPP cells, and none could be activated antidromically by VL stimulation. Thus the fsp pattern of discharge distinguished a unique class of nPP cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1993

Electrophysiological characterization of different types of neurons recorded in vivo in the motor cortex of the cat. II. Membrane parameters, action potentials, current-induced voltage responses and electrotonic structures.

1. Electrical properties of four functional classes [inactivating bursting (ib), noninactivating bursting (nib), fast spiking (fsp), and regular spiking (rsp)] of neurons in the motor cortex of conscious cats were studied with the use of intracellular voltage recording and single-electrode voltage-clamp (SEVC) techniques. Evaluations were made of action potentials and afterpotentials, current-voltage (I-V) relationships, and passive cable properties. Values of membrane potential (Vm), input resistance (RN), membrane time constant (T0), and firing threshold (T50) were also measured. The data were used to extend the electrophysiological classifications of neurons described in the companion paper. 2. Average values of Vm (from -63 to -66 mV), action-potential amplitudes (from 72 to 77 mV), and firing threshold (-54 mV) were not statistically different in different types of neurons. However, the magnitude of intracellularly injected depolarizing current required to induce spike discharge at 50% probability varied significantly (from 0.6 to 1.1 nA) among cell types. The mean RN and T0 measured at Vm varied between 8.3 and 19.8 M omega, and 7.2 and 15.1 ms, respectively, in the cell classes. 3. Action potentials were overshooting. Their mean duration at half amplitude varied from 0.25 to 0.73 ms among different cell types. Three types of action-potential configurations were distinguished. Type I action potentials found in nib and rsp neurons were relatively fast and had a depolarizing afterpotential (DAP) as well as fast and slow after hyperpolarizations (fAHPs, sAHPs). Type II action potentials found in ib and rsp cells had relatively slow rise and decay phases, DAPs, and sAHPs. Their fAHPs were small or absent. Type III action potentials were found exclusively in fsp cells, had very short durations, prominent fAHPs, but no sAHPs. 4. Steady-state I-V relationships were determined by measuring voltage responses to 0.2- to 1.0-nA hyperpolarizing, rectangular current pulses at different membrane potentials. Both RN and T0 exhibited nonlinear behavior over wide ranges of membrane potential; however, between -65 and -75 mV, the I-V relationships varied little, and they appeared constant in most cells. The steady-state values of RN increased with decreasing, and decreased with increasing the membrane potential in all but fsp cells. The I-V relationships were virtually linear in fsp neurons. 5. Transient I-V relationships were studied by measuring voltage responses to depolarizing and hyperpolarizing, rectangular current pulses of increasing amplitude from a preset membrane potential of -70 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1993

Early X-irradiation of rats. 5. Influence of irradiation on the development of extracellular field potentials evoked by antidromic stimulation.

Rat pups were treated by low, fragmented and repeated doses of X-rays, from late prenatal days until the end of the third postnatal week. Extracellular field potentials, evoked by antidromic stimulation of the lateral olfactory tract were recorded in different layers of the olfactory bulb at 1, 2, 3 and 6 weeks of age, from control (non-irradiated) and experimental rats. Development of the field potentials was analysed in both groups of animals. In controls, the amplitude of responses was gradually increasing along with age while the latency of peaks decreased; inhibitory waves were tuned even after the third postnatal week. When compared to controls at similar ages, irradiated rats had smaller peak amplitude of responses and the shortening of the response latency was delayed. In addition, a new, late-appearing excitatory wave component was observed in the granule cell layer by the sixth week. The effect of irradiation on field potentials of the olfactory bulb is discussed in light of the marked reduction of the inhibition in the local neuronal assembly, which is also indicated by the depressed development of its structural and neurochemical correlates.

Animals↗

PubMed1993

Effects of intracellularly applied aminopyridine on firing activities and synaptic responses of electrophysiologically identified cell types in the motor cortex of cats.

Effects of 3-aminopyridine (3-Ap) applied intracellularly into electrophysiologically identified cortical neurons in the cat motor cortex were studied. Actions on the membrane and firing activity properties, excitatory and inhibitory postsynaptic responses were investigated. Intracellular microelectrode techniques and single electrode voltage clamp methods were used in experiments on anesthetized and chronic nonanesthetized cats. In addition to changes in neuronal excitability and firing activity properties the evoked postsynaptic responses were significantly altered. Augmentation of EPSPs was accompanied by increases of the total duration and amplitude of the second slow component of IPSPs without influencing the early fast IPSP component. It is concluded that most actions of 3-Ap reported here are derived from direct effects of 3-Ap on the postsynaptic membrane.

Aminopyridines↗

PubMed1992

Synaptic origin of rhythmic visually evoked activity in kitten area 17 neurones.

Rhythmic patterns in neuronal activity in response to moving stimuli were observed in 28% of cells recorded extracellularly or intracellularly in area 17 of 4-16 week old anaesthetized and paralysed kittens. In both recording modes, oscillation frequencies ranged between 7 and 71 Hz, and were confined for 88% of cells in the 7-20 Hz band of the spectrum. A comparative study of firing autocorrelograms) and subthreshold activity (autocorrelation functions) indicates that the regularity of discharge stemmed from visually evoked oscillations of membrane potential at the same frequency. These oscillations are shown to result from extrinsic excitatory activity, since their amplitude, but not their frequency, depends on the resting membrane potential. The dependency on stimulus configuration supports the hypothesis that oscillations in neuronal output are dictated by periodic activity in afferent circuits selectively recruited by different attributes of the visual input which are not exclusively processed at the cortical level.

Animals↗

PubMed1991

Properties of associative long-lasting potentiation induced by cellular conditioning in the motor cortex of conscious cats.

Mechanisms of long-lasting potentiation of synaptic responses induced in the thalamocortical and recurrent collateral pathways of the pyramidal tract were studied in intracellular recordings from the motor cortex of unanesthetized, chronically implanted cats. The observations provide the first description of long-lasting potentiation in the unanesthetized neocortex in vivo. Monosynaptic excitatory postsynaptic potentials of 2-5 mV in amplitude were evoked as test responses by stimulation of the pyramidal tract and thalamic ventrolateral nucleus at 0.1-0.5 Hz frequency. Pressure microinjections of drugs and ions were also performed during intracellular recordings. In the first series of experiments, test synaptic responses were paired with intracellular current injection-induced action potentials at an interstimulus interval set between 0-200 ms and 0.1-0.5 Hz frequency. Pairings (30-100 x) induced long-lasting potentiation of the test responses in 58% of cells. The increased synaptic responses typically initiated action potentials and their potentiation usually lasted over the period of recordings. Increases in amplitude of synaptic responses were not correlated with statistically significant changes in electrical membrane properties (resting potential, input resistance, time constant, spike threshold) or parameters of action potentials and their afterpotentials. The failure to induce increases in synaptic efficacy by unpaired stimuli (pseudoconditioning) demonstrated the associative property of the long-lasting potentiation. In a second series of experiments, differential cell conditioning was employed. This paradigm induced long-lasting potentiation of the explicitly paired synaptic response without noticeable modification of unpaired or pseudorandomly paired synaptic responses tested conjointly in the same neuron. These observations demonstrated the input-specificity of long-lasting potentiation. In a third series of experiments, subthreshold depolarizing current pulses were summated with synaptic responses to induce firing in the recorded neuron during pairing. Long-lasting potentiation occurred in 55% of the summated synaptic inputs. Pseudoconditioning did not induce synaptic potentiation in these cells. In a fourth series of experiments, conditioning was employed in neurons in which firing activity was suppressed by an intracellularly injected lidocaine derivative. Long-lasting potentiation was induced in 50% of the attempts when synaptic responses were paired with current-induced depolarizations greater than 30 mV. These results suggest that postsynaptic induction of long-lasting synaptic potentiation can be successful in the absence of postsynaptic sodium spikes in neurons of the motor cortex in vivo. In a fifth series of experiments, homosynaptic high-frequency tetanization (80-200 Hz for 5-15 s) was applied to the thalamocortical and recurrent pyramidal afferents.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1990

Effects of protein kinase C inhibitor H-7 on membrane properties and synaptic responses of neocortical neurons of awake cats.

Electrophysiological effects of intracellularly pressure-injected H-7, an inhibitor of protein kinase C, were investigated in neocortical neurons of awake cats. H-7 reduced spontaneous and depolarizing current-induced firing activity and increased the latency and apparent threshold of action potentials elicited by depolarizing currents. Slow afterhyperpolarizations following action potentials and depolarizing pulses increased after injection of H-7, without detectable changes in the time course of the fast components of the action potentials. H-7 induced increases in IPSPs evoked by stimulation of the ventrolateral thalamus (VL) or the pyramidal tract (PT). Besides slight increases in the amplitude of IPSPs measured at peak, H-7 induced pronounced increases in the amplitude measured 50-100 ms after stimulation and in the total duration of IPSPs. EPSPs evoked by VL or PT stimulation did not show measurable alterations after injection of H-7. The effects occurred 2-15 min after injection of H-7 and lasted at least 90 min without essential changes in the baseline values of resting membrane potential or input resistance. The results suggest that in addition to playing a role in regulating membrane excitability, protein kinase C influences the inhibitory synaptic mechanisms of neocortical neurons.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1989

Properties of depolarizing plateau potentials in aminopyridine-induced ictal seizure foci of cat motor cortex.

The mechanisms of generation of self-sustained depolarizing plateau potentials (DPs) were studied in intracellular recordings in aminopyridine-induced ictal seizure foci in the motor cortex of the cat. In some experiments single-electrode voltage clamp techniques were used and intracellular pressure injection of aminopyridine (Ap), phorbol esters (PhEs) and tetraethylammonium (TEA) was carried out. After several ictal episodes, DPs with bursts of action potentials or with spike inactivation developed gradually in the clonic and interictal phases, without synchronism with surface ictal seizure potentials. In many cases DPs were followed by hyperpolarizing afterpotentials and neuronal inhibition. In bursting neurons DPs originated from the augmented depolarizing envelope of bursts of action potentials. In non-bursting neurons DPs were initiated from summated depolarizing afterpotentials and slow spikes with high threshold, resembling Ca-spikes. In a few neurons DPs were triggered by enlarged excitatory postsynaptic potentials. It was possible to evoke DPs by injections of depolarizing current pulses into single neurons of the Ap-focus, or by intracellular injection of AP, PhEs or TEA. We conclude that DPs are not causal cellular bases of the ictal paroxysmal discharges, rather they occur as consequences of abnormal neuronal activity. It is suggested that DPs are intrinsic regenerative membrane events induced by a transient dominance of voltage-dependent inward currents (carried primarily by calcium ions although sodium ions may contribute) by simultaneous decreases in concurrent outward potassium currents.

Aminopyridines↗

PubMed1989

An aminopyridine-sensitive, early outward current recorded in vivo in neurons of the precruciate cortex of cats using single-electrode voltage-clamp techniques.

Studies were performed in cortical neurons to determine if voltage- and time-dependent membrane currents could be recognized and characterized in the dynamic, in vivo state. Intracellular measurements made in neurons of the precruciate cortex of awake cats with single-electrode voltage-clamp (SEVC) techniques disclosed an early outward current to depolarizing command steps in 124 of 137 cells studied. The voltage-dependent properties of the early outward current closely resembled those of A-currents studied in vitro in vertebrate and invertebrate neurons. The current was activated rapidly at onset latencies of less than two ms, fell to flat plateau levels within 60-120 ms during sustained depolarization, and was reduced or eliminated in 22 of 23 cells following intracellular administration of 3- or 4-aminopyridine. The magnitude of outward current in response to depolarizing commands was increased by preceding steady hyperpolarization and reduced by preceding steady depolarization. (The steady potentials were of 9.8 s duration and +/- 40 mV apart from the holding potentials.) Since return to the holding potentials occurred 80 ms before the onset of the command steps, the changes in membrane properties that were induced lasted beyond cessation of the steady polarizing stimuli themselves. Spiking did not prevent recognition of the early outward current as judged from its appearance before and after intracellular application of QX-314 to reduce spike activity. Apart from fast inward currents associated with spike potentials, the early outward current was the most conspicuous and characteristic membrane current noted in these recordings. An additional current component that was noted but not characterized in these studies was a slow, depolarization-induced inward current that could be reduced by intracellular injection of QX-314.

Aminopyridines↗

PubMed1988

Intracellular injection of apamin reduces a slow potassium current mediating afterhyperpolarizations and IPSPs in neocortical neurons of cats.

Electrophysiologic effects of intracellularly injected apamin, a Ca2+-dependent K+ channel blocker, were investigated in neurons of the motor cortex of awake cats. Single-electrode voltage clamp techniques were used to measure changes in membrane currents including those that were synaptically activated. All changes occurred within 2-4 min after pressure injection of apamin with partial recovery observed within 8-15 min. Apamin selectively abolished an outward current that mediated a slow afterhyperpolarization (AHP) following intracellular depolarizing current pulses and action potentials without influencing the time course of the action potentials or an associated fast AHP component. In addition apamin increased the number and frequency of spike discharges evoked by the depolarizing current pulses and produced a small increase in the rate of background firing activity. The baseline resting potential and input resistance were essentially unchanged by apamin. Apamin also diminished a late, slowly decaying component of inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) elicited by stimulation of the ventrolateral thalamus or the pyramidal tract. The apamin-induced changes were concomitant with a decrease of the decay time constant of both IPSPs and IPSCs and a positive shift in their reversal potential. The results suggest that the late, slowly decaying component of these inhibitory postsynaptic responses is generated by an apamin-sensitive Ca2+-dependent K+ conductance which is also responsible for the slow AHP.

Action Potentials↗

PubMed1988

Activation of protein kinase C induces long-term changes of postsynaptic currents in neocortical neurons.

Intracellularly injected phorbol 12,13-dibutyrate (PdiB), a phorbol ester that activates protein kinase C (PKC), altered the postsynaptic responses of neurons of the motor cortex of cats. PdiB increased the amplitudes and durations of EPSPs and decreased the amplitudes and durations of IPSPs elicited by stimulation of the ventrolateral (VL) thalamus or the pyramidal tract (PT). The changes lasted for 50 min or longer. Corresponding changes in peak excitatory and inhibitory postsynaptic currents (EPSCs, IPSCs) were measured directly with the single electrode voltage clamp technique. Quantitative analysis of EPSCs in response to VL thalamic stimulation and IPSCs in response to PT stimulation made in a subgroup of fast PT cells suggested that PdiB acted within the injected neuron rather than presynaptically to alter the synaptic currents. No consistent changes in resting membrane parameters that would account for these modifications were found. Control injections of a phorbol ester that did not activate PKC failed to induce changes in synaptic responses or resting membrane properties. These observations suggest that activation of PKC, in vivo, can induce long-lasting changes in synaptic responses of neocortical neurons by direct modification of postsynaptic ion channel conductivities.

Animals↗

PubMed1987

Intracellular injection of phorbol ester increases the excitability of neurons of the motor cortex of awake cats.

The electrophysiological effects of two intracellularly injected phorbol esters (PhEs) which activate protein kinase C, phorbol 12,13-dibutyrate and phorbol 12-myristate 13-acetate, were investigated in neurons of the motor cortex of awake cats. The major finding was that intracellularly injected PhEs increased the excitability of the neurons. This was indicated by (1) an increase in spontaneous firing and depolarizing current-induced spike activity, accompanied by a decrease in the latency and threshold of current-induced spike discharges, (2) a reduction in slow afterhyperpolarizations following action potentials and depolarizing pulses, and (3) the development of bursting activity. Neither increases in input resistance nor depolarization of the resting potential sufficient to account for these excitability changes were found. Increases in the amplitudes of action potentials and their fast afterhyperpolarizations were also observed. All changes occurred within 2-8 min after injection and lasted for 50 min or longer. Control injections of 4 alpha-phorbol 12,13-didecanoate, which does not activate protein kinase C, failed to induce changes in neuronal excitability or in any of the above parameters. We conclude that the excitability of neurons of the motor cortex of the awake cats can be increased by phorbol esters that translocate and activate protein kinase C.

Action Potentials↗

PubMed1987

Effect of inhibitory amino acid antagonists on IPSPs induced in lumbar motoneurons upon stimulation of the nucleus reticularis gigantocellularis during active sleep.

The present study was performed to generate data implicating glycine or gamma-aminobutyric acid as neurotransmitter candidates mediating the IPSPs which are recorded in lumbar motoneurons following electrical stimulation of the nucleus reticularis gigantocellularis (NRGc) during the atonia of active sleep. Accordingly, intracellular records were obtained from lumbar motoneurons in unanesthetized, normally respiring cats during naturally occurring states of active sleep, while inhibitory amino acid antagonists were microiontophoretically released next to the recorded cell. Electrical stimuli, applied to the NRGc during active sleep under drug-free conditions, evoked inhibitory postsynaptic potentials (IPSPs) in all of the lumbar motoneurons which were examined. These NRGc-induced IPSPs exhibited an average latency-to-onset of 26.6 +/- 1.3 ms, a latency-to-peak of 42.5 +/- 1.3 ms, an average amplitude of 3.9 +/- 0.4 mV and a duration of 34.4 +/- 2.1 ms. Strychnine, when applied microiontophoretically, abolished or markedly suppressed these NRGc-induced IPSPs. In contrast, the microiontophoretic application of picrotoxin or bicuculline methiodide failed to block these IPSPs. To the extent that strychnine may be considered to be a specific antagonist of glycine, the present results suggest that glycine (or a structurally related amino acid) participates in the generation of NRGc-induced IPSPs during the atonia of active sleep.

Animals↗

PubMed1987

Long-lasting potentiation of synaptic transmission requires postsynaptic modifications in the neocortex.

The mechanisms of associative long-lasting potentiation (LLP) of excitatory postsynaptic potentials (EPSPs) were studied in the motor cortex of anesthetized cats. Mono- and oligosynaptic EPSPs were evoked by stimulations of thalamic VL nucleus, pyramidal tract, callosal and somatosensory system and paired with orthodromic, antidromic or current-induced action potentials. EPSP-spike stimulus pairs with 0.1-0.2 Hz frequency and 0-200 ms interstimulus intervals induced increases in the amplitudes and durations of EPSPs for 40-60 min or longer after 20-50 pairings. The LLP was prevented when postsynaptic firing was blocked by intracellular current injection or by juxtasomatic application of gamma-aminobutyric acid. LLP was also prevented when the level of intracellular free calcium was lowered by the intracellular injection of the calcium chelator EGTA or when neuronal transport was blocked by the intracellular injection of colchicine. Neither EGTA nor colchicine blocked postsynaptic firing. Thus, these findings show that LLP in the neocortex is a postsynaptic phenomenon which requires conjunctive pre- and postsynaptic activity, adequate levels of intracellular free calcium, and functional intracellular transport.

Action Potentials↗

PubMed1987

Mechanism of aminopyridine-induced ictal seizure activity in the cat neocortex.

Intracellular recordings were obtained from neurons in the motor cortex of anesthetized cats in order to examine membrane and synaptic processes involved in aminopyridine (AP)-induced ictal seizure activity. Depolarizing and hyperpolarizing membrane potential sequences which behaved as large, synchronized excitatory and inhibitory postsynaptic potentials, were found to accompany the ictal seizure potentials. After several repetitions of the seizure attack, partial responses, bursts and depolarizing plateaus with spike inactivation occurred. In layers IV and V we found non-pyramidal tract neurons showing endogenous bursting ability activated by AP. These neurons seemed to be the initiators of the rhythmic synchronous activity of the epileptic neuron population. Our results suggest that AP-induced epileptogenesis represents an adequate model of ictal events in the neocortex.

Action Potentials↗

PubMed1987

Phorbol esters that activate protein kinase C induce long-term changes of membrane excitability and postsynaptic currents in neocortical neurons.

Intracellularly injected tumor promoter phorbol esters (PhEs) that activate protein kinase C (PKC) increased the excitability and altered the postsynaptic responses of neurons of the motor cortex of awake cats. PhEs increased the amplitude and duration of EPSPs and decreased the amplitude and durations of IPSPs. No consistent changes in resting membrane parameters that would account for these modifications were found. Corresponding changes in peak excitatory and inhibitory postsynaptic currents (EPSCs, IPSCs) were measured directly with the single electrode voltage clamp technique. The changes lasted for 50 min or longer. Quantitative analysis of EPSCs in response to ventrolateral thalamic stimulation and IPSCs in response to pyramidal tract stimulation made in a subgroup of fast PT cells suggested that PhE acted within the injected neuron rather than presynaptically to alter the synaptic currents. PhE also reduced a voltage-dependent, 3-aminopyridine sensitive fast outward current (IA) and an apamin and EGTA sensitive slow outward current (IK(Ca]. Control injections of a phorbol ester that did not activate PKC failed to induce changes in synaptic responses or resting membrane properties. These observations provide the first evidence that activation of PKC, in vivo, can induce long-lasting changes in synaptic responses of neocortical neurons by direct modification of postsynaptic ion channel conductivities.

Action Potentials↗

PubMed1987

Application of the glycine labelling method to the cerebellum, hippocampus and spinal cord.

3H-glycine was applied to the cat cerebellar cortex under resting conditions and during inferior olive stimulation which activated the climbing fiber system on a restricted area. Electric recording was made. The autoradiograms showed, that under resting condition labelled glycine was incorporated mainly in granule, Golgi and basket cells and only a few Purkinje and stellate cells were active. Also cerebellar glomeruli remained without labelling. On climbing fiber stimulation Purkinje cells became activated singly and grouped, also Golgi and stellate cells increased in number. Granule cells were totally inhibited. 3H-glycine, when applied to the rat hippocampus, the dentate gyrus, CA1 and CA4 fields showed labelling at low frequency stimulation. When 400 Hz high frequency stimulation periods were interposed, long-term potentiation ensued. The overall labelling of each hippocampal region was intensified significantly, indicating that glycine incorporation may be a sign not only of excitation but also of long-term potentiation. 3H-glycine was applied to frog spinal cord during rest and dorsal root stimulation. Interneurons and motor neurons excited by the afferent fibers showed intensive glycine uptake. It is concluded that the glycine labelling method is suitable for detecting neural excitation in the structures dealt with in this paper.

Animals↗

PubMed1984

Ethanol-induced modulation of the membrane potential and synaptic activity of trigeminal motoneurons during sleep and wakefulness.

In the present study we investigated the direct actions of ethanol on the membrane properties and excitatory and inhibitory postsynaptic potentials of trigeminal motoneurons in chronic cats. During states of sleep and wakefulness, extracellular and intracellular recordings were carried out together with juxtacellular (somatic and dendritic) and intracellular pressure injections of 0.05-2.5 M ethanol solutions in femtoliter quantities. Juxtacellularly applied ethanol induced: a sequence of excitatory-inhibitory alterations in firing activity which were accompanied by depolarizing-hyperpolarizing shifts in the resting membrane potential; a decrease in the amplitude of action potentials; and a depression in excitatory and inhibitory postsynaptic potentials. Intracellular ethanol injections resulted in depolarization of the membrane potential and a decrease in the amplitude of action potentials as well as a reduction in the amplitude of excitatory and inhibitory postsynaptic potentials. Both juxtacellularly and intracellularly applied ethanol affected the membrane potential and synaptic activity in a fashion that was not dependent upon the animal's behavioral state of sleep or wakefulness.

Action Potentials↗