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PubMed1986

Tectal neurons of the frog: intracellular recording and labeling with cobalt electrodes.

With the aid of cobalt-filled intracellular electrodes, responses evoked by electrical and visual stimulation were recorded from tectal neurons. Diffuse light and "edge" and "spot" stimuli were used for visual stimulation; electrical stimuli were delivered by means of bipolar electrodes to the optic tract. The cells were subsequently filled with cobalt for a correlative histological study. The following types of neurons were distinguished: (1) Pear-shaped neurons with restricted and broad dendritic fields occurring in tectal layers 8, 6, 4, and 2. In one group, the dendrites bore beads and small protrusions and the short axon arborized within, or close to, the dendritic arbor. They responded mostly with inhibitory postsynaptic potentials to the various stimulations. This type of neuron was interpreted to be a tectal interneuron. In the second group the dendrites were smooth, the dendritic arbor was large, and the axon could be followed to layer 7 in a few cases. Excitatory activities with frequent spike discharges prevailed in their responses. They were regarded as efferent neurons of the tectum. (2) Large ganglionic neurons showed a greater variation in form than has been described in previous Golgi studies. Their responses to the different stimulations were also very variable. The axons of five neurons could be followed to the dorsal part of the thalamus, to the postoptic commissural system, and to the direct and crossed tectobulbar tract. These axons emitted several collaterals to tectal, pretectal, and tegmental structures. (3) A single stellate neuron was impaled in layer 9. It responded only to electrical stimulation with excitation. (4) Deep bipolar neurons were not mentioned in earlier works. Their somata were found in layer 6; the vertically oriented dendrites arborized in plexiform layers 7, 5, and 3, over a distance of more than 1 mm. These cells were sensitive only to electrical stimulation.

Animals↗

PubMed1993

Heterogeneity of rat corticospinal neurons.

In order to examine the degree of diversity within a population of cortical projection neurons, rat corticospinal cells were retrogradely labeled in vivo by injecting rhodamine-tagged microspheres into the cervical spinal cord, and subsequently studied electrophysiologically and anatomically in neocortical slices maintained in vitro, by use of standard current clamp techniques and a double-labeling protocol (Tseng et al., J. Neurosci. Meth. 37:121-131, 1991). Three different subgroups were distinguished on the basis of their spiking behavior: (1) Adapting cells had a marked fast (50 ms) and slow phase (200 ms) of spike frequency adaptation; (2) regular spiking (RS) cells had only a period of fast adaptation; (3) some regular spiking neurons had prominent depolarizing afterpotentials (DAPs) and could generate bursts of spikes, often in repetitive fashion (RSDAP cells). Subgroups of RSDAP cells had different patterns of burst responses to depolarizing current pulses, suggesting differences in the types and/or sites of underlying ionic conductances. Adapting cells had a slightly higher membrane input resistance and more prominent slow hyperpolarizing afterpotentials than RS and RSDAP neurons; however, the activation of presumed anomalous rectifier current by intracellular hyperpolarizations was less prominent in adapting neurons. Orthodromic stimulation in layer I evoked presumed excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs)in all three types of cells, but prominent short-latency IPSPs were found in a higher percentage of adapting neurons. The morphology of electrophysiologically characterized corticospinal neurons was studied following intracellular injection of biocytin. All three spiking types were typical layer V pyramids with apical dendrites reaching layer 1, basal dendrites in infragranular layers, and deep-directed axons that had a moderate density of local collaterals in lower cortical layers. The profuseness of dendrites, examined by Sholl's analysis of two-dimensional, camera lucida-reconstructed neurons was comparable in the three neuronal subgroups, although a smaller somatic area and more slender apical dendritic trunk were found in adapting neurons. Our results suggest that corticospinal cells in rats are a heterogeneous population of projection neurons with respect to their spiking behavior, membrane properties, synaptic connections, and, to a lesser extent, their morphology. This diversity revealed in vitro adds new complexity to the classification of corticospinal neurons.

Action Potentials↗

PubMed1995

Time-dependent rundown of GABA response in mammalian cns neuron during experimental anoxia.

Gamma-Aminobirtyric acid (GABA) is one of the major neurotransmitters in the mammalian central nervous system (CNS). The activation of post-synaptic GABAA receptor-chloride channel complex is thought to underlie inhibitory postsynaptic potentials ubiquitously in various CNS regions. GABAA receptors are modulated by convulsant, hypnotic-anticonvulsant, anxiolytic and anxiogenic agents and endogenous agents such as nurosteroids and intracellular calcium, ATP, and cyclic AMP. The function of GABAA receptor in CNS neuron is also affected by some pathophysiological processes, e.g., anoxia. For example, it is currently believed that delayed neuronal death after brain ischemia results from excessive cell excitability and/or loss of inhibition. In the present study, we investigated how the GABA-gated chloride current is affected by anoxic conditions. All experiments were carried out on neurons freshly dissociated from rat CNS by the use of both conventional and nystatin perforated patch recording configurations. The GABA response showed a considerable rundown with time in anoxic condition. The rundown was prevented by adding either ouabain or SPAI-I (Na+-K+ ATPase inhibitor-I), suggesting that the experimental anoxia reduced GABA response by decreasing intracellular ATP synthesis. This result was also confirmed by finding that the direct decrease of intracellular ATP concentration using a conventional whole-cell patch recording mode inhibited the GABA-gated chloride response in mammalian CNS neurons.

Adenosine Triphosphate↗

PubMed1994

Suppression and long latency excitation of single spinal motoneurons by transcranial magnetic stimulation in health, multiple sclerosis, and stroke.

Whether or not suppression at the level of the spinal motoneuron plays a role in motor deficits such as central paresis is unknown. In this study suppression in the firing of tonically active low threshold single motoneurons following low intensity transcranial magnetic stimulation is described in health and disease. Changes in firing probability in the absence of an early excitatory response were studied in a total of 14 motor units from 4 healthy subjects, 5 patients with multiple sclerosis, and 1 patient with stroke. Firing probability began to fall 18-59 ms after the stimulus and remained low for a period of 27-133 ms. There were no obvious differences between the three subject groups. The change in firing probability was not associated with specific physical signs. Late rises in firing probability were seen in 7 of the 14 motor units at latencies that were similar to the secondary peak which is known to occur with higher stimulus intensities. It is argued that the mechanism of partial suppression is not dependent on the full integrity of the pyramidal tract and is likely to involve a transient withdrawal of descending excitatory drive rather than an inhibitory postsynaptic potential at the spinal motoneuron.

Adult↗

PubMed1982

The ionic dependence of black widow spider venom action at the stretch receptor neuron and neuromuscular junction of crustaceans.

The effects of black widow spider venom (BWSV) on the crayfish stretch receptor and the lobster neuromuscular junction were examined. In crayfish stretch receptor neurons, BWSV caused a slight hyperpolarization followed by a large depolarization. The venom-induced depolarization of the stretch receptor was caused by an increase in membrane conductance to Na+ and Ca2+. Black widow spider venom also caused an increase in the frequency of miniature inhibitory postsynaptic potentials recorded in the stretch receptor. The ability of BWSV to increase the frequency of miniature excitatory postsynaptic potentials (MEPSPs) at the lobster neuromuscular junction was dependent on the divalent cation composition of the bathing medium. Ringer solutions containing Ca2+ supported the greatest venom-induced increase in MEPSP frequency, Mg2+ and Mn2+ supported a moderate increase in MEPSP frequency, while Co2+ and Zn2+ blocked this venom effect entirely. Black widow spider venom did not block axonal conduction in lobster walking leg axons or in the axon of the crayfish stretch receptor. The results suggest that in crustaceans, BWSV interacts specifically with membrane of the soma-dendritic region of the stretch receptor and with nerve terminal membrane, causing an increase in Na+ and Ca2+ conductance.

Animals↗

PubMed1987

Contrasting properties of K+ conductances induced by baclofen and gamma-aminobutyric acid in slices of the guinea pig hippocampus.

Properties of membrane K+ conductances induced by baclofen and gamma-aminobutyric acid (GABA) in the hippocampus were investigated by using guinea-pig brain slices. Baclofen hyperpolarized the membrane and decreased the input resistance of pyramidal cells through the activation of a membrane K+ conductance. GABA caused a biphasic response in pyramidal cells, consisting of hyperpolarizing and depolarizing components. Combined application of picrotoxin and bicuculline eliminated the major part of the depolarizing component of the biphasic response and produced a relatively pure hyperpolarizing response which was also mediated by an increase in K+ conductance. The K+ conductance change induced by baclofen showed prominent inward rectification. However, the K+ conductance induced by GABA did not show an obvious rectifying property. The K+ conductance activated by baclofen was strongly antagonized by a low concentration (5 x 10(-6) M) of 4-aminopyridine (4-AP). In contrast, the K+ conductance activated by GABA was insensitive to 4-AP even at a high concentration of 10(-3) M. The slow inhibitory postsynaptic potential (slow i.p.s.p.) evoked by stimulation of the mossy fibres was totally suppressed by a low concentration of baclofen (5 x 10(-6) M). Whereas GABA (10(-3) M) decreased the amplitude of the slow i.p.s.p., the reduction of the amplitude was proportional to the decrease in the amplitude of the electrotonic potentials produced by constant inward current injections. These results suggest that the hyperpolarizations induced by GABA and baclofen may be generated by K+ conductances of different kinetic and pharmacologic properties.

Animals↗

PubMed1987

In vitro studies of the role of gamma-aminobutyric acid in inhibition in the lateral septum of the rat.

Focal stimulation, stimulation of the fimbria, and stimulation of the medial septal area result in an inhibitory postsynaptic potential (IPSP) in lateral septal neurons. Increased stimulus intensity results in the appearance of a late hyperpolarizing potential (LHP). Treatment of the slice with bicuculline methiodide or picrotoxin results in blockade of the IPSP. When present, LHPs are enhanced in the presence of bicuculline or picrotoxin. Spontaneous and evoked IPSPs reverse near -70 mV, and LHPs reverse near -90 mV. Iontophoretic application of gamma-amino-butyric acid (GABA) results in hyperpolarizing, depolarizing, or biphasic potentials. Treatment with bicuculline or picrotoxin results in depression of biphasic GABA responses that appears selective for the depolarizing portion of the potential. At high concentrations of bicuculline, a portion of the hyperpolarizing GABA potential persists. The reversal potential of the depolarizing GABA potential is near -30 mV, and the reversal potential of monophasic hyperpolarizing GABA potential is near -70 mV. The bicuculline-resistant hyperpolarizing GABA response has a reversal potential near -90 mV. GABA activates three separate conductances on septal neurons, which are similar to those reported on hippocampal neurons. The resistance of the hyperpolarizing GABA potential to bicuculline appears to be due to the presence of a GABA-activated potassium conductance, which is similar to that activated by baclofen.

Animals↗

PubMed1988

Physiological and morphological characterization of striatal neurons transplanted into the striatum of adult rats.

Physiological and morphological properties of transplanted striatal neurons (TSNs) were examined in an in vitro slice preparation. Fetal striatal tissue (E13-14) was implanted as a dissociated cellular suspension into the striatum of adult rats. Intracellular records were obtained from TSNs 2-6 weeks after transplantation. TSNs exhibited biophysical, morphological, and synaptic properties characteristic of normal striatal neurons, despite the disruption involved in processing of the fetal tissue. Differences were observed, however, between the TSNs and host striatal neurons. TSNs consistently had higher input resistance values than host striatal neurons as determined by neuronal responses to intracellular current injection. Stimulation of adjacent host striatum elicited both excitatory and inhibitory postsynaptic potentials in TSNs. By contrast, the same stimuli elicited only excitatory responses in host striatal neurons. Morphologically, TSNs resembled host medium-size spiny neurons as demonstrated by intracellular injection of lucifer yellow. However, the complexity of dendritic branching and the density of spines on the dendrites were less than that observed for host striatal neurons. It was concluded that during the posttransplantation period studied, TSNs possess neuronal properties expected of developmentally immature striatal neurons.

Action Potentials↗

PubMed1992

ATP-sensitive K+ channels mediate an IPSP in dorsal horn neurones elicited by sensory stimulation.

Nociceptive dorsal horn neurones, which are involved in the processing of pain-related information, are inhibited by input from vibration-sensitive, large diameter primary sensory fibres (Wall and Cronly-Dillon, 1960; Salter and Henry, 1990a,b). We have reported previously that the inhibition of spinal nociceptive neurones by vibration is mediated by adenosine acting through P1-purinergic receptors (Salter and Henry, 1987). In a number of different types of cell, adenosine is known to activate K+ currents (Gerber et al., 1989; Greene and Haas, 1985; Proctor and Dunwiddie, 1987; Segal, 1982; Trussell and Jackson, 1987) and we have recently found that the adenosine-mediated inhibition of nociceptive neurones by vibration is the result of an inhibitory postsynaptic potential (IPSP), which is, indeed, caused by a K+ conductance (De Koninck and Henry, 1988, 1992). It has been reported that adenosine-activated K+ channels in cardiac muscle cells are the ATP-sensitive K+ channels (Kirsch et al., 1990). Therefore, we questioned whether these channels might mediate the purinergic IPSP we have observed in nociceptive dorsal horn neurones. We report here that glibenclamide, a blocker of ATP-sensitive K+ channels (Ashcroft, 1988; Schmid Antomarchi et al., 1987a,b), blocks the inhibition of nociceptive neurones by vibratory stimulation when this compound is administered locally by iontophoresis or systemically by intravenous injection. In addition, direct intracellular injection of ATP was found to block the IPSP evoked by vibratory stimulation. These data indicate that the purinergic IPSP in nociceptive spinal neurones is mediated via ATP-sensitive K+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1994

Differences in the Cs block of baclofen and 4-aminopyridine induced potassium currents of guinea pig CA3 neurons in vitro.

Single-electrode current- and voltage-clamp techniques were employed to study responses elicited by (-)baclofen or gamma-aminobutyric acid (GABA) and 4-aminopyridine (4-AP) induced inhibitory postsynaptic potentials in CA3 pyramidal neurons in guinea pig hippocampal slices. All drugs were applied by the bath to submerged slices in which fast synaptic transmission was blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM), bicuculline (50 microM), and picrotoxin (50 microM). (-)Baclofen (0.5 microM) and GABA (1 mM) induced equivalent-sized hyperpolarizations and input resistance decreases. The agonist induced hyperpolarization or current and 4-AP induced hyperpolarizations or currents (4-AP induced K-IPSPs or IPSCs) reversed in sign near the K-equilibrium potential (EK). The GABAB receptor antagonists, OH-saclofen (500 microM) and CGP 35348 (100 microM), reduced (-)baclofen responses, and 4-AP induced K-IPSPs, suggesting that they were mediated by GABAB receptors. Intracellular tetraethylammonium-, and extracellular barium-ions (1 mM) diminished the (-)baclofen induced current and 4-AP induced K-IPSCs. Intracellular Cs-ions blocked the (-)baclofen induced outward current at resting membrane potential but did not grossly affect the inward current recorded at membrane potentials negative to EK. 4-AP induced inwardly or outwardly directed K-IPSCs were not blocked by intracellular Cs-ions. Extracellular Cs-ions (5 mM) blocked the (-)baclofen induced inward K-current, but did not block 4-AP induced inwardly directed K-IPSCs. In conclusion, we found differences in the Cs block of activated by (-)baclofen or the endogenous transmitter GABA.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗

PubMed1997

Acute exposure to 25-hydroxy-cholesterol selectively reduces GABAb and not GABAa receptor-mediated synaptic inhibition.

Intracellular recording techniques were used to study the effects of the cholesterol oxide, 25-hydroxycholesterol (25-OH-Chol), on gamma-aminobutyric acid (GABA) receptor-mediated inhibitory postsynaptic potentials (IPSPs) in brain slices of the rat lateral septum. Superfusion of 25-OH-Chol increased the peak amplitude of the GABAa IPSP in more than half of the neurons tested, many of which exhibited a similar increase in the GABAb IPSP. However, some neurons exhibited a gradual decrease in input resistance and a selective reduction or blockade of the GABAb IPSP during prolonged exposure. Cholesterol partly mimicked the effects of 25-OH-Chol. These findings indicate that 25-OH-Chol can selectively reduce or block metabotropic GABAb while sparing ionotropic GABAa receptor-mediated synaptic inhibition. Our results indicate that brain slices can be used to study the effects of short term alterations in cholesterol on the excitability and synaptic integration properties of neurons.

Animals↗

PubMed1996

Vertical signal flow and oscillations in a three-layer model of the cortex.

A model of vertical signal flow across a layered cortical structure is presented and analyzed. Neurons communicate through spikes, which evoke an excitatory or inhibitory postsynaptic potential (spike response model). The layers incorporate two anatomical features-dendritic and axonal arborization patterns and distance-dependent time delays. The vertical signal flow through the network is discussed for various stimulus conditions using two different, but typical, axonal arborization patterns. We find stationary as well as oscillatory response, but the oscillatory response may be restricted to a single layer. Confronted with conflicting stimuli the network separates the patterns through phase-shifted oscillations. We also discuss two hypothetical animals, to be called "cat" and "mouse." These have different axonal arborizations, which give rise to a different oscillatory response (if any) of the various layers.

Axons↗

PubMed1994

Effects of strychnine on fictive swimming in the lamprey: evidence for glycinergic inhibition, discrepancies with model predictions, and novel modulatory rhythms.

1. Inhibitory postsynaptic potentials (ipsps) produced by two classes of interneurons, CC (Contralateral and caudal projecting) and lateral interneurons, were tested for strychnine sensitivity using paired intracellular recordings in the lamprey spinal cord. The ipsps were partially blocked by 0.2-0.5 microM strychnine and were completely blocked by 5 microM strychnine. Thus, the ipsps may be glycinergic. 2. These interneurons are key participants in a proposed circuit model for fictive swimming. A connectionist-type computer simulation of the model demonstrated that the cycle period of the network increased with decreasing ipsp strength. 3. Application of strychnine (0.1-0.5 microM) to the spinal cord during fictive swimming induced by an excitatory amino acid increased cycle period, consistent with previous reports, but at odds with stimulation predictions. 4. Strychnine also produced slow rhythmic modulation of fictive swimming (period = 12 s) which maintained left-right alternation and rostral-caudal coordination. Auto- and cross-correlation analyses revealed that the slow modulation was present in a weaker form in most control preparations during fictive swimming. 5. Since the proposed model for the swimming pattern generator in the lamprey spinal cord does not predict the observed speeding with strychnine, nor the slow modulatory rhythm, it appears to be deficient in its present formulation.

Animals↗

PubMed1994

Simulation of GABAB-receptor-mediated K+ current in thalamocortical relay neurons: tonic firing, bursting, and oscillations.

Until recently, the presence of gamma-aminobutyric acid (GABA) in the thalamus has usually been associated with the 'classical' GABAA Cl(-)-dependent receptor. However, the discovery of a slower, long-lasting, K(+)-dependent inhibitory postsynaptic potential (IPSP) mediated by GABAB receptors in projection cells of the dorsal lateral geniculate nucleus has led researchers to reconsider its role in modulating the behavior of these cell groups (Crunelli et al. 1988; Crunelli and Leresche 1991). Of particular interest is the role of this K+ current in the activation of the low-threshold Ca2+ current, IT, of thalamocortical relay (TCR) neurons responsible for bursting activity (Jahnsen and Llinás 1984a,b). Considering the time scale on which the GABAB-receptor-activated K+ current operates, it is ideally suited to foster sustained rhythmicity in TCR cells reciprocally connected to neurons of the nucleus reticularis thalami (NRT) as well as interneurons at frequencies observed in vivo (Steriade and Llinás 1988). In this study we show that small changes in the duration and amplitude of the K(+)-dependent IPSPs can have marked effects on TCR cell groups including a shift from single-spike firing (tonic) to bursting behavior. We further show that a single GABAB-mediated IPSP is sufficient to activate the low-threshold Ca2+ response and that sustained oscillations are possible given the presence of excitatory TCR connections to GABAergic NRT cells or interneurons of the dorsal lateral thalamus. These combined effects are examined with regard to their role in generating the well known 7-14 Hz spindle rhythm as well as slower 6-8 Hz oscillations observed in TCR cells in vivo (Steriade and Llinás 1988).

Action Potentials↗

PubMed1991

Excitation and inhibition of trigeminal motoneurons by palatal stimulation.

Excitation and inhibition of jaw-closing motoneurons (Masseteric and Temporal Motoneurons, Mass. and Temp. Mns) during transient jaw closing, the so-called jaw-closing reflex, and prolonged jaw opening elicited by palatal stimulation were studied. By pressing the anterior palatal surfaces sustained jaw opening was elicited, suggesting that sustained jaw opening results from inhibition of tonic background activity of jaw-closing motoneurons by inhibitory postsynaptic potentials (IPSPs) elicited by mechanical stimulation of the anterior palatal mucosa. Recordings showed that the onset of IPSPs was 80 ms earlier than the onset of jaw opening. Application of diffuse pressure stimulation to the posterior palatal surfaces elicited bursts of spikes triggered on excitatory postsynaptic potentials (EPSPs), suggesting that mechanosensory receptors from the posterior palatal mucosa send excitatory synaptic inputs to jaw-closing motoneurons. Furthermore, it is suggested that mechanosensory inputs from the posterior palatal mucosa may excite neurons in the central pattern generator and provide the motor patterns responsible for jaw closure during the jaw-closing reflex. We have demonstrated that excitation of Mass. Mns innervating the deep masseter muscle mainly contributed to maintaining the occlusal phase of jaw closure during the jaw-closing reflex. However, the onset of EPSPs was 100 to 160 ms (n = 27) earlier than the onset of jaw closure. In studies on spontaneously occurring jaw closure it was demonstrated that there was a proportional increase in the number of spikes of the Temp. Mn and the mechanical response (jaw closure).

Animals↗

PubMed1995

Phasic motor activity reduction occurring with horizontal rapid eye movements during active sleep in human.

We describe the phasic reduction of motor activity occurring with horizontal rapid eye movements (REMs) during active sleep in 15 children (12 healthy children and 3 patients with severe brain damage). A REM-related decrease in intercostal muscle activity was demonstrated by averaging integrated surface electromyograms. In the healthy subjects, this reduction had a mean latency from the REM onset of 37.1 ms and a duration of 225.9 ms. This phenomenon was also observed in the 3 patients who had lost cerebral function. We hypothesized a brainstem origin for the effect. A REM-related mentalis muscle activity loss, detected by averaging mentalis muscle twitches, was observed in 10 healthy children among the subjects. This loss began at 59.1 ms before the onset of REMs and lasted for 230.2 ms on average. In addition, a transient decrease in integrated REM activity surrounding mentalis muscle twitches (a twitch-related reduction of REMs) was observed. We discuss the similarity between REM-related phasic reduction of muscle activity obtained for intercostal and mentalis muscles and pontogeniculo-occipital (PGO) wave-related inhibitory postsynaptic potentials reported for feline lumbar and trigeminal motoneurons, respectively. We then assume the presence of a phasic event generator, functioning during active sleep in healthy humans, which triggers at least three generators; that is, the generator of PGO waves (or REMs), motor inhibition, and of motor excitation including muscle twitches.

Brain Stem↗

PubMed1991

Morphological characterization of rat entorhinal neurons in vivo: soma-dendritic structure and axonal domains.

We used in vivo intracellular labeling with horseradish peroxidase in order to study the soma-dendritic morphology and axonal projections of rat entorhinal neurons. The cells responded to hippocampal stimulation with inhibitory postsynaptic potentials, and thus likely received direct or indirect hippocampal input. All cells (n = 24) showed extensive dendritic domains that extended in some cases for more than 1 mm. The dendrites of layer II neurons were largely restricted to layers I and II or layers I-III, while the dendrites of deeper cells could extend through all cortical layers. Computed 3D rotations showed that the basilar dendrites of deep pyramids extended roughly parallel to the cortical layering, and that they were mostly confined to the layer containing the soma and layers immediately adjacent. Total dendritic lengths averaged 9.8 mm +/- 3.8 (SD), and ranged from 5 mm to more than 18 mm. Axonal processes could be visualized in 21 cells. Most of these showed axonal branching within the entorhinal cortex, sometimes extensive. Efferent axonal domains were reconstructed in detail in 3 layer II stellate cells. All 3 projected axons across the subicular complex to the dentate gyrus. One of these cells showed an extensive net-like axonal domain that also projected to several other structures, including the hippocampus proper, subicular complex, and the amygdalo-piriform transition area. The axons of layer III and IV cells projected to the angular bundle, where they continued in a rostral direction. In contrast to the layer II, III and IV cells, no efferent axonal branches leaving the entorhinal cortex could be visualized in 5 layer V neurons. The data indicate that entorhinal neurons can integrate input from a considerable volume of entorhinal cortex by virtue of their extensive dendritic domains, and provide a further basis for specifying the layers in which cells receive synaptic input. The extensive axonal branching pattern seen in most of the cells would support divergent propagation of their activity.

Animals↗

PubMed1987

Long-term effects of 3-acetylpyridine-induced destruction of cerebellar climbing fibers on Purkinje cell inhibition of vestibulospinal tract cells of the rat.

The inhibitory action of Purkinje cells on vestibulospinal tract (VST) cells was examined in rats deprived of climbing fibers with 3-acetylpyridine (3-AP) intoxication. In order to resolve discrepancies raised in previous studies with various means, special efforts were devoted to directly estimate Purkinje cell inhibition at synaptic levels by using intracellular recording, to avoid sampling bias by using a systematic survey of VST cells in each rat, and to evaluate the time-dependence of the effects of climbing fiber deafferentation by regular testing at 10 day intervals until 160 days after 3-AP intoxication. As compared with 661 VST cells impaled in 15 control rats, 1771 VST neurons impaled in 29 3-AP-treated rats revealed four basic changes in the monosynaptic inhibitory postsynaptic potentials (IPSPs) induced by stimulation of Purkinje cell axons in the white matter of the cerebellar anterior lobe. First, the rate of IPSP occurrence among VST cells was 0.64 in control rats; at more than 10 days after 3-AP intoxication it decreased gradually, down to 0.37-0.38 at the 70th-81st days, and thereafter increased up to 0.53 by the 160th day. The rate of IPSP occurrence varied considerably between the rostral and caudal regions, and also between the dorsal and ventral divisions of the VST cell population, but its reduction after 3-AP intoxication occurred approximately in parallel in all divisions. Second, IPSPs evoked with standard 500 microA pulse stimuli were smaller in size on and after day 10. The reduction of IPSP size was by as much as 53% of control values at the 70th-101st days in the dorsal division, but no significant change occurred in the ventral division of the VST cell population. Third, the latency of the IPSPs was prolonged by about 0.25 ms on and after day 10. Analysis of the relationship between the IPSP latency and the dorsoventral location of VST cells in the medulla suggests that the major cause for the prolongation of IPSP latency is an increased synaptic delay at Purkinje cell axon terminals. Fourth, the cerebellar stimulation threshold for evoking IPSPs was almost always below 100 microA in control rats, but values of 100-250 microA were common after the 40th day. Thus, climbing fiber deafferentation exerts long-term influences on excitability of Purkinje cell axons, and on the connectivity and synaptic transmission from Purkinje cell axons to VST cells.

Animals↗