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Results for “Inhibitory Postsynaptic Potentials”

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PubMed2001

Potentially epileptogenic dysfunction of cortical NMDA- and GABA-mediated neurotransmission in Otx1-/- mice.

Knockout Otx1 mice present a microcephalic phenotype mainly due to reduced deep neocortical layers and spontaneous recurrent seizures. We investigated the excitable properties of layer V pyramidal neurons in neocortical slices prepared from Otx1-/- mice and age-matched controls. The qualitative firing properties of the neurons of Otx1-/- mice were identical to those found in wild-type controls, but the proportion of intrinsically bursting (IB) neurons was significantly smaller. This is in line with the lack of the Otx1 gene contribution to the generation and differentiation of neurons destined for the deep neocortical layers, in which IB neurons are located selectively in wild-type rodents. The pyramidal neurons recorded in Otx1-/- mice responded to near-threshold electrical stimulation of the underlying white matter, with aberrant polysynaptic excitatory potentials often leading to late action potential generation. When the strength of the stimulus was increased, the great majority of the Otx1-/- neurons (78%) responded with a prominent biphasic inhibitory postsynaptic potential that was significantly larger than that observed in the wild-type mice, and was often followed by complex postinhibitory depolarizing events. Both late excitatory postsynaptic potentials and postinhibitory excitation were selectively suppressed by NMDA receptor antagonists, but not by AMPA antagonists. We conclude that the cortical abnormalities of Otx1-/- neocortex due to a selective loss of large projecting neurons lead to a complex rearrangement of local circuitry, which is characterized by an excess of N-methyl-d-aspartate-mediated polysynaptic excitation that is counteracted by GABA-mediated inhibition in only a limited range of stimulus intensity. Prominent postsynaptic inhibitory potentials may also act as a further pro-epileptogenic event by synchronizing abnormal excitatory potentials.

2-Amino-5-phosphonovalerate↗

PubMed1992

Presynaptic dopamine D1 receptors attenuate excitatory and inhibitory limbic inputs to the shell region of the rat nucleus accumbens studied in vitro.

1. Intracellular recordings were made from the shell region of the nucleus accumbens in an in vitro slice preparation. The mean resting membrane potential, input resistance, and action potential amplitude of these neurons were -76 +/- 1 mV, 87 +/- 5 M omega and 94 +/- 2 mV (N = 108), respectively. A sample of these neurons (N = 18) was identified as medium spiny neurons with the use of the biocytin-avidin labeling technique. 2. Electrical stimulation of the fornix, subcortical fibers, or neuropil within the nucleus accumbens shell itself elicited a depolarizing postsynaptic potential (PSP). Dopamine (10-100 microM) attenuated PSPs elicited by stimulation of all of these sites. In a paired-pulse stimulation protocol, dopamine was observed to enhance the facilitation of the test response with respect to the conditioning response. 3. The suppressive effect of dopamine was mimicked by the D1 receptor agonist SKF 82958 (10-30 microM), whereas the D2 receptor agonist quinpirole (10-30 microM) was ineffective. The action of dopamine was antagonized by the D1 receptor antagonist Sch 23390 (10-30 microM), but not by the D2 receptor antagonist sulpiride (10-50 microM) or various adrenergic receptor antagonists. 4. The PSP was usually composed of an excitatory postsynaptic potential (EPSP)-inhibitory postsynaptic potential (IPSP) sequence. Dopamine equally attenuated the excitatory and inhibitory component of the synaptic response. The attenuation of both EPSP and IPSP did not depend on membrane potential. 5. Dopamine effects on the resting membrane potential and input resistance were variable and did not correlate with changes in the PSP. Two further indications were found in favor of a presynaptic locus of dopaminergic modulation. First, the time course of the PSP was not altered during dopamine application. Second, dopamine did not attenuate depolarizations induced by bath-applied L-glutamate. In extracellular recordings, it was found that dopamine reduced the population spike but not the presynaptic fiber volley. 6. These findings strongly indicate that dopaminergic modulation of synaptic responses in neurons located in the accumbens shell region is mediated by presynaptic D1 receptors. Notably, dopamine does not exert a purely inhibitory effect on synaptic excitability in the nucleus accumbens, because it suppresses both the excitatory and inhibitory component of the synaptic response.

Afferent Pathways↗

PubMed1992

Excitatory synaptic potentials in neurons of the deep nuclei in olivo-cerebellar slice cultures.

Excitatory postsynaptic potentials evoked in neurons of the deep cerebellar nuclei, either by electrical stimulation within the nuclei in cerebellar slice cultures or by electrical stimulation of olivary explants in olivo-cerebellar co-cultures, were investigated in the rat by means of intracellular recordings. In neurons of the deep cerebellar nuclei, stimulation of the nuclear tissue, as well as stimulation of the olivary tissue, induced a fast rising excitatory postsynaptic potential, followed by an inhibitory postsynaptic potential and a long-lasting excitation. The fast rising excitatory postsynaptic potential and the following inhibitory postsynaptic potential were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione. The remaining depolarization was abolished by D-(-)-2-amino-5-phosphonovalerate, suggesting that this potential was mediated by N-methyl-D-aspartate receptors. With only D-(-)-2-amino-5-phosphonovalerate added to the bath, the slow excitation was depressed, whereas the fast excitatory and inhibitory postsynaptic potentials were not affected. In the presence of bicuculline, the 6-cyano-7-nitroquinoxaline-2,3-dione- and the D-(-)-2-amino-5-phosphonovalerate-sensitive excitatory postsynaptic potentials elicited by stimulation of the olivary tissue had the same latency, and were both graded with stimulation strength. The time-to-peak and the duration of the D-(-)-2-amino-5-phosphonovalerate-sensitive excitatory postsynaptic potentials were considerably longer than those of the 6-cyano-7-nitroquinoxaline-2,3-dione-sensitive excitatory postsynaptic potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1989

Role of excitatory amino acid receptors in synaptic transmission in area CA1 of rat hippocampus.

The new antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), which blocks responses to kainate and quisqualate, has been used in conjunction with D-2-amino-5-phosphonovalerate (APV), which blocks selectively responses to N-methyl-D-aspartate (NMDA), to determine the role of excitatory amino acid receptors in synaptic transmission. An excitatory postsynaptic potential (EPSP)-inhibitory postsynaptic potential (IPSP) sequence was evoked in CA1 neurons by stimulation of the Schaffer collateral-commissural pathway in rat hippocampal slices. CNQX (10 microM) substantially reduced the EPSP without having any effect on input resistance or membrane potential. The IPSP was also reduced provided that the stimulating electrode was place approximately 1 mm from the recording electrode. The EPSP that remained in the presence of CNQX had characteristics of an NMDA receptor-mediated potential; it had a slow timecourse, summated at high frequencies, was blocked reversibly by APV, increased greatly in size in Mg2+-free medium, and showed an anomalous voltage dependence in Mg2+-containing medium. In the presence of CNQX, an APV-sensitive polysynaptic GABAergic IPSP could be evoked, indicating that NMDA receptors can mediate suprathreshold EPSPS in inhibitory interneurons. It is suggested that either NMDA or non-NMDA receptors can, under different circumstances, mediate the synaptic excitation of pyramidal neurons and inhibitory interneurons in area CA1 of the hippocampus.

2-Amino-5-phosphonovalerate↗

PubMed1995

Pharmacological characterization of pre- and postsynaptic GABAB receptors in the deep nuclei of rat cerebellar slices.

Whole-cell current-and voltage-clamp recordings were made from deep nuclear neurons in cerebellar slices from seven- to nine-day-old rats. Baclofen, a GABAB agonist, produced a slow postsynaptic hyperpolarization associated with a decrease in input resistance. The hyperpolarization was G-protein-dependent, blocked by intracellular Cs+ and antagonized by CGP 35348, a GABAB antagonist. In dialysed neurons recorded with Cs+ -containing pipettes, baclofen suppressed deep nuclear neuronal inhibitory postsynaptic potentials and inhibitory postsynaptic currents evoked by electrical stimulations of the Purkinje cell axons. This effect was blocked by CGP 35348, indicating that the suppressions were mediated by presynaptic GABAB receptors. The inability of CGP 35348 or uptake inhibitors (nipecotic acid and NO-711) to alter the decay of inhibitory postsynaptic currents evoked by maximal stimulation suggested that GABAB receptors are not activated by the stimulation of the GABAergic input. Paired-pulse depression of inhibitory postsynaptic currents was not blocked by CGP 35348. Moreover, neither uptake inhibitors nor CGP 35348 produced any significant changes to the whole-cell current produced by a tetanic stimulation of Purkinje cell axons, suggesting that GABAB autoreceptors were also not activated by endogenous GABA release. Our findings indicate that while pre- and postsynaptic GABAB receptors are present in the deep nuclei of the rat cerebellum, they are not activated by electrical stimulation of the Purkinje cell axons.

Animals↗

PubMed1996

Diffusion, not uptake, limits glycine concentration in the synaptic cleft.

1. The question of whether active uptake limits the duration of action of the inhibitory transmitter glycine has been addressed in vivo at inhibitory synapses on the goldfish Mauthner (M) cell. The kinetics of inhibitory postsynaptic potentials and inhibitory postsynaptic currents (IPSCs) evoked antidromically and by eighth-nerve stimulation were recorded in control and in conditions expected to block glycine uptake or slow its diffusion. Theoretical considerations, based on simulated quantal currents, predicted that if diffusion was slow, rapid uptake of glycine would be required and its block would prolong the synaptic responses. 2. Temperature coefficient values for IPSC decay time constants (tau S) are in the range of 2.0 for temperatures between 15 and 23 degrees C, suggesting that diffusion is not the rate-limiting step. 3. Li+, Ch+, or N-methyl-D-glucamine were substituted for 80% of the Na+ in the extracellular fluid to analyze the effects of blocking the Na(+)-dependent glycine uptake. These procedures enhanced the maximum inhibitory shunt produced by glycine iontophoresis, leading to the suggestion that uptake may buffer the concentration of the transmitter in the cleft. In contrast, the Na+ substitutes had no effect on the tau of the recurrent collateral IPSC, which involves synchronous activation of a pool of interneurons and has a monoexponential decay (tau approximately 10-11 ms). 4. The decay phase of the disynaptic IPSCs produced by stimulating the contralateral eighth nerve has fast and slow components, with a prolonged tail lasting up to 100 ms, particularly in the case of repetitive nerve stimulation. The tail is inhibitory, as revealed by its shunt of the antidromic action potential, and it is at least partially Cl- dependent. However, it can be accelerated by superfusion with the glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and DL-2-amino-5-phosphonopentanoic acid (APV). In the presence of these blockers, the IPSC decay remains biexponential (tau fast = 5.2 and 5.9 ms, tau slow = 94 and 130 ms for single and burst stimuli, respectively). Blocking uptake in this condition did not modify tau fast or tau slow. 5. We conclude that an active uptake mechanism does not shape glycinergic IPSCs, including the longer-lasting components that might include a contribution due to persistence of the transmitter. Rather, diffusion alone is sufficient to remove glycine at a rate faster than channel unbinding. 6. To test whether glycine might diffuse to adjacent excitatory synapses and enhance activation of N-methyl-D-aspartate receptors, CNQX and APV were applied locally, by pressure, to the M cell soma, but they had no effect on the prolonged decay of eighth-nerve-evoked responses. Thus the effects of the antagonists when added to the superfusate are exerted at the network level.

2-Amino-5-phosphonovalerate↗

PubMed1992

Glucose regulation of synaptic transmission in the dorsolateral septal nucleus of the rat.

Intracellular recordings were made from neurons in the dorsolateral septal nucleus (DLSN) of rat brain slices. Lowering the concentration of extracellular glucose resulted in a concentration-dependent membrane hyperpolarization associated with a cessation of spontaneous firing. The amplitude of the excitatory postsynaptic potential (EPSP), inhibitory postsynaptic potential (IPSP), and late hyperpolarizing potential (LHP) evoked by a single stimulus applied to the fimbrial/fornix pathway was decreased when the concentration of glucose was reduced to 0-2 mM. Substitution of glucose with 2-deoxy-D-glucose (11 mM), an antimetabolite of glucose substrate, mimicked the effects of glucose depletion. Mannoheptulose (10-20 mM), a potent hexokinase blocker, and dinitrophenol (50 microM), a potent inhibitor of oxidative phosphorylation, produced both the hyperpolarization and inhibition of postsynaptic potentials, even in the presence of 11 mM glucose. The sulphonylureas, glibenclamide (10 microM) and tolbutamide (1 mM), did not antagonize the hyperpolarization and the inhibition of the postsynaptic potentials produced by glucose depletion. The amplitude of membrane depolarizations produced by pressure application of glutamate (10 mM) and the membrane hyperpolarizations produced by pressure application of either muscimol (1 mM) or baclofen (1 mM) were almost unchanged, even when glucose was reduced to 1-2 mM. These results indicate that intracellular glucose metabolism regulates the function of septal neurons, not only by changing the resting membrane potential, but also by presynaptically affecting neurotransmission between the hippocampal formation and the lateral septum.

Action Potentials↗

PubMed1997

Subthreshold receptive fields and baseline excitability of "silent" S1 callosal neurons in awake rabbits: contributions of AMPA/kainate and NMDA receptors.

The contribution of NMDA and non-NMDA receptors to excitatory subthreshold receptive fields was examined in callosal efferent neurons (CC neurons) in primary somatosensory cortex of the fully awake rabbit. Only neurons showing no traditional (suprathreshold) receptive fields were examined. Subthreshold responses were examined by monitoring the thresholds of efferent neurons to juxtasomal current pulses (JSCPs) delivered through the recording microelectrode. Changes in threshold following a peripheral conditioning stimulus signify a subthreshold response. Using this method, excitatory postsynaptic potentials and inhibitory postsynaptic potentials are manifested as decreases and increases in JSCP threshold, respectively. NMDA and non-NMDA agonists and antagonists were administered iontophoretically via a multibarrel micropipette assembly attached to the recording/stimulating microelectrode. Receptor-selective doses of both AMPA/kainate and NMDA antagonists decreased the excitability of CC neurons in the absence of any peripheral stimulation. Threshold to JSCPs rose by a mean of 20% for both classes of antagonist. Despite the similar effects of NMDA and non-NMDA antagonists on baseline excitability, these antagonists had dramatically different effects on the subthreshold excitatory response to activation of the receptive field. Whereas receptor-selective doses of AMPA/kainate antagonists either eliminated or severely attenuated the subthreshold excitatory responses to peripheral stimulation, NMDA antagonists had little or no effect on the subthreshold evoked response.

Animals↗

PubMed1994

Actions of 5-hydroxytryptamine on ventral tegmental area neurons of the rat in vitro.

Intracellular recordings were made with conventional microelectrodes and with whole-cell patch-clamp electrodes from neurons of the rat ventral tegmental area and substantia nigra zona compacta in vitro. Neurons were distinguished as principal cells and secondary cells; it is known from previous work that most principal cells contain dopamine whereas secondary cells do not. 5-Hydroxytryptamine (5-HT; 3-100 microM) depolarized (or evoked an inward current at -60 mV) 46% of 153 principal cells; a small proportion (11%) of cells were hyperpolarized (or showed outward current at -60 mV). Secondary cells were equally likely to be depolarized (or inward current at -60 mV, 30% of 80 cells) or hyperpolarized (or outward current at -60 mV, 28%). approximately 40% of each type of cell were unaffected by 5-HT. Depolarizing responses of 5-HT were mimicked by (+/-)-1-(2,5-dimethoxy-4-iodophenyl)- 2-aminopropane (DOI) and blocked by ketanserin. Hyperpolarizing responses were mimicked by dipropyl-5-carboxamidotryptamine and reversed polarity at the K+ equilibrium potential. Inhibitory postsynaptic potentials (or currents) mediated at GABAA receptors occurred spontaneously in some principal cells; they were reversibly blocked by tetrodotoxin and bicuculline. 5-HT either increased or decreased the frequency of these synaptic potentials but did not change their mean amplitude or decay time.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamines↗

PubMed1987

Observations on the actions of substance P and [D-Arg1,D-Pro2,D-Trp7,9,Leu11)substance P on single neurons of the guinea pig submucous plexus.

Intracellular recordings were made from neurons of the guinea pig submucosal plexus and the effects of substance P and the substance P analogue [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P were examined. Substance P (20-200 nM) depolarized all submucosal neurons; these depolarizations were shown to be due to a decrease in the resting (or "leak") potassium conductance of the membrane. In approximately 50% of the 46 neurons tested, superfusion with [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P (0.2-20 microM) produced a dose-dependent membrane hyperpolarization. This hyperpolarization was prevented by the alpha 2-adrenoceptor antagonist idazoxan (300 nM) or by concentrations of cobalt which abolished all spontaneous and evoked synaptic potentials, indicating that it resulted from release of noradrenaline from sympathetic nerve terminals. [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P depressed the amplitude of the three synaptic potentials recorded from submucosal neurons; the concentrations that caused 50% of the maximal inhibition of the fast excitatory postsynaptic potential, the inhibitory postsynaptic potential, and slow excitatory postsynaptic potential were 40 microM, 600 nM and 20 microM, respectively. When idazoxan was present, the substance P analogue was less effective in depressing the amplitudes of the fast and slow excitatory synaptic potentials suggesting that much of its presynaptic inhibition also resulted from release of noradrenaline. These results provide evidence that [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P releases noradrenaline from sympathetic nerves in the submucosal plexus. One effect of this is a membrane hyperpolarization; another is a presynaptic inhibition of transmitter release. These actions much limit the usefulness of this "substance P antagonist" in efforts to show that synaptic potentials, such as the slow excitatory synaptic potential, are mediated by substance P.

Animals↗

PubMed1987

Peroxide alters neuronal excitability in the CA1 region of guinea-pig hippocampus in vitro.

Effects of peroxidative damage on neuronal excitability were investigated with electrophysiological techniques in CA1 pyramidal cells of the hippocampal slice preparation. Hydrogen peroxide alone or combined with ferrous ions (peroxide/iron) is likely to produce hydroxyl free radicals through the Fenton reaction. Intracellularly recorded excitatory postsynaptic potentials and inhibitory postsynaptic potentials were significantly reduced by exposure to peroxide, while responses to iontophoretically applied GABA and glutamate were unaffected. These results suggest that peroxide has presynaptic actions. Peroxide and peroxide/iron also increased frequency adaptation; after exposure, neurons fired fewer action potentials at a lower frequency in response to the same depolarizing current step. A voltage clamp analysis revealed that the potassium currents were unaffected by peroxide/iron. Calcium current was not obviously altered by exposure to peroxide. Sodium spike threshold was also unaffected. Calcium spike threshold was significantly increased by peroxide. This action of peroxide may underlie its presynaptic actions. It is concluded that peroxide produces both presynaptic and postsynaptic damage. This damage is likely to result from the production of free radicals which have been postulated to underlie a number of pathological states.

Action Potentials↗

PubMed1988

Electrophysiology of the mammalian cerebellar cortex in organ culture.

A direct comparison was made between the electrical properties of rat Purkinje cells in cerebellar organotype cultures and those in acute slices from age-matched animals. Cultures were prepared from 9-11-day-old animals. Intracellular recordings were made 5-12 days later, at which time the folia architecture of the cerebellum was still well preserved. The resting membrane potentials and input resistances of Purkinje cells in cultured and acute slice preparations from young animals were comparable to those of mature Purkinje cells in slices. Neurons from animals younger than 14 days differed from mature Purkinje cells in that they fired at low frequencies in response to outward current pulses. The latter property was found in all cultured neurons studied, independent of their time in culture. These action potentials were generated by Na+ and Ca2+ conductances as shown by the application of selective channel blockers. Cultured or acute slice preparations from animals younger than 11 days shared other immature electroresponsive features. In both groups, Na+-dependent plateau depolarizations were observed in less than 10% of Purkinje cells unless K-conductances were blocked, and considerable membrane depolarization was often required to elicit Ca2+-dependent action potentials. These findings are compatible with the relative prominence of voltage-dependent outward currents in immature Purkinje cells, a property which may be enhanced in culture. The injection of hyperpolarizing current pulses revealed a marked time-dependent anomalous rectification in all Purkinje cells. At the breaks of such pulses, several events were observed. In all cells, a rebound conductance was identified which could generate post-anodal spike bursts. In cultured neurons, however, hyperpolarizing pulses were also followed by a slow return to resting potential. This membrane potential profile was similar to that produced by the activation of an A conductance. Experiments on acute slices from animals of different ages (P9-P17) showed that this A-like conductance was expressed only during a brief period in Purkinje cell development. A higher level of spontaneous synaptic activity was observed in cultured than in acute slice preparations. Both unitary excitatory postsynaptic potentials and inhibitory postsynaptic potentials could be elicited in the former by parallel fiber stimulation, and could be fully reversed by outward or inward transmembrane current injections, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗

PubMed2000

Roles of ion channels in EPSP integration at neuronal dendrites.

Many different kinds of voltage-gated ion channels (Na+ channels, K+ channels, Ca2+ channels) exist at neuronal dendrites. Integration of dendritic electric signals (excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs) and action potentials) and/or non-electric signals (Ca2+ and second messengers) occurs in restricted dendritic compartments consisting of spines and adjacent fine dendrites. Voltage-gated ion channels at neuronal dendrites play crucial roles in the integration of dendritic signals. Dendritic signals, in turn, play important roles in the modulation of local dendritic physiological functions (e.g. input-specific synaptic plasticity, long-term potentiation (LTP) and long term depression (LTD)). A combined experimental and theoretical approach is a good way to clarify the biophysical behaviors of dendritic ion channels. Analyses of dendritic ion channels can open the door to a new wave of discoveries about EPSP integration at neuronal dendrites.

Animals↗

PubMed1992

Membrane and synaptic properties of developing lateral geniculate nucleus neurons during retinogeniculate axon segregation.

During the first postnatal month in the ferret (Mustela putorius furo), the projections from the retina to the lateral geniculate nucleus (LGN) become segregated into eye-specific layers and ON and OFF sublayers, a process that is thought to depend in part on neuronal activity. Remarkably, virtually nothing is known about the physiological features of LGN neurons during this period. We have recorded intracellularly from 46 A-layer neurons in slices of the ferret LGN between the ages of postnatal days 7 and 33. The passive membrane properties and current-voltage relationships of the developing neurons were similar in many, though not all, respects to those of adult LGN neurons. Action potentials in younger animals were smaller in amplitude and longer in duration than in older animals, but cells at all ages were capable of producing spike trains whose latency and spike number varied with stimulus intensity. In addition, cells at all ages responded with low-threshold potentials upon release from hyperpolarization. Slightly more than half of the LGN neurons responded to optic tract stimulation with excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), or EPSP-IPSP pairs, beginning with the youngest ages. Thus, as early as the second postnatal week, and much before the onset of pattern vision, LGN neurons have many of the membrane and synaptic properties of adult thalamic neurons. These data are consistent with LGN cells playing a significant role in activity-dependent reshaping of the retinogeniculate pathway.

Action Potentials↗

PubMed1992

Synaptic mechanisms in sympathetic preganglionic neurons.

Intracellular recordings from sympathetic preganglionic neurons (SPNs) in adult cat and neonatal rat spinal cord slices reveal four types of synaptic potentials, namely, excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and slow EPSPs in both preparations, and a slow IPSP in cat SPNs. Pharmacological studies show that glutamate or a related excitatory amino acid and glycine are the probable mediators of EPSPs and IPSPs. There may be heterogenous mediators of slow EPSPs; substance P, serotonin, norepinephrine, and epinephrine are all probable mediators of slow EPSPs in subpopulations of SPNs. In the case of slow IPSPs, norepinephrine appears to be the likely transmitter. Finally, stimulation of ventral roots elicits a synaptic potential that appears to be caused by glutamate released from afferent fibers in the ventral roots. Our results indicate that a multitude of synaptic mechanisms exist in the rat SPNs by means of which inputs arising from sensory and supraspinal neurons are processed in a timely and orderly manner, thus ensuring highly organized but differentiated outputs to multiple peripheral target cells.

Animals↗

PubMed2004

Coupling between feline cerebellum (fastigial neurons) and motoneurons innervating hindlimb muscles.

The aims of the study were twofold: (1) to verify the hypothesis that neurons in the fastigial nucleus excite and inhibit hindlimb alpha-motoneurons and (2) to determine both the supraspinal and spinal relays of these actions. Axons of fastigial neurons were stimulated at the level of their decussation in the cerebellum, within the hook bundle of Russell, in deeply anesthetized cats with only the right side of the spinal cord intact. The resulting excitatory postsynaptic potentials and inhibitory postsynaptic potentials were analyzed in motoneurons on the left side of the lumbar enlargement. Postsynaptic potentials evoked by the first effective stimulus were induced at latencies <2 ms from descending volleys and <1 ms from interneuronally relayed volleys, indicating a trisynaptic coupling between the fastigial neurons and alpha-motoneurons, via commissural interneurons on the right side. Cerebellar stimulation facilitated the synaptic actions of both vestibulospinal and reticulospinal tract fibers. However, the study leads to the conclusion that trisynaptic fastigial actions are mediated via vestibulospinal rather than reticulospinal tract fibers [stimulated within the lateral vestibular nucleus (LVN) and the medial longitudinal fascicle (MLF), respectively]. This is indicated firstly by collision between descending volleys induced by cerebellar stimulation and volleys evoked by LVN stimuli but not by MLF stimuli. Second, similar cerebellar actions were evoked before and after a transection of MLF. Mutual facilitation between the fastigial and reticulospinal, as well as between the fastigial and vestibulospinal actions, could be due to the previously reported integration of descending vestibulospinal and reticulospinal commands by spinal commissural interneurons.

Animals↗

PubMed2003

Electrophysiological properties and input-output organization of callosal neurons in cat association cortex.

Intracellular recordings from association cortical areas 5 and 7 were performed in cats under barbiturate or ketamine-xylazine anesthesia to investigate the activities of different classes of neurons involved in callosal pathways, which were electrophysiologically characterized by depolarizing current steps. Excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and/or antidromic responses were elicited by stimulating homotopic sites in the contralateral cortical areas. Differential features of EPSPs related to latencies, amplitudes, and slopes were detected in closely located (50 microm or less) neurons recorded in succession along the same electrode track. In contrast to synchronous thalamocortical volleys that excited most neurons within a cortical column, stimuli applied to homotopic sites in the contralateral cortex activated neurons at restricted cortical depths. Median latencies of callosally evoked EPSPs were 1.5 to 4 ms in various cortical cell-classes. Fast-rhythmic-bursting neurons displayed EPSPs whose amplitudes were threefold larger, and latencies two- or threefold shorter, than those found in the three other cellular classes. Converging callosal and thalamic inputs were recorded in the same cortical neuron. EPSPs or IPSPs were elicited by stimulating foci spaced by <1 mm in the contralateral cortex. In the overwhelming majority of neurons, latencies of antidromic responses were between 1.2 and 3.1 ms; however, some callosal neurons had much longer latencies, <or=18.5 ms. Some neurons were excited monosynaptically through the callosal pathway and identified antidromically from appropriate thalamic nuclei, thus revealing a callosal-corticothalamic pathway. Data are discussed in relation to the commissural spread of fast and slow normal oscillations as well as paroxysmal activities.

Animals↗

PubMed1982

Role of the cortical neuron: integrator or coincidence detector?

A model was constructed of the relations between the incoming excitatory postsynaptic potentials and inhibitory postsynaptic potentials to the intracellular membrane potential fluctuations and to the firing rate of a single neuron. From this model, the strength of synapses was assessed in two ways: 1) the ability of several synchronous presynaptic spikes to initiate a postsynaptic spike, termed the synchronous gain of the synapse; and 2) the ability of several asynchronous presynaptic spikes to add a spike to the output spike train, called the asynchronous gain. It was found that for the conditions prevailing in the brain's cortex, the synchronous gain is almost always higher. It appears that the cortical neurons act as coincidence detectors, and that the appropriate code for the higher cortical functions is coincidence and not firing rate.

Action Potentials↗