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At least 595 records · Page 33Linked to original sources
PubMed1997

Deafferentation weakens excitatory synapses in the developing central auditory system.

Decreased excitatory synaptic activity during development often leads to pre- and postsynaptic atrophy, as assessed anatomically. The present study considers the effect of decreased excitatory transmission on the maturation of synaptic strength. Towards this end, cochlear nucleus neurons, which project to the ipsilateral lateral superior olive (LSO), were denervated in gerbils at postnatal day 7, before the onset of hearing. This manipulation was intended to disrupt spontaneous glutamatergic transmission in the LSO while sparing the glycinergic afferents from the medial nucleus of the trapezoid body (MNTB). Afferent-evoked synaptic activity was assessed 1-6 days after ablation in a brain slice preparation using whole-cell current- and voltage-clamp recordings. In control animals, ipsilaterally evoked excitatory postsynaptic potentials (EPSPs) were present in 91% of neurons tested, but were observed in only 60% of neurons following cochlea removal. The maximum EPSP amplitude was significantly smaller in manipulated neurons compared with controls, and this was accompanied by a higher incidence of ipsilaterally evoked inhibitory postsynaptic potentials (IPSPs). To study the efficacy of excitatory synapses in greater detail, voltage-clamp recordings were made in the presence of strychnine and AP-5 [D(O)-2-amino-5-phosphonopentanoic acid]. The minimum excitatory postsynaptic current (EPSC) amplitude, presumed to reflect the efficacy of a single glutamatergic afferent, was approximately 40% smaller in manipulated neurons. In contrast, MNTB-evoked IPSPs were similar in neurons from control and ablated animals. However, manipulated neurons often exhibited a rebound depolarization after a hyperpolarizing current pulse or an afferent-evoked IPSP. In 70% of manipulated neurons, synaptically evoked rebound depolarizations were reduced, but not eliminated, by glutamate receptor antagonists. The glycine receptor antagonist strychnine did eliminate the IPSP-associated depolarization in these neurons. Collectively, these results suggest that functional denervation of excitatory afferents decreases their synaptic efficacy as result of both cell loss as well as decreased strength of individual surviving synapses.

Acoustic Stimulation↗
PubMed2002

Short-term plasticity of descending synaptic input to phrenic motoneurons in rats.

Respiratory afferent stimulation can elicit increases in respiratory motor output that outlast the period of stimulation by seconds to minutes [short-term potentiation (STP)]. This study examined the potential contribution of spinal mechanisms to STP in anesthetized, vagotomized, paralyzed rats. After C(1) spinal cord transection, stimulus trains (100 Hz, 5-60 s) of the C(1)-C(2) lateral funiculus elicited STP of phrenic nerve activity that peaked several seconds poststimulation. Intracellular recording revealed that individual phrenic motoneurons exhibited one of three different responses to stimulation: 1) depolarization that peaked several seconds poststimulation, 2) depolarization during stimulation and then exponential repolarization after stimulation, and 3) bistable behavior in which motoneurons depolarized to a new, relatively stable level that was maintained after stimulus termination. During the STP, excitatory postsynaptic potentials elicited by single-stimulus pulses were larger and longer. In conclusion, repetitive activation of the descending inputs to phrenic motoneurons causes a short-lasting depolarization of phrenic motoneurons, and augmentation of excitatory postsynaptic potentials, consistent with a contribution to STP.

Animals↗
PubMed1996

Activity-dependent decay of early LTP revealed by dual EPSP recording in hippocampal slices from young rats.

The early maintenance of long-term potentiation (LTP) was studied in the CA1 region of hippocampal slices from 12- to 18-day-old rats in a low-magnesium solution (0.1 mM). The alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated components of the field excitatory postsynaptic potential were estimated in parallel using early and late measurements of the composite potential. At the normal test stimulus frequency of 0.1 Hz, LTP was seen initially as a predominant increase in the AMPA component, but converted, via a substantial decay of this component and a gradual growth of the NMDA component, into nearly equal changes of the two components. Interrupting the test stimulation for 10 min, changing the test stimulus frequency to 1/60 Hz after LTP induction, or using a test stimulus frequency of 1/60 Hz during the entire experiment significantly reduced the decay of the potentiation of the AMPA component while enhancing the potentiation of the NMDA one. The ratio between the magnitudes of the two excitatory postsynaptic potential (EPSP) components showed a decaying time course that was independent of the manipulations used. Application of the NMDA antagonist D(-)-2-amino-5-phosphonopentanoic acid (50 microM) after LTP induction stabilized the LTP of the AMPA component until washout was started. On the other hand, the phosphatase inhibitor okadaic acid (1 microM) resulted in decay of the potentiation of both EPSP components back to around baseline and altered the time course of the ratio between the components. Our results show that the early maintenance of LTP is controlled in an activity-dependent and NMDA-dependent manner. This process accelerates the decay of LTP of both AMPA and NMDA components in parallel, suggesting that it is similar to homosynaptic long-term depression, although it operates at the normal test stimulus frequency. The data support a scenario in which LTP ensues as a selective AMPA receptor modification and subsequently converts to another modification, possibly a presynaptic one.

Animals↗
PubMed1992

Regulation of the M current: transduction mechanism and role in ganglionic transmission.

Slow excitatory postsynaptic potentials in sympathetic ganglia often involve suppression of a voltage-dependent potassium current termed the M current. This current is suppressed by the muscarinic action of acetylcholine, by peptides such as luteinizing hormone releasing hormone, and sometimes by alpha-adrenoceptor agonists. Activation of beta-adrenoceptors sometimes produces weak potentiation. The voltage dependence of the M current is such that its suppression increases the excitability of ganglionic neurones. Since this sometimes leads to spontaneous discharge, activation of the slow excitatory postsynaptic potential mechanism (or modulation of M current) within a sympathetic ganglion produces effects that manifest in the autonomic outflow to the target organ. In frogs, M currents are present in the neurones of both paravertebral sympathetic ganglia and cardiac parasympathetic ganglia. Since the M current is suppressed by adrenaline in the parasympathetic ganglia and these ganglia often receive adrenergic fibres from sympathetic ganglia, this might reflect an important means of interaction between the two branches of the autonomic system. At the cellular level, M-current suppression is little affected by drugs that interfere with membrane phosphorylation--dephosphorylation processes. This observation is discussed in relationship to the current understanding of the transduction mechanism for agonist-induced M-current suppression.

Animals↗
PubMed2002

Temperature dependence of synaptic responses in guinea pig hippocampal CA1 neurons in vitro.

1. Temperature-dependent properties of synaptic transmission were studied by recording orthodromic responses of the population spike and excitatory postsynaptic potential in CA1 pyramidal neurons of guinea pig hippocampal slices. 2. Increasing the temperature of the perfusing medium from 30 to 43 degrees C resulted in a decrease in the amplitude of the population spike (A-PS) and a reduced slope of the excitatory postsynaptic potential (S-EPSP). Bath application of the gamma-aminobutyric acid receptor antagonist, picrotoxin, or a change in the calcium concentration of the perfusate did not affect the A-PS during heating. 3. Increasing the strength of the synaptic input to that eliciting a PS with an amplitude 50, 75, or 100% of maximal at 30 degrees C resulted in a significant increase in the A-PS during the middle phase of hyperthermia (35-39 degrees C). 4. The long-term potentiation (LTP) induced at either 30 or 37 degrees C showed the same percentage increase in both the amplitude of the population spike and the S-EPSP after delivery of a tetanus (100 Hz. 100 pulses) to CA1 synapses. 5. The results of the present study, therefore, indicate that the decrease in CA1 field potential was linearly related to the temperature of the slice preparation, while LTP was induced in these responses during heating from 30 to 37 degrees C.

Action Potentials↗
PubMed1983

Lobster muscle and synapse respond to cortisol, a vertebrate hormone.

Cortisol (0.28 mumol X L-1) applied to lobster (Homarus americanus) neuromuscular preparations produces a hyperpolarization in muscle fibers and an increase in amplitude of excitatory postsynaptic potentials. The effect appears to be surface-mediated, because of its rapid onset (within seconds). It is also Na+-K+ ATPase dependent, because ouabain blocks the effects. The effects are relatively short-lasting, and gradually subside within 15 min. The increase in excitatory postsynaptic potentials is attributed in part to increased quantal output of transmitter, and not to changes in muscle fiber membrane resistance. The effects of cortisol on neuromuscular transmission and membrane potential indicate that cortisol may have a physiological role in crustaceans.

Animals↗
PubMed1998

Limbic gamma rhythms. II. Synaptic and intrinsic mechanisms underlying spike doublets in oscillating subicular neurons.

Gamma oscillations were evoked in the subiculum in rat transverse hippocampal slices by tetanic stimulation (200 ms/100 Hz) of either CA1 or subiculum. Gamma oscillations in the subiculum differed from those in CA1 in containing population spike doublets as well as singlets. The present study addresses the origin of this more complex form of gamma oscillation in the subiculum. Intracellular recordings from subicular neurons revealed that 63% of them fired double action potentials on cycles of the gamma oscillation that generated population spike doublets after tetanic stimulation of either CA1 or subiculum. The remaining cells produced excitatory postsynaptic potentials (EPSPs), and occasional single spikes, on each cycle. Neurons that fired occasional single action potentials during gamma rhythms were "regular spiking" cells. They did not produce burst discharges during depolarizing steps, had minimal membrane potential sags on hyperpolarizing steps, and responded to single afferent volleys with a single action potential on an EPSP followed by a large inhibitory postsynaptic potential complex. Fast spiking cells were observed too infrequently to be studied in detail. Neurons that fired doublets during gamma rhythms were "intrinsic burst" (IB) cells. They generated bursts of action potentials on step membrane depolarizations, had significant membrane potential sags on step hyperpolarizations with an anodal break potential on return to rest, and fired multiple action potentials in response to high-intensity single afferent volleys. IB neurons did not fire action potential doublets during 1-s membrane depolarizations. Double action potentials, however, were evoked in these cells by depolarizing pulses at 40 Hz from hyperpolarized membrane potentials (-100 mV). Computer simulations suggest that the hyperpolarization between the depolarizations was essential for action potential doublets. The results in this and the previous paper suggest the following: either CA1 or subiculum alone can generate gamma oscillations gated by local networks of interneurons, oscillations in CA1 project through pyramidal cell axons to subiculum with a time lag expected from axon conduction delays, and oscillating sequences of EPSPs and intrinsic and/or synaptic hyperpolarizing potentials in IB subicular neurons generate gamma frequency spike doublets, which depend on both the intrinsic properties of these neurons and their temporally patterned synaptic input. This phenomenon could amplify gamma output from CA1 and modify its coupling to gamma oscillations in the wider limbic system.

Action Potentials↗
PubMed1985

Effects of K+-channel blockers on transmitter release in bullfrog sympathetic ganglia.

Effects of K+-channel blockers, tetraethylammonium (TEA), 4-aminopyridine (4-AP) and Cs+ on synaptic transmission were studied with an intracellular electrode in bullfrog sympathetic ganglia. TEA (25-500 microM), 4-AP (0.6-5 microM) and Cs+ (50 microM-10 mM) all increased the quantal content of the fast excitatory postsynaptic potential in a dose-dependent manner. The effects of TEA were rapid in onset and recovery, whereas those of 4-AP and Cs+ appeared with a notable delay and reversed slowly. All blockers lengthened synaptic delay. When compared at approximately equipotent concentrations for potentiation of transmitter release, TEA and 4-AP were found to produce a similar lengthening of the synaptic delay whereas Cs+ caused a much greater prolongation. The quantal size of the fast excitatory postsynaptic potential and the amplitude of the acetylcholine potential were not affected by 4-AP or Cs+, but were depressed by TEA. These results indicate that TEA, 4-AP and Cs+ enhance evoked transmitter release in bullfrog sympathetic ganglia. It is suggested that the potentiation is caused, at least in part, by a mechanism that increases Ca++ influx in the nerve terminal. The enhanced influx is presumed to be mediated by a broadening of the presynaptic action potential after K+-channel blockade.

4-Aminopyridine↗
PubMed2003

Fast synaptic connections from CBIs to pattern-generating neurons in Aplysia: initiation and modification of motor programs.

Consummatory feeding movements in Aplysia californica are organized by a central pattern generator (CPG) in the buccal ganglia. Buccal motor programs similar to those organized by the CPG are also initiated and controlled by the cerebro-buccal interneurons (CBIs), interneurons projecting from the cerebral to the buccal ganglia. To examine the mechanisms by which CBIs affect buccal motor programs, we have explored systematically the synaptic connections from three of the CBIs (CBI-1, CBI-2, CBI-3) to key buccal ganglia CPG neurons (B31/B32, B34, and B63). The CBIs were found to produce monosynaptic excitatory postsynaptic potentials (EPSPs) with both fast and slow components. In this report, we have characterized only the fast component. CBI-2 monosynaptically excites neurons B31/B32, B34, and B63, all of which can initiate motor programs when they are sufficiently stimulated. However, the ability of CBI-2 to initiate a program stems primarily from the excitation of B63. In B31/B32, the size of the EPSPs was relatively small and the threshold for excitation was very high. In addition, preventing firing in either B34 or B63 showed that only a block in B63 firing prevented CBI-2 from initiating programs in response to a brief stimulus. The connections from CBI-2 to the buccal ganglia neurons showed a prominent facilitation. The facilitation contributed to the ability of CBI-2 to initiate a BMP and also led to a change in the form of the BMP. The cholinergic blocker hexamethonium blocked the fast EPSPs induced by CBI-2 in buccal ganglia neurons and also blocked the EPSPs between a number of key CPG neurons within the buccal ganglia. CBI-2 and B63 were able to initiate motor patterns in hexamethonium, although the form of a motor pattern was changed, indicating that non-hexamethonium-sensitive receptors contribute to the ability of these cells to initiate bursts. By contrast to CBI-2, CBI-1 excited B63 but inhibited B34. CBI-3 excited B34 and not B63. The data indicate that CBI-1, -2, and -3 are components of a system that initiates and selects between buccal motor programs. Their behavioral function is likely to depend on which combination of CBIs and CPG elements are activated.

Action Potentials↗
PubMed2005

Spatiotemporal patterns of dorsal root-evoked network activity in the neonatal rat spinal cord: optical and intracellular recordings.

Spatiotemporal patterns of dorsal root-evoked potentials were studied in transverse slices of the rat spinal cord by monitoring optical signals from a voltage-sensitive dye with multiple-photodiode optic camera. Typically, dorsal root stimulation generated two basic waveforms of voltage images: dual-component images consisting of fast, spike-like signal followed by a slow signal in the dorsal horn, and small, slow signals in the ventral horn. To qualitatively relate the optical signals to membrane potentials, whole cell recordings were combined with measurements of light absorption in the area around the soma. The slow optical signals correlated closely with subthreshold postsynaptic potentials in all regions of the cord. The spike-like component was not associated with postsynaptic action potentials, suggesting that the fast signal was generated by presynaptic action potentials. Firing in a single neuron could not be detected optically, implying that local voltage images originated from synchronously activated neuronal ensembles. Blocking glutamatergic synaptic transmission inhibited excitatory postsynaptic potentials (EPSPs) and significantly reduced the slow optical signals, indicating that they were mediated by glutamatergic synapses. Suppressing glycine-mediated inhibition increased the amplitude of both optical signals and EPSPs, while blocking GABA(A) receptor-mediated synapses, increased the amplitude and time course of EPSPs and prolonged the duration of voltage images in larger areas of the slice. The close correlation between evoked EPSPs and their respective local voltage images shows the advantage of the high temporal resolution optical system in measuring both the spatiotemporal dynamics of segmental network excitation and integrated potentials of neuronal ensembles at identified sites.

2-Amino-5-phosphonovalerate↗
PubMed1998

Transgenic mice with cerebral expression of human immunodeficiency virus type-1 coat protein gp120 show divergent changes in short- and long-term potentiation in CA1 hippocampus.

The human immunodeficiency virus type-1 envelope glycoprotein gp120 is shed from the virus and from infected cells and thus can diffuse and interact with a variety of central nervous system cells. Transgenic mice constitutively expressing glial fibrillary acidic protein-driven gp120 from brain astrocytes display neuronal and glial changes resembling abnormalities in human immunodeficiency virus type-1-infected human brains. To assess the neurophysiology of these transgenic mice and determine whether gp120 expression impairs synaptic plasticity, we examined CA1 population excitatory postsynaptic potentials in hippocampal slices from transgenic mice and from non-transgenic controls, using a double-blind protocol. Compared with slices from non-transgenic littermate controls, slices from gp120 transgenic mice showed four significant alterations: (i) increased mean slopes of normalized population excitatory postsynaptic potentials; (ii) larger paired-pulse facilitation after induction of long-term potentiation at 50 ms interpulse intervals; (iii) markedly elevated short-term potentiation after 10 and 20 shocks at 100 Hz; and (iv) a significant reduction in the magnitude of CA1 long-term potentiation. In slices from transgenic mice expressing Escherichia coli beta-galactosidase from the same promoter, paired-pulse facilitation and long-term potentiation were normal. These results indicate that brain slice preparations from gp120 transgenic mice can be used to assess pathophysiological effects of gp120 on neuronal networks. Because short-term potentiation involves presynaptic mechanisms, our results suggest that gp120 expression in these mice enhances either presynaptic glutamate release or postsynaptic glutamate receptor function, or both. These changes could lead to increased Ca2+ influx, thereby contributing to neuronal dysfunction and injury. As long-term potentiation is a cellular model of learning and memory, our results may be relevant to memory (cognitive) impairments seen in patients with AIDS.

Animals↗
PubMed2000

Reciprocal modulation of glutamate and GABA release may underlie the anticonvulsant effect of phenytoin.

Although conventional wisdom suggests that the effectiveness of phenytoin as an anticonvulsant is due to blockade of Na+-channels this is unlikely to be it's sole mechanism of action. In the present paper we examined the effects of phenytoin on evoked and spontaneous transmission at excitatory (glutamate) and inhibitory (GABA) synapses, in the rat entorhinal cortex in vitro. Evoked excitatory postsynaptic potentials at glutamate synapses exhibited frequency-dependent enhancement, and phenytoin reduced this enhancement without altering responses evoked at low frequency. In whole-cell patch-clamp recordings the frequency of excitatory postsynaptic currents resulting from the spontaneous release of glutamate was reduced by phenytoin, with no change in amplitude, rise time or decay time. Similar effects were seen on miniature excitatory postsynaptic currents, recorded in the presence of tetrodotoxin. Evoked inhibitory postsynaptic potentials at GABA synapses displayed a frequency-dependent decrease in amplitude. Phenytoin caused a reduction in this decrement without affecting the responses evoked at low frequency. The frequency of spontaneous GABA-mediated inhibitory postsynaptic currents, recorded in whole-cell patch mode, was increased by phenytoin, and this was accompanied by the appearance of much larger amplitude events. The effect of phenytoin on the frequency of inhibitory postsynaptic currents persisted in the presence of tetrodotoxin, but the change in amplitude distribution largely disappeared. These results demonstrate for the first time that phenytoin can cause a simultaneous reduction in synaptic excitation and an increase in inhibition in cortical networks. The shift in balance in favour of inhibition could be a major factor in the anticonvulsant action of phenytoin.

2-Amino-5-phosphonovalerate↗
PubMed1996

Quantal secretion from visualized boutons on rat pelvic ganglion neurones.

Synaptic transmission from single preganglionic hypogastric nerves innervating monopolar pelvic ganglion neurones has been studied with intracellular electrodes to record transmission from all the boutons and with extracellular electrodes placed over boutons visualized with DiOC2(5) in order to record transmission from selected boutons. Intracellular electrodes revealed spontaneous excitatory postsynaptic potentials (EPSPs) with amplitude histograms that show increasing numbers of large EPSPs as the external calcium ([Ca2+]o) was increased from 0.15 to 1.0 mM. These histograms were in general well fitted by a Poisson mixture of gamma distributions. Extracellular electrodes placed over visualized boutons revealed evoked excitatory postsynaptic potentials (extracellular EPSPs) with amplitude histograms that were best described by single gamma distributions in most cases in low [Ca2+]o (less than 0.5 mM). The standard deviation of these gammas was not much larger than that of the electrical noise. In a minority of extracellular recordings the amplitude histogram of evoked extracellular EPSPs was best described by a gamma distribution in which the standard deviation was much greater than that of the noise. Confocal microscopy of boutons orthogradely labelled with dextran-rhodamine showed that about 30% of these formed closely apposing pairs on the surface of the neurones. These observations are discussed in terms of the hypothesis that multiquantal release at boutons occurs as a consequence of the coupled secretion from closely apposed boutons.

Animals↗
PubMed1986

Neurophysiology of limbic system pathways in the rat: projections from the subicular complex and hippocampus to the entorhinal cortex.

We studied the responses of rat entorhinal neurons to electrical stimulation of the dentate gyrus, hippocampus and subicular complex. Three main results were obtained. Excitatory postsynaptic potentials were recorded in entorhinal neurons in response to electrical stimulation. Cell in layers II, III and V of the entorhinal cortex were responsive. Frequency potentiation of excitatory responses was observed when 10/s stimulation was used. Excitatory responses were followed by inhibitory postsynaptic potentials. The results provide evidence for an excitatory projection from the hippocampus and subiculum to the entorhinal cortex, and are consistent with the existence of feed-forward inhibition of entorhinal principal neurons.

Animals↗
PubMed1990

Synaptic integration in hippocampal CA1 pyramids.

Excitatory synapses on hippocampal pyramids are exclusively located to dendritic spines, usually in a 1:1 proportion. The number of spines indicates a convergence of as many as 25,000-30,000 excitatory boutons per CA1 pyramidal cell in rats. Activation of a single afferent fibre produces a unitary excitatory postsynaptic potential (EPSP) of about 150 microV, probably produced by a single quantum of transmitter. The release probability is normally low, but may be increased by facilitatory processes. On the average, each afferent fibre has few boutons (mostly 1, but up to 5) in contact with a given CA1 pyramid. Surprisingly, in view of the large synaptic convergence, only 100-300 synchronously active excitatory synapses seem necessary to make the cell discharge. Synapses in various parts of the dendritic tree are nearly equally effective in this regard. Excitatory postsynaptic potentials produced by neighbouring synapses sum linearly, both with each other and with hyperpolarizing, inhibitory potentials. Cable theoretical considerations suggest that the summation effect will be greater for synapses contacting the same secondary dendrite than for more distributed dendritic contacts. Three types of inhibitory neurones provide different classes of interference. The chandelier cells (axoaxonic cells) terminate upon the initial axons of a large number of pyramidal cells, and are thus capable of producing a wide-spread and effective inhibition. By hyperpolarizing the somata of a smaller number of cells, basket cells counteract all excitatory inputs to these cells, irrespective of synaptic location. In contrast to these two forms of global inhibition, stellate cells may cause a shunting form of inhibition at specific dendritic sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Tetanus toxin blocks inhibition of granule cells in the dentate gyrus of the urethane-anaesthetized rat.

Field potentials of dentate granule cells in response to stimulation of the perforant path have been studied before and after injecting tetanus toxin (200 mouse LD50; or phosphate-buffered saline in controls) into the hilus of the dentate gyrus of rats under urethane anaesthesia. Within 1 h of toxin injection, the population spike, but not the slope of the excitatory postsynaptic potential, had increased markedly in amplitude and double or treble population spikes appeared in response to perforant path stimulation. Both paired pulse inhibition (15-ms interval between conditioning and test stimuli) and commissural inhibition (10-ms interval) were substantially reduced by the toxin. Neither multiple spikes nor the reduction in inhibition were seen in controls. Apparent inhibition of the excitatory postsynaptic potential, seen with paired stimuli to the perforant path, was not affected by the toxin. At later times after the injections, a progressive increase in the size of the spikes was seen in the controls while in the toxin animals there was often a secondary decrease in size. It is concluded that tetanus toxin can block both feed-back and feed-forward inhibitory components acting on dentate granule cells. The results are discussed with respect to the role of inhibitory processes in the control of epileptogenesis.

Action Potentials↗
PubMed2001

Spatial distribution of the vestibulospinal neurons in the frog vestibular nuclei.

In experiments on the preparation of a frog perfused brain (Rana ridibunda), intracellular potentials were recorded from neurons of the vestibular nuclei following stimulation of the vestibular nerve and the spinal cord. The vestibulospinal neurons were identified on the basis of excitatory postsynaptic potentials evoked by the stimulation of the ipsilateral vestibular nerve and antidromic activation from the stimulation of the cervical and lumbar enlargements of the spinal cord. The cells that could be activated antidromically only by cervical cord stimulation have been designated as C cells, and the cells that could also be activated antidromically as a result of lumbar stimulation have been termed L cells. The average conduction velocity determined for C neurons was 10.67 m/s and for L neurons 15.84 m/s. The ratio of C and L neurons over the vestibular nuclear complex was very similar to each other: 52% C neurons and 48% L neurons. The majority of both types of neurons were localized in the lateral vestibular nucleus (58.6%), to a lesser extent in the descending vestibular nucleus (30.7%) and very little in the medial vestibular nucleus (10.6%). In the lateral vestibular nucleus, C neurons prevailed in the caudal part of the nucleus and L neurons prevailed in the rostral part. By contrast, in the descending and medial vestibular nuclei there was a gradual increase of C and L cells quantitatively from the rostral to the caudal part. Fast and slow cells were detected among the vestibulospinal neurons. The fast neurons of L cells did not prevail greatly over the slow ones, whereas the slow neurons of C cells prevailed comparatively largely over the fast neurons. Thus, it became possible to reconstruct the spatial distribution of the identified vestibulospinal neurons. The results of spatial distribution of C and L vestibulospinal neurons in the frogs failed to conform to definite somatotopy, which is characteristic of mammalian vestibular nuclei. The results of this study have confirmed an earlier assumption that C and L neurons in the frog's vestibular nuclei as a source of vestibulospinal fibers, are scattered separately or more frequently in groups, so that they establish a 'patch-like' somatotopy and do not form a distinctly designed field as in mammals.

Action Potentials↗