Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Synaptic Potentials”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed1983

Convergence of trigeminal afferents on retractor bulbi motoneurones in the anaesthetized cat.

Retractor bulbi motoneurones were identified by intracellular recording of their antidromic invasion following stimulation of the motor axons. Characteristics of excitatory post-synaptic potentials (e.p.s.p.s) evoked by electrical stimulation of long ciliary nerves (corneal afferents), the supraorbital nerve and the ipsilateral or contralateral vibrissae were analysed. Comparison of the orthodromic responses induced by supra-threshold stimulation of the four trigeminal inputs showed that the most powerful excitatory effect was due to corneal afferent stimulation. Excitatory synaptic potentials were followed in some cases by a period of hyperpolarization lasting 15-20 msec. It is suggested that this is an inhibitory potential of post-synaptic origin. Interaction between condition and test e.p.s.p.s evoked by long ciliary nerve and supraorbital nerve stimulation revealed a partial blocking of test e.p.s.p.s over a longer period (more than 30 msec), and it is suggested that inhibitory mechanisms within the trigeminal nucleus may be in part responsible for the absence of facilitation at the level of the motoneurone.

Action Potentials↗
PubMed1992

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

1. Intracellular recordings were obtained from pyramidal-type neurons in the basolateral amygdaloid nucleus (BLA) in slices of rat ventral forebrain and used to compare the actions of exogenously applied cholinomimetics to the effects produced by electrical stimulation of amygdalopetal cholinergic afferents from basal forebrain. 2. Bath application of carbachol depolarized pyramidal cells with an associated increase in input resistance (Ri), reduced the slow after-hyperpolarization (AHP) that followed a series of current-evoked action potentials and blocked spike frequency accommodation. All of these effects were reversed by the muscarinic antagonist atropine but not by the nicotinic antagonist hexamethonium. 3. Electrical stimulation of amygdaloid afferents within the external capsule evoked a series of synaptic potentials consisting of a non-cholinergic fast excitatory postsynaptic potential (EPSP), followed by early and late inhibitory postsynaptic potentials (IPSPs). Each of these synaptic potentials was reduced by carbachol in an atropine-sensitive manner. 4. Local application of carbachol to pyramidal cells produced a short-latency hyperpolarization followed by a prolonged depolarization. The hyperpolarization and depolarization to carbachol were blocked by atropine but not hexamethonium. 5. The carbachol-induced hyperpolarization was associated with a decrease in Ri and had a reversal potential nearly identical to that of the early IPSP. The inhibitory response was blocked by perfusion of medium containing tetrodotoxin (TTX), bicuculline or picrotoxin, while the subsequent depolarization was unaffected. On the basis of these data, it is concluded that the muscarinic hyperpolarization is mediated through the rapid excitation of presynaptic GABAergic interneurons in the slice. 6. The findings that the carbachol-induced depolarization was associated with an increase in Ri, often had a reversal potential below -80 mV, was sensitive to changes in extracellular potassium concentration and was blocked by intracellular ionophoresis of the potassium channel blocker caesium suggest that it resulted from a muscarinic blockade of one or more potassium conductances. 7. Repetitive stimulation of sites within the slice containing cholinergic afferents evoked a series of fast EPSPs followed by IPSPs. These non-cholinergic potentials were followed by a slow EPSP that lasted from 10 s-4 min. The slow EPSP was enhanced by eserine and blocked by atropine. It was also blocked by TTX or cadmium, indicating that it was dependent on spike propagation and calcium-dependent release of acetylcholine (ACh). 8. Stimulation of cholinergic afferents in the slice mimicked other effects produced by carbachol including blockade of the slow AHP and accommodation of action potential discharge and these actions were potentiated by eserine and blocked by atropine.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2002

Metabotropic glutamate receptors: electrical and chemical signaling properties.

Over the last two decades, glutamate has been established as the main excitatory neurotransmitter in the mammalian brain. Glutamate released from synapses activates ion channel-forming receptors at postsynaptic cells and consequently mediates fast postsynaptic potentials. These receptors are termed ionotropic glutamate receptors (iGluRs). The subsequent discovery of metabotropic glutamate receptors (mGluRs) revealed that glutamate can also mediate slow synaptic potentials, modulate ion channels, and directly couple to GTP binding proteins. In contrast to the iGluRs, the mGluRs possess seven transmembrane domains and a large intracellular C-terminus that involves interactions with a variety of other intracellular signaling systems. Eight functionally distinct mGluR subtypes are known to be localized to specific neuron types at presynaptic and/or postsynaptic membranes. Their physiological functions involve the generation of slow excitatory and inhibitory synaptic potentials, modulation of synaptic transmission, synaptic integration, and plasticity. The classical role of glutamate as a fast excitatory synaptic transmitter was largely extended by mGluRs acting as a neuromodulator and even as an activator of inhibitory mechanisms at certain synapses.

Animals↗
PubMed1991

Involvement of excitatory amino acid receptors in long-term potentiation in the Schaffer collateral-commissural pathway of rat hippocampal slices.

The present article reviews studies from our laboratory, which have shown that excitatory amino acids receptors of the N-methyl-D-aspartate type are involved in the induction of long-term potentiation in the Schaffer collateral-commissural pathway of rat hippocampal slices. The nature of the excitatory amino acid receptors that mediate the response that is modified by the induction of long-term potentiation is also considered. The mechanism of induction of long-term potentiation is discussed, as are some possible stages that are required for the maintenance of this process. Some new data are presented concerning the ability of N-methyl-D-aspartate to potentiate synaptic transmission and to depress the amplitude of the presynaptic fibre volley. Concerning the potentiation, it is shown that brief (1-2 min) perfusion of slices with N-methyl-D-aspartate is sufficient to potentiate synaptic transmission for at least 3 h. The N-methyl-D-aspartate induced depression of the presynaptic fibre volley is shown to be transient and independent of synaptic transmission.

Animals↗
PubMed1983

Comparison of antidromic and orthodromic action potentials of identified motor axons in the cat's brain stem.

Recordings were made from identified central axons at a known distance from their somata, to compare the action potentials resulting from antidromic and synaptic excitation. By taking advantage of the anatomical configuration within the brain stem of the motoneurones innervating the retractor bulbi muscle in the orbit, their axons were penetrated in the VIth nucleus and labelled by electrophoretic injection of horseradish peroxidase. Excitatory post-synaptic potentials recorded in the retractor bulbi axons at about 3 mm from the soma were six times smaller than in the soma. The space constant of the axonal segment between the retractor bulbi and the abducens nucleus was estimated to be 1.7 mm. When the axons propagated action potentials the attenuation was increased to eighteen times due to the nodes of Ranvier intercalated between the soma and the site of recording. Antidromic action potentials displayed stepwise changes in amplitude and shape when stimuli were applied at intervals decreasing from 5 ms to 0.7 ms. The changes were related to the different lengths of refractoriness of the soma, initial segment and axon. Orthodromic action potentials evoked by synaptic excitation displayed similar changes in amplitude and shape. These observations lead to the conclusion that the soma, initial segment and neighbouring nodes of Ranvier contribute significantly to the shape of the action potential. Contrary to the generally accepted view, it appears that the efferent discharge along motor axons can be initiated without a simultaneous activation of the somato-dendritic or even the initial segment membrane, as revealed by the lack of somato-dendritic and/or initial segment contribution to the shape of the synaptically evoked action potentials.

Action Potentials↗
PubMed2004

Acute and chronic cocaine-induced potentiation of synaptic strength in the ventral tegmental area: electrophysiological and behavioral correlates in individual rats.

The initiation of the psychostimulant sensitization process depends on the mesolimbic system, which projects from the ventral tegmental area (VTA) to the nucleus accumbens. Although such initiation is primarily dependent on glutamatergic activity in VTA neurons, the exact role VTA excitatory synapses play in this process is poorly understood. Here, we examine the effects of repeated in vivo injections of cocaine on the magnitude and duration of the increase in strength at VTA excitatory synapses reported previously to be elicited by a single in vivo exposure to cocaine (Ungless et al., 2001; Saal et al., 2003). We also compare the synaptic modifications induced by cocaine with its effects on locomotor activity. Surprisingly, repeated cocaine exposure potentiated the ratio of AMPA receptor-mediated to NMDA receptor-mediated EPSCs to a similar extent and duration as a single in vivo cocaine exposure. In naive animals, the magnitude of the cocaine-induced locomotor activity after a single injection of cocaine correlated with the magnitude of the accompanying synaptic enhancement. This correlation was lost on the seventh day of repeated cocaine administration, as well as when a challenge injection was given 10 d after the cessation of repeated cocaine administration. These results suggest that the cocaine-induced synaptic plasticity at VTA excitatory synapses is transient, and its duration depends on the last exposure to cocaine. Furthermore, chronic cocaine exposure disrupts the normal, presumably adaptive relationship between synaptic enhancement in the VTA and behavior.

Animals↗
PubMed1984

Penicillin induced hyperexcitability in the in vitro hippocampal slice can be unrelated to impairment of somatic inhibition.

The effects induced by penicillin (PEN) upon the synaptic responses of CA1 hippocampal pyramidal cells (HPCs) were studied in the 'in vitro' slice. Low concentrations of PEN (0.17-0.34 mM) evoked an increase in amplitude and duration of the orthodromic excitatory post-synaptic potential induced by stratum radiatum, while stimuli which were subthreshold in control conditions became effective in eliciting action potentials. These changes were not paralleled by any decrease of the recurrent inhibitory post-synaptic potential due to inhibitory interneurons located at or near the soma. However, the latter decreased and then disappeared as PEN concentrations were brought to levels higher than 0.68 mM. Since low concentrations of PEN increase CA1 HPCs responsiveness without decreasing somatic inhibition, it is concluded that this action is probably due to a reduced dendritic inhibitory mechanism.

Animals↗
PubMed1995

Opposing roles for dopamine and serotonin at presynaptic receptors in the ventral tegmental area.

1. Dopamine D1 and 5HT1D receptors are found on the terminals of afferent GABA neurons that synapse on the ventral tegmental area (VTA) dopamine neurons. The role of these receptors in the actions of cocaine was investigated using intracellular recordings in a brain slice preparation. Synaptic potentials were generated in the slice and GABA-mediated inhibitory post-synaptic potentials (IPSP) were identified. 2. Stimulation of dopamine D1 receptors selectively enhanced the GABAB IPSP, and their effect was blocked by D1 antagonists. The magnitude of the IPSP was decreased when D1 antagonists were applied in isolation, suggesting tonic D1 receptor stimulation via dendritically released dopamine. 3. Cocaine had an opposite effect and selectively decreased the magnitude of GABAB IPSP. This action was mimicked by 5HT and the 5HT1D agonist sumatriptan, and attenuated by the 5HT1D/2C antagonist, metergoline. The action of cocaine was also mimicked by the 5HT-releasing agent, fenfluramine, and blocked by pre-incubation of the slice with the 5HT-depleting agent, para-chloroamphetamine. 4. The results of this study suggest that dopamine and 5HT have opposing roles in modulating GABA input into VTA dopamine neurons. The actions of cocaine on this interplay may have implications for understanding its addictive properties.

Animals↗
PubMed1990

Serotonin (5-HT) induces IPSPs in pyramidal layer cells of rat piriform cortex: evidence for the involvement of a 5-HT2-activated interneuron.

In a slice preparation of rat piriform cortex, both intracellular and extracellular techniques were used to examine the pharmacological and electrophysiological actions of serotonin (5-HT). Bath application of 5-HT resulted in either depolarization (57%), hyperpolarization (34%) or no change (9%) in membrane potential of cells in the pyramidal cell layer (layer II) of piriform cortex. Additionally, when KCl-containing electrodes were used, 5-HT induced an increase in depolarizing synaptic potentials in 41% of these cells. It was concluded that these potentials were reverse inhibitory post-synaptic potentials (IPSPs) because they were blocked by bicuculline and tetrodotoxin. The induction of IPSPs by 5-HT was blocked by the 5-HT2-selective antagonist ritanserin. By recording extracellularly in the presence of 5-HT, a group of 5-HT-activated, putative interneurons was found at the border of layers II and III of piriform cortex, 5-HT but not norepinephrine activation was blocked by ritanserin. The actions of 5-HT were mimicked by the 5-HT2 agonist alpha-methyl-5-HT; the 5-HT2 partial agonist, 2,5-dimethoxy-4-methyl-amphetamine had a small agonist action of its own and blunted the effect of 5-HT. Activation of a larger group of putative interneurons by the more universal excitant N-methyl-D-aspartate showed that the 5-HT-activated interneurons represented 23% of the interneurons located on the border between layers II and III. We conclude that 5-HT induces IPSPs in layer II pyramidal cells by activating a subpopulation of interneurons at the border of layers II and III of piriform cortex.

Animals↗
PubMed1981

Nigro-reticular pathway in the rat: an intracellular study.

Stimulation of substantia nigra produced short latency excitatory and inhibitory post-synaptic potentials in neurons located in nucleus reticularis gigantocellularis in the reticular formation. These post-synaptic potentials were considered to be monosynaptic on the basis of constant latency at varying stimulus strength. It is suggested that substantia nigra is the source of the inhibition and that excitatory potentials are due to stimulation of cortico-reticular fibers.

Animals↗
PubMed1968

Reticulospinal inhibition of transmission in reflex pathways.

1. The effect of electrical stimulation of the brain stem on reflex transmission has been investigated in decerebrate cats after partial transection of the spinal cord.2. Brain stem stimuli that do not evoke inhibitory post-synaptic potentials (IPSPs) in motoneurones or primary afferent depolarization may still effectively depress the excitatory and inhibitory synaptic actions evoked from the flexor reflex afferents (FRA) and from Ib afferents. There is no effect on post-synaptic potentials from Ia afferents or on Renshaw IPSPs. The depression is not associated with any measurable change in conductance over the motoneuronal membrane.3. There is also inhibition from the brain stem of transmission from the FRA (but not from Ia and Ib afferents) to primary afferent terminals and to ascending spinal pathways.4. It is concluded that this inhibition from the brain stem is exerted at an interneuronal level in spinal reflex paths.5. The inhibitory action is evoked from the region of Magoun's inhibitory centres in the brain stem and is mediated by axons with a conduction velocity of at least 20 m/sec. The axons are distributed in the dorsal part of the lateral funicle.6. The pathway mediating the inhibition from the brain stem is named the dorsal reticulospinal system. Its possible role in maintaining the decerebrate control of reflexes is discussed and related to the problem of a selective control of some paths from a primary afferent system.

Animals↗
PubMed1979

Functions of different receptor systems in the reptilian labyrinth.

Different biopotentials, following a mechanical stimulus, were recorded from single hair cells of the reptilian labyrinth, with electronoptically circumscript localizations: 1. From the apical cell pole, the receptor potential, intracellular or from the ciliary surface, within the physiological range proportional to stimulus amplitude, frequency or phase, without delay, and with no real threshold of mechanosensitivity, as measured by ciliary displacement amplitude or velocity. 2. From the synaptic zone, in the basal region of the hair cell, or from contacting nerve endings, the synaptic potentials, local excitatory or inhibitory processes, respectively, with measurable latencies and with non-linear distortion. 3. From the (dendritic) endings of the first afferent neuron (or neurons), spike-shaped action potentials, synchronized by the (excitatory) synaptic potentials. Characteristic curves were plotted as a quantitative representation of the mechano-electric input-output relations of the different types of hair cells. For proceeding morphological and physiological system analysis, the comparison of the different submammalian inner-ear receptor systems gives us some new possibility of a closer correlation between ultrastructure and function.

Acoustic Stimulation↗
PubMed1996

Myenteric neurons of the rat descending colon: electrophysiological and correlated morphological properties.

Conventional intracellular electrophysiological recordings were made from 502 myenteric neurons of the rat descending colon. Myenteric neurons could be classified into three groups on the basis of distinct electrophysiological properties. The first group of neurons (51% of all neurons) fired tetrodotoxin-sensitive action potentials in response to direct somal depolarization and the majority (98%) of this group generated fast cholinergic excitatory synaptic potentials in response to focal stimulation and were therefore designated S/Type 1 neurons. The second group (40%) of neurons fired tetrodotoxin-insensitive action potentials which were followed by long-lasting membrane afterhyperpolarizations, hence were termed AH neurons. These neurons did not receive fast cholinergic synaptic inputs but ionophoretic application of acetylcholine induced rapid nicotinic cholinoceptor-mediated depolarizations. The final group of neurons (9%), named Type 3 neurons, received fast cholinergic synaptic inputs but could never be made to fire action potentials. Rundown in amplitude of successive fast excitatory synaptic potentials evoked by a short train of presynaptic nerve stimuli was observed in only a small proportion of neurons (8/37; 22%) with the majority of neurons (29/37; 78%) showing no such decrease in amplitude, even at frequencies of stimulation as high as 10 Hz. Superfusion of 5-hydroxytryptamine could induce both an inhibition and a facilitation of cholinergic fast synaptic transmission. Evidence was adduced that these presynaptic inhibitory and facilitatory actions appeared to be mediated via 5-hydroxytryptamine 1A and 5-hydroxytryptamine 4 receptors, respectively. Muscarinic slow excitatory synaptic potentials were not detected (9/9 neurons tested) and non-cholinergic slow excitatory synaptic potentials following repetitive focal presynaptic nerve stimulation were observed in only 39/502 (8%) of all neurons. In those neurons in which a demonstrable change in membrane input resistance was detectable, slow excitatory potentials were accompanied by an increased input resistance. In addition, in a small subset (4%) of S/Type 1 neurons, slow membrane hyperpolarizations accompanied by an increased membrane input resistance were observed following tetanic presynaptic nerve stimulation. Superfusion of 5-hydroxytryptamine induced both membrane depolarizations and hyperpolarizations. Membrane depolarizations were observed in 40% of all neuronal types (34% of S/Type 1 neurons, 58% of AH neurons and 11% of Type 3 neurons) and were accompanied by an increased membrane input resistance and occasionally, in S/Type 1 and AH neurons, by anodal break excitation or spontaneous action potential firing. Membrane hyperpolarizations were observed in S/Type 1 neurons (5%) only and were accompanied, unexpectedly, by an increased membrane input resistance. In those neurons that responded both to application of 5-hydroxytryptamine and tetanic presynaptic nerve stimulation, 5-hydroxytryptamine always mimicked the slow synaptic response indicating that 5-hydroxytryptamine may function as a slow synaptic mediator in some myenteric neurons. Myenteric neurons identified by intracellular injection of the neuronal marker Neurobiotin TM were found to conform to the morphological classification schemes proposed for myenteric neurons of the guinea-pig and porcine intestine, that is, Dogiel Types I and II and Stach Type IV neurons were present. Simultaneous electrophysiological recording and intracellular staining techniques revealed that a correlation existed between the electrophysiological and morphological properties of myenteric neurons of the rat colon, with electrophysiological classified S/Type 1 neurons having Dogiel Type I morphologies (95/108 neurons; 88%) and electrophysiological classified AH neurons having Dogiel Type II morphologies (87/94 neurons; 93%)...

Animals↗
PubMed1975

Heterosynaptic facilitation in the giant cell of Aplysia.

1. Heterosynaptic facilitation, defined as an increase of the efficacy of synaptic transmission between a test interneurone and a post-synaptic neurone, produced by the stimulation of a separate pathway, was studied in the left pleural ganglion. The experimental procedure consisted of detecting the effects of a brief tetanus, applied to tentacular and tegumentary nerves, on the amplitude of monosynaptic and unitary post-synaptic potentials (p.s.p.s) recorded in the left giant cell and generated by stimulating the test interneurone every 10 sec. The membrane potential of the test interneurone was simultaneously recorded. 2. Following heterosynaptic stimulation, the amplitude of the test p.s.p. increased, after a delay of about 30 sec, up to 250% of its original size; this increase subsided after 2-3 min or more. 3. Only the interneurones producing in the giant cell the e.i.p.s.p. (excitatory-inhibitory post-synaptic potential) were affected by hetero-synaptic facilitation. Other interneuronal types showed no changes in their synaptic transmission on the giant cell after heterosynaptic stimulation. 4. Heterosynaptic stimulation did not produce either orthodromic or antidromic spikes in the test interneurones clearly indicating that facilitation of test p.s.p. did not result from increased spike activity in the test interneurone. 5. Often heterosynaptic facilitation of the test p.s.p. was observed due to spontaneous activity in the heterosynaptic pathway, demonstrating the normal occurrence of the phenomenon. 6. Iontophoretic injection of 5-HT at critical, presumably synaptic, sites in the neuropil, evoked a facilitation of the test p.s.p. similar to heterosynaptic facilitation. Only the e.i.p.s.p.s. were so affected by 5-HT. On the contrary, other p.s.p. types were depressed by 5-HT as a result of conductance changes in the left giant cells. 7. Both heterosynaptic facilitation and 5-HT facilitation were suppressed by the presence in the bath of 5-HT (10(-5) M) and of LSD-25 (3 X 10(-4) M). The action of injected 5-HT on the membrane conductance of the left giant cell was also depressed in the pressence of 5-HT in the bath, but was unaffected by LSD-25 (3 X 10(-4) M). 8. From the parallelism of properties of heterosynaptic and 5-HT facilitation, it is suggested that 5-HT is the probable transmitter mediating heterosynaptic facilitation. It seems likely that 5HT is released from the heterosynaptic pathway at the level of the synaptic ending of the test interneurone on to the giant cell and that it increases the efficacy of this synapse, probably acting on the quantity of synaptic transmitter liberated.

Animals↗
PubMedDate not supplied

Neurophysiological changes associated with selective neuronal damage in hippocampus following transient forebrain ischemia.

Neurophysiological changes of hippocampal neurons were compared before and after transient forebrain ischemia using intracellular recording and staining techniques in vivo. Ischemic depolarization (ID) was used as an indication of severe ischemia. Under halothane anesthesia, approximately 13 min of ID consistently produced severe neuronal damage in the CA1 region of rat hippocampus, while CA3 pyramidal neurons and dentate granule cells remained intact. After such severe ischemia, approximately 60% of the CA1 neurons exhibited a synaptic potentiation. The excitability of these neurons progressively decreased following reperfusion. Approximately 30% of the CA1 neurons showed a synaptic depression following ischemia. The excitability of these neurons transiently decreased following reperfusion. After ischemia of the same severity, both synaptic transmission and excitability of CA3 and granule cells transiently depressed. These data suggest that ischemia-induced synaptic potentiation may be associated with the pathogenesis of neuronal damage following ischemia, and that the synaptic depression may have protective effects on hippocampal neurons after ischemic insult.

Animals↗
PubMed1970

Synaptic connexions of alpha extensor motoneurones with ipsilateral and contralateral cutaneous nerves.

1. Synaptic responses of alpha extensor motoneurones to stimulation of cutaneous nerves of the hind limb were recorded from the lumbosacral region in decerebrate and decerebrate-spinal unanaesthetized cats. Responses to ipsi- and contralateral stimulation are compared.2. Usually a single volley in an ipsilateral cutaneous nerve led to an inhibitory post-synaptic potential while one in a contralateral cutaneous nerve led to an excitatory post-synaptic potential or to discharge of the cell, thus demonstrating the classical reciprocal innervation pattern. In some cells either ipsilateral or crossed spinal action was of opposite sign to normal.3. Tests using graded stimulation showed the range of myelinated afferents associated with crossed spinal actions to be narrower than that for ipsilateral actions; for the sural nerve the ranges are 1-6 mu and 1-9 mu respectively. A substantial proportion of the coarser myelinated afferents do not make connexion with alpha motoneurones on either side of the cord; in the sural nerve this proportion includes the range 10-17 mu.4. Central transmission times for ipsilateral and crossed-spinal actions were estimated after making systematic allowance for conduction time to the cord in the associated cutaneous afferents. Mean values for inhibitory pathways from ipsilateral cutaneous nerves were about 2 msec, while those for crossed spinal facilitatory pathways were notably greater, 3-5 msec.5. Crossed spinal actions were more profoundly depressed by anaesthesia than were corresponding ipsilateral actions.6. Interpretation of the results was aided by a separate study of the input to the spinal cord; stimulus strength is related to the diameters of the cutaneous fibres excited and to peripheral conduction time in those fibres.

Animals↗
PubMed1999

Inputs from three brainstem sources to identified neurons of the mouse inferior colliculus slice.

A total of 40 neurons from of the central nucleus of the mouse inferior colliculus (IC) were recorded intracellularly from brain slices to determine input properties by electrical stimulation of the ipsilateral lateral lemniscus (LL), commissure of Probst (CP), and commissure of the IC (CoIC) together with cellular morphology (in 25 neurons) by biocytin injection and staining. Nine neurons had oriented (bipolar), 16 neurons non-oriented (multipolar) dendritic trees of various sizes. Axon collaterals of a given neuron often ran in several directions to provide multiple input to adjacent isofrequency laminae, the lateral nucleus of the IC, the brachium of the IC, the LL, the CP, and the IC commissure. Neurons were classified by spike response patterns to depolarizing current injection into onset- and sustained-spiking cells. The former had significantly shorter membrane-time constants, significantly less frequently and smaller hyperpolarizations after spike occurrence, and more Ca2+-humps. These properties and their preferred position in the dorsolateral ICC suggest a participation in binaural temporal processing. Almost all oriented cells showed only excitatory post-synaptic potentials (EPSPs) after LL stimulation, while in non-oriented cells inhibitory post-synaptic potentials (IPSPs) after the EPSPs were significantly more frequent. Neurons with largest dendritic trees and many dorsalward projecting axon collaterals were found in the ventral IC. There, neurons had average 4 ms (two synapses) shorter response latencies to LL stimulation than dorsally located neurons. Thus, neurons in the central and dorsal IC may receive mono- and disynaptic input from ventrally located neurons.

Animals↗
PubMed1986

The effect of percutaneous motor cortex stimulation on H reflexes in muscles of the arm and leg in intact man.

The technique of electrical stimulation of the brain via scalp electrodes has been used to activate corticospinal pathways in intact man. The intensity of stimulation was adjusted to be below the threshold necessary to evoke a direct electromyographic response when the muscles being tested were totally relaxed. Changes in spinal cord excitability were measured using H-reflex (monosynaptic) testing. By this means it was found that subthreshold scalp stimulation can produce a descending corticospinal volley even in the absence of a direct muscle response. The time course of changes in spinal cord excitability was evaluated by evoking test H reflexes at different intervals relative to the scalp stimulus. In wrist and finger flexor muscles of seven subjects, a single subthreshold scalp shock produced an initial peak facilitation of the H reflex which on average lasted for 2.5 ms. The end of the initial facilitation was marked by a return of the H reflex towards basal levels and on one occasion by a frank inhibition. It is suggested that the initial facilitation is produced by arrival at the motoneurones of monosynaptic excitatory post-synaptic potentials (e.p.s.p.s) and is truncated by the subsequent arrival of disynaptic inhibitory post-synaptic potentials (i.p.s.p.s). The initial facilitation was followed by a second phase of facilitation of the H reflex. The second phase was weaker, more variable and longer lasting (from 5 to 20 ms) than the first phase. The threshold of scalp stimulus intensity required to produce an effect on the H reflex was the same for the first and second phases of facilitation. Several possible explanations are discussed for the mechanism responsible for the late and long-lasting facilitation. In two subjects wrist and finger extensor muscles were studied. The time course of H-reflex changes was similar to that of the flexors except that the initial facilitation was followed by a frank inhibition in both subjects. In one subject thenar muscles and tibialis anterior were studied and behaved similarly to wrist and finger flexor muscles. Effects on the soleus H reflex was studied in seven subjects. In five of these subjects, in contrast to the other muscles studied, the initial event was an inhibition of the H reflex. This inhibition also could be seen preceding the usual period of facilitation in averaged rectified surface electromyogram (e.m.g.) records when scalp stimuli were given during weak voluntary activation of soleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Arm↗