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PubMed1996

Central modulation of stretch receptor neurons during fictive locomotion in lamprey.

1. In lamprey, stretch receptor neurons (SRNs), also referred to as edge cells, are located along the lateral margin of the spinal cord. They sense the lateral movements occurring in each swim cycle during locomotion. The isolated lamprey spinal cord in vitro was used to investigate the activity of SRNs during fictive locomotion induced by bath-applied N-methyl-D-aspartate (NMDA). Intracellular recordings with potassium acetate filled electrodes showed that 63% of SRNs had a clear locomotor-related modulation of their membrane potential. 2. Of the modulated SRNs, two-thirds had periods of alternating excitation and inhibition occurring during the ipsilateral and the contralateral ventral root bursts, respectively. The phasic hyperpolarization could be reversed into a depolarizing phase after the injection of chloride ions into the cells; this revealed a chloride-dependent synaptic drive. The remaining modulated SRNs were inhibited phasically during ipsilateral motor activity. 3. Experiments with barriers partitioning the recording chamber with the spinal cord into three pools, allowed an inactivation of the locomotor networks within one pool by washing out NMDA from the pool in which the SRN was recorded. This resulted in a marked reduction, but not an abolishment, of the amplitude of the membrane potential oscillations. Both the excitatory and the inhibitory phases were reduced, resulting from removal of input from inhibitory and excitatory interneurons projecting from the adjacent pools. If the glycine receptor antagonist strychnine (1 microM) was applied in one pool, the phasic hyperpolarizing phase disappeared without affecting the excitatory phase. 4. Bath application of the gamma-aminobutyric acid (GABA)A receptor antagonist, bicuculline (50-100 microM) blocked the spontaneous large unitary inhibitory postsynaptic potentials, which occurred without a clear phasic pattern. Bicuculline had no significant effect on the peak to peak amplitude of the locomotor-related membrane potential oscillations. The inhibition in SRNs therefore has a dual origin: glycinergic interneurons provide phasic inhibition, while the GABA system can exert a tonic inhibition via GABAA receptors. 5. These data show that, in addition to the stretch-evoked excitation, which SRNs receive during each locomotor cycle, most of them also receive excitation from the central pattern generator network during the ipsilateral contraction, which may ensure a maintained high level of sensitivity to stretch during the shortening phase of the locomotor cycle. This arrangement is analogous to the efferent control of muscle spindles exerted by gamma-motoneurons in mammals, which as a rule are coactivated with alpha-motoneurons to the same muscle (alpha-gamma linkage).

Animals↗

PubMed1991

Postsynaptic and presynaptic effects of the calcium chelator BAPTA on synaptic transmission in rat hippocampal dentate granule neurons.

When applied to rat hippocampal slices, the permeable calcium chelator, BAPTA-AM, caused a reduction of both post-spike train slow afterhyperpolarizations (AHPs) and spike-frequency adaptation in dentate granule cells. This indicated that BAPTA-AM can, like microinjected EGTA, block calcium-activated potassium channels. At perforant pathway synapses, BAPTA-AM caused a reduction of inhibitory postsynaptic potentials (IPSPs) and an initial increase and later decrease of excitatory postsynaptic potentials (EPSPs). The initial increase in EPSPs may be caused by presynaptic spike-broadening owing to inhibition of calcium-activated potassium channels which normally regulate the duration of the presynaptic action potential. These channels may be affected at lower doses of chelator than synaptic transmitter release. BAPTA salt injected into individual dentate granule cells caused, as expected, decreased AHPs and spike-frequency adaptation. Also, paradoxically, both excitatory and inhibitory synaptic potentials were increased although input resistance was not.

Action Potentials↗

PubMed2001

Substance P stimulates inhibitory synaptic transmission in the guinea pig basolateral amygdala in vitro.

To determine the physiological role of tachykinin NK1 receptors in the basolateral nucleus of the amygdala (BLN) we have studied the electrophysiological effects of substance P (SP) in the absence and presence of selective tachykinin receptor antagonists in guinea pig brain slices. Recordings were made from two populations of neurones; spiny pyramidal and stellate neurones, both thought to be projection neurones. Activation of NK1 receptors with SP increased the frequency of spontaneous inhibitory postsynaptic potentials in the majority of cells. This effect was blocked by bicuculline or tetrodotoxin, but not ionotropic glutamate receptor antagonists. The enhanced synaptic activity induced by SP was antagonised by the NK1 receptor antagonist L-760,735 but not by the less active enantiomer L-781,773 or the NK3 receptor antagonist L-769,927. Thus in the basolateral nucleus of the guinea pig amygdala, NK1 receptor activation preferentially stimulates inhibitory synaptic activity. Consistent with this observation, immunohistochemistry revealed NK1 receptor immunoreactivity to be largely restricted to a subset of GABA interneurones. These studies support a physiological role for SP in the regulation of pathways involved in the control of emotional behaviour.

Amygdala↗

PubMed2005

Neural mechanisms of the ultrafast activities.

A brief review of previous studies is presented on ultra-fast activities > 300 Hz (high frequency oscillations, HFOs) overlying the cortical response in the somatosensory evoked potential (SEP) or magnetic field (SEF). The characteristics of somatosensory HFOs are described in terms of reproducibility and origin (area 3b and 1) of the HFOs, changes during a wake-sleep cycle, effects of higher stimulus rate or tactile interference, etc. Also, several hypotheses on the neural mechanisms of the HFOs are introduced; the early HFO burst is probably generated from action potentials of thalamocortical fibers at the time when they arrive at the area 3b (and 1), since this component is resistant to higher stimulus rate > 10Hz or general anesthesia: by contrast, the late HFO burst is sensitive to higher stimulus rate, reflecting activities of a postsynaptic neural network in the somatosensory cortices, area 3b and 1. As to possible mechanisms of the late HFO burst genesis, an interneuron hypothesis, a fast inhibitory postsynaptic potential (IPSP) hypothesis of the pyramidal cell and a chattering cell hypothesis will be discussed on the basis of physiological and pathological features of the somatosensory HFOs.

Action Potentials↗

PubMedDate not supplied

Facilitation of transmission via inhibitory pathway 1a to spinal extensor motoneurons in response to stimulation of the forelimb nerves in cats.

Activation of forelimb flexor reflex afferent in cats anesthetized with a mixture of Chloralose and Nembutal evoked temporospatial facilitation in the reciprocal inhibitory pathways to spinal extensor motoneurons. The amplitude of disynaptic reciprocal 1a inhibitory postsynaptic potentials (IPSP) evoked in the extensor motoneurons by activation of the most excitable fibers of the nerve supplying the antagonist muscle increased several-fold using conditioning stimulation of the forelimb nerve. Facilitation of 1a IPSP occurred on a background of IPSP evoked by descending inter-limb discharges. Facilitation of 1a IPSP had a latent period of 18-20 msec and could last to 60 msec. The possible role of inhibitory 1a interneurons in interlimb coordination is discussed.

Animals↗

PubMed1993

Metabotropic glutamate receptors mediate a post-tetanic excitation of guinea-pig hippocampal inhibitory neurones.

1. Inhibitory cell activity and inhibitory postsynaptic potentials impinging spontaneously on pyramidal cells were recorded in the CA3 region of hippocampal slices from guinea-pig. We compared the effects on synaptic inhibition, of tetanic stimuli in the presence of antagonists of ionotropic excitatory amino acid receptors, and of application of agonists of metabotropic glutamate receptors. 2. Tetanic stimulation of afferent fibres caused an increase, of duration 0.5-2.5 min, in the frequency of spontaneous Cl(-)-mediated IPSPs. Inhibitory cell firing increased due to a depolarization and a reduction of after-hyperpolarizing potentials. 3. Tetanic stimulation induced, in some experiments, rhythmic bursts of IPSPs and transformed the firing pattern of some inhibitory cells from a discharge of single action potentials to rhythmic bursts of three to five action potentials. 4. Application of the metabotropic glutamate receptor agonist, trans-1-amino-cyclopentane-1,3-dicarboxylic acid (tACPD), at concentrations from 3-10 microM increased the frequency of spontaneous IPSPs. In some slices tACPD caused IPSPs to occur rhythmically. IPSP frequency did not continue to increase with concentrations of tACPD above 20 microM. 5. tACPD depolarized inhibitory cells and reduced after-hyperpolarizing potentials. High concentrations (50-100 microM) of tACPD excited inhibitory cells to potentials at which they no longer discharged fast action potentials. 6. Both tetanic stimulation and tACPD led to the appearance in pyramidal cell pairs of simultaneous IPSPs which were not previously observed, suggesting that the same group of inhibitory cells was excited in both cases. 7. Low concentrations of tACPD (3-10 microM) enhanced IPSP responses to tetanic stimuli, while the effects of tetanic stimuli were occluded in the presence of high concentrations (20-30 microM) of tACPD. 8. We suggest that activation of metabotropic glutamate receptors during tetanic stimulation leads to a post-tetanic excitation of inhibitory cells that mediate Cl(-)-dependent IPSPs.

2-Amino-5-phosphonovalerate↗

PubMed1980

Dendrodendritic inhibition: demonstration with intracellular recording.

The isolated turtle olfactory bulb was used to characterize synaptic interactions between mitral and granule cell dendrites. First, blockade of antidromic invasion of mitral cell dendrites caused a large decrease in the size of the inhibitory postsynaptic potential (IPSP) recorded in mitral cells, indicating that the IPSP results in large part from activity in the dendrites of mitral cells. Second, direct depolarization of mitral cells was followed by an IPSP. In the presence of tetrodotoxin, depolarization of mitral cells evoked calcium spikes (as would be expected for presynaptic membranes) followed by IPSP's. These findings demonstrate that regenerative sodium spikes and axonal pathways are not required for this inhibitory pathway and that the inhibition is indeed a result of local dendritic interaction. Such a pathway provides an obligatory synaptic inhibition of mitral cells following their activation and emphasizes the tight coupling that exists with reciprocal dendrodendritic synapses.

Action Potentials↗

PubMed1987

Models of synchronized hippocampal bursts in the presence of inhibition. I. Single population events.

1. We constructed model networks with 520 or 1,020 cells intended to represent the CA3 region of the hippocampus. Model neurons were simulated in enough detail to reproduce intrinsic bursting and the electrotonic flow of currents along dendritic cables. Neurons exerted either excitatory or inhibitory postsynaptic actions on other cells. The network models were simulated with different levels of excitatory and inhibitory synaptic strengths in order to study epileptic and other interesting collective behaviors in the system. 2. Excitatory synapses between neurons in the network were powerful enough so that burst firing in a presynaptic neuron would evoke bursting in its connected cells. Since orthodromic or antidromic stimulation evokes both a fast and a slow phase of inhibition, two types of inhibitory cells were simulated. The properties of these inhibitory cells were modeled to resemble those of two types of inhibitory cells characterized by dual intracellular recordings in the slice preparation. 3. With fast inhibition totally blocked, a stimulus to a single cell lead to a synchronized population burst. Thus the principles of our epileptic synchronization model, developed earlier, apply even when slow inhibitory postsynaptic potentials (IPSPs) are present, as apparently occurs in the epileptic hippocampal slice. The model performs in this way because bursting can propagate through several generations in the network before slow inhibition builds up enough to block burst propagation. This can occur, however, only if connectivity is sufficiently large. With very low connection densities, slow IPSPs will prevent the development of full synchronization. 4. We performed multiple simulations in which the fast inhibitory conductance strength was kept fixed at various levels while the strength of the excitatory synapses was varied. In each simulation, we stimulated either one or four cells. For each level of inhibition, the peak number of cells bursting depended sensitively on excitatory synaptic strength, showing a sudden increase as this strength reached a critical level. The critical excitation, which depended on the level of inhibition, corresponded to the level at which bursting can propagate from cell to cell at the particular level of inhibition. 5. We performed an analogous series of simulations in which the strength of excitatory synapses was held constant while the strength of fast inhibitory synapses was varied, stimulating a single neuron in each case. These simulations correspond to experiments that have been done in the hippocampal slice as low doses of picrotoxin are washed into a slice, gradually abolishing fast inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1985

Electrophysiology of identified neurosecretory and non-neurosecretory cells in the cockroach pars intercerebralis.

Two cell types can be distinguished with intracellular recording from the pars intercerebralis of the American cockroach (Periplaneta americana). The first type, which corresponds morphologically to the medial neurosecretory cell, always had spontaneously occurring, overshooting action potentials. These action potentials are probably endogenously produced. Tetrodotoxin experiments revealed that sodium is the dominant ion of the action potential. The action potentials are followed by a relatively long after-hyperpolarization. The input resistance of these cells ranged from 120 to 390 M omega. A mathematical model, based on cellular morphology and response to current pulses, revealed a membrane time constant of about 100 msec and an axonal:somatic conductance ratio of approximately 13. Area-specific membrane resistance was estimated at 33 k omega cm2. These cells also often had reversible and spontaneous inhibitory postsynaptic potentials. The second cell type, which is non-neurosecretory, never produced spontaneous action potentials and rarely had synaptic potentials. Action potentials could be evoked by current injection into the cell body or by extracellular stimulation of their axons in the posteroventral portion of the the protocerebrum. These action potentials also depend on sodium ions. Their input resistance ranged from 16 to 35 M omega. They had a membrane time constant of approximately 15 msec and an axonal:somatic conductance ratio of about 9. Their area specific membrane resistance was estimated at 14 k omega cm2.

Action Potentials↗

PubMed1986

Role of inhibitory mechanisms in staring spells.

Phenomena of a negative nature--a motionless stare with arrest of mental activity--characterize absence seizures and some complex partial seizures. In agreement with this clinical observation, it has been found that the slow waves of the spike-wave complex are associated with inhibitory postsynaptic potentials and cessation of neuron firing in both humans and experimental animals. Gamma-aminobutyric acid (GABA) concentration is increased in the cerebral cortex in some experimental models of spike-wave discharge, and GABA agonists exacerbate spike-wave discharges in a variety of experimental models. GABAergic neurons and terminals are also increased in the hippocampus of seizure-sensitive gerbils, and kindling of the hippocampus and amygdala appears to enhance GABAergic inhibitory mechanisms. Antiabsence drugs selectively depress inhibitory pathways in the central nervous system, providing further evidence in support of the hypothesis that absences represent inhibitory paroxysms. Antiabsence drugs also appear to be useful adjunctive drugs in the treatment of complex partial seizures associated with spike-wave discharges, suggesting that here too inhibitory mechanisms may play a prominent role. All these clinical, physiological, and pharmacological observations would indicate that staring spells represent inhibitory seizures, occurring primarily in absences and secondarily in some complex partial seizures.

Anticonvulsants↗

PubMed1992

Serotonin-containing neurons in lobsters: their role as gain-setters in postural control mechanisms.

1. The electrophysiological properties of two pairs of identified serotonin-containing neurons in the fifth thoracic (T5) and first abdominal (A1) ganglia of the lobster, Homarus americanus, were studied with the use of intracellular recording methods. Intracellular dye injection combined with immunocytochemistry verified the neurochemical status of the recorded neurons. 2. The serotonin-containing neurons usually are spontaneously active at 0.5-1.0 Hz and produce large, overshooting action potentials with a prominent after-hyperpolarization. The action potentials appear to be generated by a pacemaking mechanism endogenous to the cells. Extracellular recordings from thoracic connectives and from second thoracic roots show that action potentials from the cells in A1 and T5 are propagated rostrally along their axons and invade axon collaterals that innervate neurohemal organs in the second thoracic roots and the pericardial organs. These observations suggest that these serotonin-containing cells may function in part as important neurosecretory cells in the lobster. 3. Members of the pairs of serotonin-containing cells are not synaptically connected. They receive prominent inhibitory inputs in the form of inhibitory postsynaptic potentials (IPSPs), which exhibit discrete size classes and probably arise from several sources. Most IPSPs are temporally synchronized among the two pairs of serotonin-containing cells. 4. The serotonin-containing cells respond to stimulation of postural command fibers, with flexion command fibers exciting and extension command fibers inhibiting the cells, suggesting that these cells are a part of the postural flexion circuitry. 5. Intracellular activation or inhibition of the serotonin-containing cells has no effect on the spontaneous readout of postural motor programs recorded from motor nerve roots. Coactivation of the serotonin-containing cells and command fibers, or inhibition of the serotonin-containing cells while activating command fibers, however, shows that the cells act as "gain-setters," modulating the interaction between command inputs and motoneuron outputs. 6. About 24% of the motor neuron units analyzed are influenced by the serotonin-containing cells. There is a bias toward facilitation of the readout of flexion motor programs, particularly with stimulation of strong and moderate flexion command fibers. 7. The serotonin-containing cells in T5 and A1 ganglia are hypothesized to serve two functions, one tonic and the other phasic, in modulating behavioral output in lobsters. Tonic firing of the cells should result in a sustained release of serotonin from central and peripheral sets of nerve terminals, which, in turn, could influence peripheral and central targets of the amine.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed2005

Blockade of the membranal GABA transporter potentiates GABAergic responses evoked in pyramidal cells by mossy fiber activation after seizures.

The presence of a neurotransmitter within a synaptic terminal is normally due to its local synthesis. However, uptake of the neurotransmitter from the extracellular milieu by a specific membranal transporter can also explain its intraterminal accumulation. A specific vesicular transporter carries the neurotransmitter into synaptic vesicles, enabling it to be released in a calcium-dependent manner when the terminal is invaded by an action potential. Under certain circumstances, a neurotransmitter can also be released by the reversal in the direction of its membranal transporter, in a calcium-independent manner. Interestingly, gamma-aminobutyric acid (GABA) can be released in this manner after epileptic activity. With intracellular recordings, in this work we show that in rats subjected to seizures, but not in naive rats, mossy fiber stimulation in the presence of glutamate receptor blockers produces bicuculline-sensitive inhibitory postsynaptic potentials (IPSPs) in pyramidal cells. The blockade of the membranal GABA transporter (GAT-1) strongly enhances the amplitude and decay time of the IPSPs in both high and low extracellular calcium concentrations. This electrophysiological evidence, together with previous neurochemical and immunohistological data, show that GAT-1 contributes to the termination of the synaptic action of mossy fiber-released GABA and rules out its involvement in depolarization-dependent GABA release.

Animals↗

PubMedDate not supplied

Synaptic transmission in ammonia intoxication.

Ammonia intoxication allegedly plays a significant role in the pathophysiology of hepatic encephalopathy. In order to understand the pathogenesis of this encephalopathy it is necessary to know the effects of ammonia on the mechanisms by which neurons communicate, i.e., excitatory and inhibitory synaptic transmissions. NH4+ decreases excitatory synaptic transmission mediated by glutamate. Possibly, this effect is related to a depletion of glutamate in presynaptic terminals. NH4+ decreases inhibitory synaptic transmission mediated by hyperpolarizing Cl(-)-dependent inhibitory postsynaptic potentials. This effect is related to the inactivation of the extrusion of Cl- from neurons by NH4+. By the very same action, NH4+ also decreases the hyperpolarizing action of Ca2+- and voltage-dependent Cl- currents. These currents may modify the efficacy of the synaptic input to neurons and increase neuronal excitability. Estimates derived from experimental observations suggest that an increase of CNS tissue NH4+ to 0.5 mumol/g is sufficient to disturb excitatory and inhibitory synaptic transmission and to initiate the encephalopathy related to acute ammonia intoxication. Chronic portasystemic shunting of blood, as in hepatic encephalopathy, significantly changes the relation between CNS NH4+ and function of synaptic transmission. A portacaval shunt increases the tissue NH4+ necessary to disturb synaptic transmission. However, after a portasystemic shunt, synaptic transmission becomes extremely sensitive to any acute increase of NH4+ in the CNS.

Ammonia↗

PubMed2005

Intracellular analysis of reflex pathways underlying the stumbling corrective reaction during fictive locomotion in the cat.

In cat and humans, contact between an obstacle and the dorsum of the foot evokes the stumbling corrective reaction (reflex) that lifts the foot to avoid falling. This reflex can also be evoked by short trains of stimuli to the cutaneous superficial peroneal (SP) nerve in decerebrate cats during the flexion phase of fictive locomotion. Here we examine intracellular events in hindlimb motoneurons accompanying stumbling correction. SP stimulation delivered during the flexion phase excites knee flexor motoneurons at short latency [minimum excitatory postsynaptic potential (EPSP) latency 1.8 ms; mean 2.7 ms]. Although a similar short latency excitation occurs in ankle extensors (mean latency, 2.8 ms), recruitment is delayed until successive shocks in the stimulus train overcome the locomotor-related hyperpolarization of ankle extensors. In ankle flexor motoneurons, SP stimulation evokes an inhibition (mean latency, 2.7 ms) that briefly reduces or stops their firing during the flexion phase. There is a phase-dependent modulation of SP-evoked EPSP amplitude as well as latency during locomotion. However, the more obvious change in SP reflex pathways with the onset of fictive locomotion is the reduced inhibition of ankle extensor motoneurons and the increased inhibition of ankle flexors. These results show that the characteristic pattern of hindlimb motoneuron activation during SP nerve-evoked stumbling correction results from 1) di- and trisynaptic excitation of knee flexor and ankle extensor motoneurons; 2) increased inhibitory postsynaptic potentials in ankle flexors and a suppression of inhibition in extensors, 3) sculpting of the short-latency SP postsynaptic effects by motoneuron membrane potential, and 4) longer latency excitatory effects that are likely evoked by lumbar interneurons involved in the generation of fictive locomotion.

Animals↗

PubMed1988

Physiological heterogeneity of nonpyramidal cells in rat hippocampal CA1 region.

Functional differentiation of nonpyramidal cells was studied by intracellular recording and staining of cells located in the stratum pyramidale or along the border between the stratum radiatum and the stratum lacunosum-moleculare of slices prepared from rat hippocampal CA1 region. In the stratum pyramidale, nonpyramidal cells (fast-spiking cells, type I cells) exhibited brief-duration action potentials (mean spike-width at one-half amplitude = 0.28 ms, N = 9) and little or no frequency adaptation of spike discharge to depolarizing current pulse. These cells ramified axon collaterals mainly in the stratum pyramidale or in the apical side of the stratum oriens. The HRP-injected nonpyramidal cells located between the stratum radiatum and the stratum lacunosum-moleculare (type II cells) showed different physiological characteristics from fast-spiking cells in the stratum pyramidale. The spike width was longer than that of fast-spiking cells (mean duration measured at one-half amplitude = 0.61 ms, N = 11) and these cells exhibited adaptation of spike discharge in response to depolarizing current pulses. Following hyperpolarizing current pulses, a depolarizing potential was produced in some type II cells. Although most cells of this group sent axon collaterals into the stratum radiatum or into the stratum lacunosum-moleculare, there were also cells whose axon collaterals extended to and ramified in the stratum pyramidale. In contrast to pyramidal cells, spikes of both types of nonpyramidal cells did not broaden during repetitive firing evoked by large depolarizing current pulses. Stimulation of the stratum radiatum caused excitatory and inhibitory postsynaptic potentials in both type I and II cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1996

Photoinactivation of the giant neuropil glial cells in the leech Hirudo medicinalis: effects on neuronal activity and synaptic transmission.

1. We studied the effects of photoinactivation of neuropil glial (NG) cells of the leech Hirudo medicinalis on neuronal activity and synaptic transmission. Each segmental ganglion contains two of these giant glial cells, which are electrically and dye coupled. 2. One of the two NG cells in an isolated segmental ganglion was filled with the dye Lucifer yellow (LY). Subsequent irradiation of the ganglion with laser light (440 nm) to photolyze LY caused irreversible depolarization of both NG cells. The NG cells that were filled with LY depolarized from -73 +/- 1.1 (SE) mV to -22 +/- 2.4 mV within 25 +/- 2.8 min of continuous irradiation (n = 22). The other NG cell, which was not directly filled with LY, depolarized with some delay. 3. Photoinactivation of the NG cells caused an irreversible depolarization of Retzius neurons and noxious (N) sensory cells by a mean of 14 mV (n = 36) and 9 mV (n = 24), respectively. In addition, the input resistance was reduced by 54% in Retzius cells and by 34% in N cells. Spikes could not be evoked in Retzius cells after the inactivation of the NG cells, either by intracellular current injection or by electrical nerve stimulation. Similarly, anterior pagoda neurons, annulus erector neurons, and the excitor neurons of the ventrolateral circular muscles became inexcitable. However, N cells, heart interneurons, and most of the heart motor neurons, touch cells, and pressure cells could still generate spontaneous or evoked action potentials. 4. Photoinactivation of the NG cells impaired the electrical connection between the two Retzius neurons. The electrical coupling was completely eliminated in six of eight cell pairs and reduced by 66% in two others. 5. Photoinactivation of the NG cells in the 3rd and 4th segmental ganglion caused a complete block of the chemical synapse between reciprocal inhibitory heart interneurons in these ganglia; the bursting rhythm either stopped or changed to a tonic activity, whereas inhibitory postsynaptic potentials could not be recorded in either heart interneuron anymore. 6. Laser irradiation alone had no effect on neuronal activity and synaptic transmission. Addition of glutathione (10 mM) and ascorbic acid (10 mM) to the saline to bind extracellular radicals that might be produced by the irradiation did not suppress the effects caused by photoinactivation of NG cells. 7. Elevation of bath K+ concentration to 12 mM, acidification of the saline to pH 5.5, and alkalinization to pH 8.5 for 6 min each did not mimick the effects on membrane properties of Retzius cells as produced by inactivation of NG cells. The results suggest some role of glial cells in the maintenance of neuronal activity and electrical and chemical synaptic transmission.

Animals↗

PubMed1993

Effects of interferons and hydrogen peroxide on CA3 pyramidal cells in rat hippocampal slice cultures.

In viral diseases of the CNS, both interferon-alpha/beta and interferon-gamma are produced intrathecally. At least some of the neurological symptoms associated with these diseases may be due to the effects of these cytokines. We have studied the actions of interferons on CA3 pyramidal cells in hippocampal slice cultures. Bath application of interferon-alpha/beta and interferon-gamma produced an excitatory effect on CA3 pyramidal cells and a decrease in evoked inhibitory postsynaptic potential amplitude, eventually leading to epileptiform bursting. These effects were slow in onset (several minutes), suggesting an indirect mechanism of action. Several lines of evidence suggest that the actions of interferons on pyramidal cells may at least in part be mediated by reactive oxygen intermediates, known to be released from non-neuronal cells: the effects of interferon on CA3 pyramidal cells were blocked by the free radical scavengers catalase and superoxide dismutase. Hydrogen peroxide reduced evoked inhibitory synaptic transmission, eventually leading to epileptiform bursting, thus mimicking several of the effects of interferons on pyramidal cells.

Action Potentials↗

PubMed1993

Synaptic organization of the vestibulo-collic pathways from six semicircular canals to motoneurons of different neck muscles.

The pattern of inputs from six semicircular canals to neck motoneurons was investigated by stimulating six ampullary nerves electrically and recording intracellular potentials from motoneurons of the rectus capitis dorsalis (RD), the complexus (COMP) and the obliquus capitis caudalis (OCA) muscles at the upper cervical cord of the cat. RD and COMP motoneurons received disynaptic excitation from bilateral anterior and contralateral horizontal ampullary nerves and disynaptic inhibition from bilateral posterior and ipsilateral horizontal ampullary nerves. OCA motoneurons received excitation from ipsilateral vertical and contralateral horizontal ampullary nerves and inhibition from contralateral vertical and ipsilateral horizontal ampullary nerves. Ipsilateral disynaptic inhibitory postsynaptic potentials and contralateral disynaptic excitatory postsynaptic potentials to these motoneurons were mediated by the medial longitudinal fasciculus (MLF) and the other postsynaptic potentials by the extra-MLF pathways. The results indicated that motoneurons of a neck muscle have its own characteristic pattern of inputs from six semicircular canals.

Animals↗