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PubMed1984

Synaptic hyperpolarization and inhibition of turtle cochlear hair cells.

Intracellular recordings were made from turtle cochlear hair cells in order to examine the properties of the post-synaptic potentials evoked by electrical stimulation of the efferent axons. Single shocks to the efferents generated a hair cell membrane hyperpolarization with an average amplitude generally less than 1 mV and lasting for about 100 ms. With short trains of shocks, the size of the post-synaptic potential grew markedly to a maximum of 20-30 mV. The interaction between pairs of shocks separated by a varying interval was studied. For an interval of 4 ms, the response to the second shock was increased on average by a factor of 3 and the conditioning effect of the first shock decayed with a time constant of about 100 ms. We suggest the augmentation in response to trains of shocks may be partly due to facilitation of efferent transmitter release. The efferent post-synaptic potentials could be reversibly abolished by perfusion with perilymphs containing 3 microM-curare or atropine, and infusion of acetylcholine gave a transient membrane hyperpolarization. These observations are consistent with efferent action being mediated via a cholinergic synapse onto the hair cells. The post-synaptic potentials could be reversed in polarity by injection of hyperpolarizing currents through the recording electrode. The reversal potential was estimated as about -80 mV, 30 mV negative to the resting potential. Near reversal, a small brief depolarization was evident and may constitute a minor component of the synaptic response. The value of the reversal potential was unaffected by substitution of the perilymphatic chloride, but was altered in a predictable manner by changes in extracellular potassium concentration indicating that the post-synaptic potentials arise mainly by an increase in the permeability of the hair cell membrane to potassium ions. Throughout the post-synaptic hyperpolarization there was a reduction in the sensitivity of the hair cell to tones at its characteristic frequency. The desensitization, maximal for low sound pressures, varied in different cells from a factor of 1.6 to 28. At the peak of the largest synaptic potentials, the receptor potential remained negative to the resting potential with all but the loudest characteristic frequency tone s. We suggest that there are two factors in efferent inhibition; one a r duction in the receptor potential at the hair cell's characteristic frequency and the other a hyperpolarization of its membrane potential which should reduce the release of excitatory transmitter onto the afferent terminals.

Acetylcholine↗
PubMed1992

Effects of the novel NMDA receptor antagonist, CGP 39551, on field potentials and the induction and expression of LTP in the dentate gyrus in vivo.

The effects of the novel competitive N-methyl-D-aspartate (NMDA) receptor antagonist, CGP 39551 [the carboxyethylester of CGP 37849; DL-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid], on extracellular field potentials and long-term potentiation (LTP) induced in the dentate gyrus by stimulation of the perforant path were studied in anesthetized rats. CGP 39551 attenuated the population spike (PS) and excitatory postsynaptic potential (EPSP) amplitude of dentate field potentials, reduced the NMDA receptor-mediated component of train-evoked burst potentials, and prevented the induction of LTP. The decrease in PS and EPSP amplitude produced by CGP 39551 was observed mainly in non-potentiated synaptic populations; potentiated field potentials were only minimally affected by drug treatment. These results are consistent with receptors may contribute in a tonic manner to the state of dentate granule cell excitability. Finally, the differential modulation of potentiated and non-potentiated synapses by CGP 39551 suggests that a change in some properties of postsynaptic AMPA receptors is involved in the expression of LTP.

2-Amino-5-phosphonovalerate↗
PubMed1995

Long-term potentiation and synaptic protein phosphorylation.

Long-term potentiation (LTP) is a well known experimental model for studying the activity-dependent enhancement of synaptic plasticity, and because of its long duration and its associative properties, it has been proposed as a system to investigate the molecular mechanisms of memory formation. At present, there are several lines of evidence that indicate that pre- and postsynaptic kinases and their specific substrates are involved in molecular mechanisms underlying LTP. Many studies focus on the involvement of protein kinase C (PKC). One way to investigate the role of PKC in long-term potentiation is to determine the degree of phosphorylation of its substrates after in situ phosphorylation in hippocampal slices. Two possible targets are the presynaptic membrane-associated protein B-50 (a.k.a. GAP 43, neuromodulin and F1), which has been implicated in different forms of synaptical plasticity in the brain such as neurite outgrowth, hippocampal LTP and neurotransmitter release, and the postsynaptic protein neurogranin (a.k.a. RC3, BICKS and p17) which function remains to be determined. This review will focus on the protein kinase C activity in pre- and postsynaptic compartment during the early phase of LTP and the possible involvement of its substrates B-50 and neurogranin.

Animals↗
PubMed1986

Properties of rat medial septal neurones recorded in vitro.

Activity of neurones of the rat medial septal nucleus (m.s.) was recorded in in vitro slice preparations. The recorded population could be divided into low (less than 30 M omega)- and high-input-resistance (greater than 30 M omega) neurones. The high-resistance neurones tended to fire spontaneous action potentials and post-synaptic potentials. Some of the spontaneously active cells fired rhythmically at rates of 2-10 Hz. The rhythmicity disappeared following hyperpolarization of the recorded cell. The cells could fire repetitive Ca2+ spikes in the presence of tetrodotoxin (TTX) and intracellular Cs+. Cd2+ blocked this rhythmicity. Most of the m.s. cells had a non-linear voltage-current relation in both the hyperpolarizing and depolarizing directions. Hyperpolarizing rectification was selectively blocked by extracellular Cs+ whereas depolarizing rectification could be blocked by TTX. A recovery from hyperpolarization was associated in many cells with a transient depolarization (anodal break (a.b.) potential). A 20 ms 15 mV hyperpolarization could trigger an a.b. potential. The a.b. potential was reduced by TTX and Cs+ but not by Cd2+ or Mn2+. Depolarization of quiescent neurones triggered action potential discharges. A common pattern of discharge was a burst of two spikes which kept a fairly constant interspike interval. The second spike in a doublet could not follow a rate of 10 Hz depolarizing current pulses. It was also sensitive to topical application of Cd2+. It is therefore suggested that Ca2+ might be involved in the generation of the doublet. Long depolarizing current pulses produced trains of action potentials, showing little accommodation and little after-hyperpolarization, indicating that these cells possess little Ca2+-dependent K+ current. Many cells emitted spontaneous post-synaptic potentials at high rates. These could be blocked by picrotoxin. Stimulation of the lateral septal (l.s.) nucleus produced a Cl-dependent i.p.s.p. The i.p.s.p. was blocked by picrotoxin. Topical application of gamma-aminobutyric acid (GABA) produced a marked Cl(-)-dependent increase in conductance. It is suggested that l.s. projects a GABA-mediated inhibitory connexion to the m.s. Acetylcholine (ACh) depolarized m.s. neurones and caused an increase in input resistance. The response was present in TTX or Cd2+-containing medium. Atropine blocked responses to ACh. 5-Hydroxytryptamine (5-HT) hyperpolarized m.s. neurones in a manner consistent with an increase in K+ conductance. The effects of 5-HT were seen in TTX- and Cd2+-treated m.s. slices.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1997

Nucleus-specific chloride homeostasis in rat thalamus.

Synchronous thalamic network activity occurring during slow wave sleep and paroxysmal discharges critically depends on the ability of thalamocortical relay cells and inhibitory neurons of the nucleus reticularis thalami (nRt) to fire bursts of action potentials. Inhibitory synaptic potentials (IPSPs) originating from nRt cells are crucial in deinactivating T-channels and thus promoting burst firing in relay cells, but the functional role of intra-nRt IPSPs is less well understood. A major factor that regulates the net effects of IPSP generation is the chloride equilibrium potential (ECl). Here we applied the perforated patch-clamp technique, using the cation-selective ionophore gramicidin to assess the reversal potential of chloride in nRt and relay cells in brain slices. We found that the reversal potential of GABA-induced membrane currents (EGABA) was significantly more hyperpolarized in relay (-81 +/- 2.6 mV), as compared with nRt cells (-71 +/- 2.5 mV). EGABA was not significantly different from the reversal potential of evoked IPSCs (EIPSC; -82 +/- 4.4 mV) in relay cells. In both relay and reticular neurons the chloride gradient was collapsed partially by the chloride cation cotransport blocker furosemide, suggesting an active chloride extrusion mechanism in thalamic neurons. Given the relatively hyperpolarized resting potentials (approximately -70 mV) reported for nRt and relay cells during in vitro thalamic oscillations, we conclude that under these conditions GABAA IPSPs lead to significant hyperpolarization in relay cells. By contrast, intra-nRt inhibition essentially would be shunting, i.e., would produce minimal membrane polarization but still could reduce the amplitude of excitatory events.

2-Amino-5-phosphonovalerate↗
PubMed1977

Physiological and anatomical characteristics of reticulospinalneurones in lamprey.

1. Intracellular records were obtained from giant reticulospinal cells (Müller cells) in the brain of adult lamprey. The cells had maximum resting potentials of -80 mV and action potentials with overshoots of 30 mV. Input resistances varied from 2 to 8 MOmega.2. Individual spontaneous excitatory and inhibitory synaptic potentials (e.p.s.p.s and i.p.s.p.s) were observed, as well as occasional high frequency bursts of excitatory potentials. Much of the spontaneous synaptic activity could be eliminated by elevating the Ca(2+) concentration in the bathing solution to 10-15 mM, suggesting that the synaptic potentials were due to spike activity in elements presynaptic to Müller cells.3. Electrical stimulation of cranial nerves produced synaptic responses in Müller cells. Ipsilateral vestibular nerve stimulation produced i.p.s.p.s; contralateral stimulation, e.p.s.p.s. Stimulation of either optic nerve produced mixed synaptic responses with e.p.s.p.s dominating in cells with large resting potentials. Trigeminal nerve stimulation produced mixed responses. Olfactory nerve stimulation produced excitation. Spinal cord stimulation produced e.p.s.p.s and i.p.s.p.s, the dominant effect being inhibition.4. In favourable preparations strong electrical stimulation of cranial nerves produced afterdisharges in Müller cells, lasting from a few seconds after stimulation of the olfactory and vestibular nerves to as long as several minutes after optic, trigeminal or spinal cord stimulation.5. Natural stimulation of tactile, visual and vestibular receptors resulted in synaptic responses similar to those produced by electrical stimulation of the cranial nerves. Fish odour applied to the olfactory mucosa produced no response.6. Iontophoretic application of L-glutamate to Müller cells produced depolarization accompanied by a decrease in input resistance. In addition, glutamate produced bursts of inhibitory and excitatory synaptic potentials, presumably by depolarizing excitatory or inhibitory nerve terminals or nearby cell bodies.7. Iontophoretic application of gamma-aminobutyric acid (GABA) resulted in a slight hyperpolarization, accompanied by a large reduction in input resistance. The reversal point both of the hyperpolarizations and of the spontaneous inhibitory post-synaptic potentials was about 6 mV greater than the resting potential.8. There were two types of synaptic ending on Müller cell bodies, one type containing round vesicles and the other containing ellipsoidal vesicles. These terminals were intermixed over the surface of the cell bodies and dendrites with no readily apparent segregation.9. Intracellular records from the spinal axons of Müller cells during electrical stimulation of cranial nerves and spinal cord showed, in addition to the normal propagating action potential activity which normally originates in the cell bodies, depolarizing, hyperpolarizing and biphasic evoked potentials. These membrane responses were grossly similar in appearance to synaptic potentials except that the large depolarizing potentials had unusually long decay times. The physiological basis of these potentials remains unclear.10. Electron microscopic examination showed very few synaptic endings afferent to Müller axons, a finding in contrast to the abundance of synaptic-like potentials recorded. However, the occasional synapses afferent to Müller axons were invariably located near an efferent synaptic region of the axon itself. This raises the possibility that a very limited number of synaptic regions of Müller axons may be subject to presynaptic modulation of transmitter release.11. The observations reported here support the idea that Müller cells in lamprey are an important motor outflow from the brain and serve to coordinate the lamprey's trunk responses to external sensory stimulation.

Action Potentials↗
PubMed1991

Selective suppression of afferent but not intrinsic fiber synaptic transmission by 2-amino-4-phosphonobutyric acid (AP4) in piriform cortex.

Differences in the glutaminergic modulation of afferent and intrinsic fiber synaptic transmission in piriform (olfactory) cortex were investigated using extracellular and intracellular recording techniques in a transverse slice preparation. 2-Amino-4-phosphonobutyric acid (AP4) strongly suppressed synaptic potentials evoked by afferent fiber stimulation in layer 1a, while having a much weaker effect on synaptic potentials evoked by intrinsic fiber stimulation in layer 1b. Both the racemic mixture and L-(+)-enantiomer of AP4 showed this differential effect. Suppression of afferent fiber synaptic potentials was accompanied by an increase in paired pulse facilitation, suggesting a pre-synaptic mechanism, while intrinsic fiber synaptic potentials showed little change in facilitation. Previous work has shown that cholinergic modulation in piriform cortex appears selective for intrinsic fiber synapses. The present data describes a pre-synaptic glutaminergic modulation complementary to the cholinergic modulation.

Afferent Pathways↗
PubMed1990

Excitatory postsynaptic potentials in rat neocortical neurons in vitro. III. Effects of a quinoxalinedione non-NMDA receptor antagonist.

1. Intracellular microelectrodes were used to obtain recordings from neurons in layer II/III of rat frontal cortex. A bipolar electrode positioned in layer IV of the neocortex was used to evoke postsynaptic potentials. Graded series of stimulation were employed to selectively activate different classes of postsynaptic responses. The sensitivity of postsynaptic potentials and iontophoretically applied neurotransmitters to the non-N-methyl-D-asparate (NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) was examined. 2. As reported previously, low-intensity electrical stimulation of cortical layer IV evoked short-latency early excitatory postsynaptic potentials (eEPSPs) in layer II/III neurons. CNQX reversibly antagonized eEPSPs in a dose-dependent manner. Stimulation at intensities just subthreshold for activation of inhibitory postsynaptic potentials (IPSPs) produced long-latency (10 to 40-ms) EPSPs (late EPSPs or 1EPSPs). CNQX was effective in blocking 1EPSPs. 3. With the use of stimulus intensities at or just below threshold for evoking an action potential, complex synaptic potentials consisting of EPSP-IPSP sequences were observed. Both early, Cl(-)-dependent and late, K(+)-dependent IPSPs were reduced by CNQX. This effect was reversible on washing. This disinhibition could lead to enhanced excitability in the presence of CNQX. 4. Iontophoretic application of quisqualate produced a membrane depolarization with superimposed action potentials, whereas NMDA depolarized the membrane potential and evoked bursts of action potentials. At concentrations up to 5 microM, CNQX selectively antagonized quisqualate responses. NMDA responses were reduced by 10 microM CNQX. D-Serine (0.5-2 mM), an agonist at the glycine regulatory site on the NMDA receptor, reversed the CNQX depression of NMDA responses.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2003

The effects of protein kinase C activity on synaptic transmission in two areas of rat hippocampus.

The effects of three protein kinase C (PKC) agonists (phorbol ester, ingenol and indolactam-V) and two PKC antagonists (D-erythro-sphingosine and chelerythrine) on input-output (I-O) relations in the Schaffer collateral pathway to CA1 (SC-CA1) and mossy fiber pathway to CA3 (MF-CA3) were determined in rat hippocampus brain slices. In the SC-CA1 pathway, phorbol esters and indolactam-V had only small effects on field excitatory post-synaptic potentials (fEPSP) in slices from 60-day animals, although ingenol, an activator of novel PKC isozymes, caused a significant decrease of the field excitatory post-synaptic potentials amplitude in 60-day animals, but not in 30-day animals. In contrast, in the MF-CA3 pathway, PKC agonists induced a significant increase in the field excitatory post-synaptic potentials. PKC antagonists depressed the field excitatory post-synaptic potentials in the SC-CA1 pathway, but had no significant effect in the MF-CA3 pathway. In the MF-CA3 pathway, paired-pulse facilitation was abolished by PKC agonists and unaffected by antagonists. In SC-CA1, it was depressed by agonists to levels below control, whereas it was significantly increased by chelerythine. We conclude that PKC plays important but different roles in both regions. In the SC-CA1 pathway, PKC is almost maximally active under control circumstances, and PKC antagonists significantly reduce synaptic responses. In contrast, in the MF-CA3 pathway, there is no apparent activation under resting circumstances, but significant potentiation of synaptic transmission is induced when PKC is activated. There are developmental changes in the pattern of PKC isozymes, and both pre- and post-synaptic actions are important.

Alkaloids↗
PubMed1999

Chemically induced, activity-independent LTD elicited by simultaneous activation of PKG and inhibition of PKA.

Although it is widely agreed that cyclic AMP is necessary for the full expression of long-term potentiation of synaptic strength, it is unclear whether cyclic AMP or cyclic AMP-dependent protein kinase (PKA) play roles in the induction of long-term depression (LTD). We show here that two PKA inhibitors, H-89 (10 microM) and KT5720 (1 microM), are unable to block induction of LTD at Schaffer collateral-CA1 synapses in hippocampal slices in vitro. Rather, H-89 enhanced the magnitude of LTD induced by submaximal low-frequency stimulation. Raising [cGMP] with zaprinast (20 microM), a selective type V phosphodiesterase inhibitor, reversibly depressed synaptic potentials. However, coapplication of H-89 plus zaprinast converted this to a robust LTD that depended critically on activation of cyclic GMP-dependent protein kinase (PKG). Chemically induced LTD is activity-independent because it could be induced without stimulation and in tetrodotoxin (0.5 microM). Additionally, chemical LTD did not require activation of N-methyl-D-aspartate or GABA receptors and could be reversed by LTP. Stimulus-induced LTD occluded chemical LTD, suggesting a common expression mechanism. In contrast to bath application, postsynaptic infusion of H-89 into CA1 pyramidal neurons did not enhance LTD, suggesting a presynaptic site of action. Further evidence for a presynaptic locus was supplied by experiments where H-89 applied postsynaptically along with bath application of zaprinast was unable to produce chemical LTD. Thus simultaneous presynaptic generation of cyclic GMP and inhibition of PKA is sufficient to induce LTD of synaptic transmission at Schaffer collateral-CA1 synapses.

Animals↗
PubMedDate not supplied

Determinants of BDNF-induced hippocampal synaptic plasticity: role of the Trk B receptor and the kinetics of neurotrophin delivery.

The neurotrophins are a class of signaling molecules known for their growth and survival-promoting activities during neuronal development. Recent studies suggest that the neurotrophins, including brain-derived neurotrophic factor (BDNF), can also dramatically influence synaptic transmission in the adult hippocampus. The experiments described in this paper indicate that ability of BDNF to potentiate synaptic transmission in the hippocampus relies on functional Trk B receptors. Moreover, the rate at which BDNF is applied to hippocampal synapses is also a potent determinant of whether synaptic potentiation will result. Hippocampal slices perfused with BDNF at a very slow flow rate (e.g., < or = 25 ml/hr) did not show synaptic potentiation. Increasing the rate of BDNF application resulted in synaptic potentiation in which the magnitude and onset kinetics of the potentiation were determined by the rate of BDNF delivery. Immunocytochemical analysis of BDNF detected with confocal microscopy confirmed these electrophysiological observations, indicating that the penetration of BDNF into hippocampal slices is influenced dramatically by the perfusion rate.

Animals↗
PubMed2000

Detection of synchrony in the activity of auditory nerve fibers by octopus cells of the mammalian cochlear nucleus.

The anatomical and biophysical specializations of octopus cells allow them to detect the coincident firing of groups of auditory nerve fibers and to convey the precise timing of that coincidence to their targets. Octopus cells occupy a sharply defined region of the most caudal and dorsal part of the mammalian ventral cochlear nucleus. The dendrites of octopus cells cross the bundle of auditory nerve fibers just proximal to where the fibers leave the ventral and enter the dorsal cochlear nucleus, each octopus cell spanning about one-third of the tonotopic array. Octopus cells are excited by auditory nerve fibers through the activation of rapid, calcium-permeable, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate receptors. Synaptic responses are shaped by the unusual biophysical characteristics of octopus cells. Octopus cells have very low input resistances (about 7 M Omega), and short time constants (about 200 microsec) as a consequence of the activation at rest of a hyperpolarization-activated mixed-cation conductance and a low-threshold, depolarization-activated potassium conductance. The low input resistance causes rapid synaptic currents to generate rapid and small synaptic potentials. Summation of small synaptic potentials from many fibers is required to bring an octopus cell to threshold. Not only does the low input resistance make individual excitatory postsynaptic potentials brief so that they must be generated within 1 msec to sum but also the voltage-sensitive conductances of octopus cells prevent firing if the activation of auditory nerve inputs is not sufficiently synchronous and depolarization is not sufficiently rapid. In vivo in cats, octopus cells can fire rapidly and respond with exceptionally well-timed action potentials to periodic, broadband sounds such as clicks. Thus both the anatomical specializations and the biophysical specializations make octopus cells detectors of the coincident firing of their auditory nerve fiber inputs.

Acoustic Stimulation↗
PubMed1983

Tetanus toxin: convulsant action on mouse spinal cord neurons in culture.

The effects of direct application of tetanus toxin on fetal mouse spinal cord neurons in culture are described. Tetanus toxin produces increased excitation characterized by paroxysmal depolarizing events (PDE). In contrast to the abrupt onset of convulsant action produced by postsynaptic glycine antagonist strychnine, the convulsant action of tetanus occurs after a dose-dependent latent period. The onset of the convulsant action of tetanus toxin is paralleled by a reduction in observed spontaneous inhibitory synaptic potentials. Excitatory synaptic events can be identified as components of some tetanus-PDE. The toxin does not alter postsynaptic responses to the inhibitory amino acids glycine and gamma-aminobutyric acid. The latency and convulsant action of tetanus toxin are consistent with an irreversible presynaptic membrane interaction that reduces inhibitory transmission, a mechanism of action distinct from those of convulsants that antagonize inhibitory transmitters at the postsynaptic membrane.

Action Potentials↗
PubMed1971

Excitatory input from the distal colon to the inferior mesenteric ganglion in the guinea-pig.

1. Intracellular recordings were obtained from ganglion cells in the guinea-pig inferior mesenteric ganglion (IMG) with a segment of the distal colon attached to the lumbar colonic nerves.2. Continuous electrical activity consisting of excitatory synaptic potentials and action potentials was recorded from ganglion cells in all regions of the IMG.3. The ;spontaneous' synaptic potentials were indistinguishable from those elicited by submaximal stimulation of any of the nerve trunks connected to the IMG.4. The excitatory activity was irreversibly abolished when the lumbar colonic nerves were cut and reversibly abolished when tetrodotoxin (5 x 10(-7) g/ml.) was added to the colon side of a two-compartment organ bath.5. Addition of dihydro-beta-erythroidine (5 x 10(-6) g/ml.) to the ganglion side of the bath abolished the synaptic activity of colonic origin and the synaptic responses to stimulation of any of the nerve trunks connected to the IMG.6. Addition of dihydro-beta-erythroidine (1 x 10(-5) g/ml.) to the colon side of the bath markedly depressed the synaptic input of colonic origin but had no effect on synaptic responses produced by preganglionic nerve stimulation.7. Distension of the colonic segment and the application of 5-HT (1 x 10(-5) g/ml.) to the mucosal surface of the colon increased the frequency of synaptic input.8. The synaptic input from the colon was transiently blocked following repetitive stimulation of any of the nerve trunks connected to the IMG. The discharge of miniature synaptic potentials was unaffected.9. Addition of noradrenaline (1 x 10(-7) to 1 x 10(-6) g/ml.) to the colon side of the bath reduced, and in some cases completely abolished, the synaptic input to the IMG. Phentolamine (1 x 10(-6) g/ml.), when added to the colon side of the bath, blocked the effect of noradrenaline and the transient inhibition following repetitive nerve stimulation.10. Addition of noradrenaline (1 x 10(-4) g/ml.) to the ganglion side of the bath reduced but never abolished the amplitude of the synaptic potentials of colonic origin.11. It was concluded that in the guinea-pig, the IMG is involved in a peripheral reflex whose afferent limit of this reflex consists of the axons of cholinergic neurones within the wall of the colon. Many of these neurones are driven either directly or indirectly by cholinergic synapses. The efferent noradrenergic neurones of the IMG function as a group of inhibitory neurones which depress the activity of the excitatory neurones of the colon which are driving them.

Action Potentials↗
PubMed1995

Intracellular in vivo recording of inferior colliculus auditory neurons from awake guinea-pigs.

Intracellular recordings of identified inferior colliculus (ICc) auditory neurons, were analyzed in in vivo awake, chronically implanted guinea-pigs. The passive membrane characteristics as well as the spontaneous and click evoked synaptic potentials and spike activity, were studied. The injection of current pulses revealed little, if any, adaptation and membrane voltage shifts that outlasted the electrical stimuli. The spontaneous action potentials, observed in all the units studied, were of the short-duration type. During wakefulness, spontaneous synaptic potentials of higher amplitude were observed in comparison to the anesthetized preparation as well as an enhanced firing rate. The click evoked synaptic potentials far outlasted the sound (click, 0.1 ms) duration. The binaural, contralateral and ipsilateral sound stimulation evoked different sequences of synaptic potentials and firing. This was mostly in agreement with studies of extracellular recordings from the ICc, in anesthetized and behaving animals.

Acoustic Stimulation↗
PubMed2006

Physiological changes of premotor nonspiking interneurons in the central compensation of eyestalk posture following unilateral sensory ablation in crayfish.

We investigated how the physiological characteristics and synaptic activities of nonspiking giant interneurons (NGIs), which integrate sensory inputs in the brain and send synaptic outputs to oculomotor neurons innervating eyestalk muscles, changed after unilateral ablation of the statocyst in order to clarify neuronal mechanisms underlying the central compensation process in crayfish. The input resistance and membrane time constant in recovered animals that restored the original symmetrical eyestalk posture 2 weeks after operation were significantly greater than those immediately after operation on the operated side whereas in non-recovered animals only the membrane time constant showed a significant increase. On the intact side, both recovered and non-recovered animals showed no difference. The frequency of synaptic activity showed a complex pattern of change on both sides depending on the polarity of the synaptic potential. The synaptic activity returned to the bilaterally symmetrical level in recovered animals while bilateral asymmetry remained in non-recovered ones. These results suggest that the central compensation of eyestalk posture following unilateral impairment of the statocyst is subserved by not only changes in the physiological characteristics of the NGI membrane but also the activity of neuronal circuits presynaptic to NGIs.

Adaptation, Physiological↗
PubMed2003

Voltage-clamp-controlled current-clamp recordings from neurons: an electrophysiological technique enabling the detection of fast potential changes at preset holding potentials.

Investigations of the properties of fast, transient potential changes (e.g. receptor potentials or synaptic potentials) in excitable cells by means of current-clamp recording techniques require the exact adjustment and control of membrane potentials. Usually, the desired membrane potential values are set by current injection via the recording electrode and are controlled manually by regulating the current strength necessary to maintain a constant potential. However, this technique is associated with a number of disadvantages. A single-electrode current- and voltage-clamp amplifier was therefore modified to compensate for slow membrane potential changes without affecting faster voltage responses. Basically, low-pass filters with selectable time constants were incorporated into the voltage-clamp feedback circuit to control the amplifier's response speed. In addition, the amplifier's electronic circuits were altered to enable current pulse injection into the cells. Thus, while recording at preset and controlled membrane potentials, it was possible to monitor the cell's input resistance or current/voltage relationship. This new recording technique has been designated "voltage-clamp-controlled current clamp" (VCcCC) and its performance was tested by intracellular recordings from neocortical and neostriatal neurons in vitro using either conventional microelectrodes or patch-clamp electrodes.

Amplifiers, Electronic↗
PubMed2005

Neuroeffector connections of giant multimodal neurons in the African snail Achatina fulica.

A new method of making preparations was used to analyse the neuroeffector connections of the paired giant neurons of the African snail Achatina fulica. These neurons were found to induce postsynaptic potentials in the muscles of the mantle, heart, the wall of the pulmonary cavity, and the muscular elements of the renal complex, the pericardium, the sexual apparatus, the walls of the cerebral arteries, the filaments of the columellar muscles, the wall of the abdomen, and the tentacle retractor muscles. Rhythmic neuron activity led to the development of marked facilitation and long-term potentiation of synaptic potentials. The possible significance of the multiple neuroeffector connections of giant neurons is discussed.

Adaptation, Physiological↗