PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Synaptic Potentials”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 73 records · Page 4Linked to original sources
PubMed1988

Synaptic organization of the tectal-facial pathways in the cat. I. Synaptic potentials following collicular stimulation.

1. The synaptic pathways underlying tectal influence over pinna movements were studied using an acute electrophysiological approach. Under pentobarbital anesthesia, postsynaptic potentials were recorded intracellularly in antidromically identified, cat facial motoneurons following electrical stimulation of the superior colliculus. How collicular topography is reflected in these synaptic potentials was examined using multiple stimulation sites. The pathways responsible for tectally evoked synaptic potentials were studied by making acute brain stem lesions and by intra-axonal horseradish peroxidase (HRP) staining. 2. Monosynaptic excitatory potentials (EPSPs) with latencies ranging from 0.7 to 1.1 ms and amplitudes that were always less than 1 mV were recorded in motoneurons following stimulation of the contralateral superior colliculus. Larger disynaptic EPSPs ranging in latency from 1.2 to 2.0 ms were recorded both in isolation and in association with monosynaptic EPSPs. In addition, disynaptic inhibitory synaptic potentials (IPSPs) with latencies ranging from 1.5 to 2.5 ms were observed, often in combination with monosynaptic EPSPs. Both disynaptic EPSPs and IPSPs were graded, augmented by multiple stimuli and found in all categories of motoneurons. 3. Stimulation of the ipsilateral superior colliculus produced nearly the same spectrum of potentials and latencies as did contralateral tectal stimulation. Occlusion between ipsi- and contralaterally evoked IPSPs suggests there might be a common element in the inhibitory disynaptic pathways. 4. More discrete populations of facial motoneurons were investigated. Specifically, motoneurons innervating the platysma and orbicularis oculi muscles, the intrinsic ear muscles, and muscles that move the vibrissae all displayed tectally elicited mono- and di-synaptic potentials. Collicular input was not restricted to motoneurons involved in orienting the pinnae. 5. The presence, polarity, and amplitude of the synaptic potentials evoked in individual facial motoneurons exhibited variations that were related to the site of stimulation in either the ipsi- or contralateral colliculus. These variations are compatible with the idea that the collicular input to facial motoneurons is topographically organized. 6. Acute lesions at the level of the superior olive indicated that the pathway producing the contralateral monosynaptic EPSPs runs, near the midline, ipsilateral to the target facial nucleus, whereas the contralateral disynaptic and the ipsilateral mono- and disynaptic pathways lie further lateral.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1994

Hippocampal long-term potentiation is not accompanied by presynaptic spike broadening, unlike synaptic potentiation by K+ channel blockers.

The expression of hippocampal long-term potentiation (LTP) is thought to be at least partly due to increased transmitter release. To test whether this increase is due to a broadening of the presynaptic action potential, we have compared the presynaptic fibre volley before and after LTP induction, or application of K+ channel blockers, in CA1 of rat hippocampal slices. Tetraethylammonium (TEA; 1 mM) induced a parallel increase in the fibre volley duration of the slope of the field EPSP, indicating that a presynaptic spike broadening underlying synaptic potentiation can be detected. In contrast, induction of LTP did not produce any measurable change in the fibre volley, although the average increase in the EPSP slope was larger than with TEA. These results indicate that LTP expression is not primarily due to a presynaptic spike broadening.

Action Potentials↗
PubMed1997

Transient synaptic potentiation in the visual cortex. II. Developmental regulation.

In our previous study, pairing-induced transient synaptic potentiation in supragranular layers of the visual cortex was described in mature guinea pigs. In the present study, the development of this type of synaptic plasticity and the underlying cellular mechanisms that mediate it were evaluated in animals from postnatal day (PND) 5 to 180. Potentiation is more reliably evoked in younger animals (likelihood: 75%, PND 5-30; 51%, PND > or = 34), and the magnitude of the effect is greater (+40 +/- 3%, mean +/- SE, PND 5-30; +26 +/- 3%, PND > or = 34). Similar to data obtained from the mature animals, visual cortical transient synaptic potentiation in the immature cortex occurs at excitatory synaptic sites directly activated by the stimulation, and activation by local recurrent cortical circuits is not necessary for the induction of this potentiation. This is demonstrated by 1) experiments in which action potential output from the paired neuron was blocked by Lidocaine, N-ethyl bromide quaternary salt applied into the neuron (5 of 5), and 2) experiments in which the contribution to the compound postsynaptic potential by inhibitory synapses was eliminated by selective, intracellular blockade by gamma-aminobutyric acid-mediated inhibitory postsynaptic potentials only onto the recorded neuron (7 of 11). Thus these perturbations do not reduce the likelihood or magnitude of this synaptic potentiation. In contrast to the N-methyl-D-aspartate (NMDA) receptor dependence for induction of this synaptic potentiation in the cortex of mature animals, in the young animals' cortices (PND 11-27) potentiation is readily induced during blockade of NMDA receptors (72%, 13 of 18, did not different from control: 75%, 40 of 53). Thus the NMDA receptor becomes functionally linked to a synaptic potentiation cascade during development, replacing another 2-amino-5-phosphonovaleric acid (APV)-insensitive potentiation process in the neonatal cortex. Postsynaptic intracellular calcium has a critical role in the induction of this form of synaptic potentiation in all ages studied. Synaptic potentiation was prevented (8 of 11 cases) or was replaced by synaptic depression (3 of 11 cells) in experiments in which postsynaptic calcium levels were reduced by intracellular application of 1,2-bis-2-aminophenoxy ethane-N,N,N',N'-tetraacetic acid (BAPTA) in the cortex of young (PND 7-14) animals, or in which the extracellular calcium concentrations was lowered. Inhibition of postsynaptic calcium-induced calcium release blocked synaptic potentiation (4 of 4 cells). Prolonged superfusion (3 h) of the nitric oxide synthase inhibitor L-nitro-arginine (LNA) did not significantly affect the likelihood (in LNA, 81%; 13 of 16 cells), or the magnitude (+38 +/- 7% increase in LNA vs. +40 +/- 3% in control cases) of potentiation, in contrast to its effects in the mature cortex.

Aging↗
PubMed2007

Dissociation between apoptosis, neurogenesis, and synaptic potentiation in the dentate gyrus of adrenalectomized rats.

Removal of adrenal hormone corticosterone in rats aged 3-4 months results within 3 days in acceleration of apoptosis and proliferation of newborn cells in the dentate gyrus (DG). A critical question is whether such a shift in the maturity of dentate cells after adrenalectomy (ADX) affects synaptic plasticity. To address this question, male rats were adrenalectomized and synaptic potentiation was recorded in vitro in hippocampal slices, as well as in vivo, in response to high frequency stimulation of the perforant path, 3 days after ADX. At this time-point, cell loss was assessed and proliferation was examined. Based on two independent parameters, bromodeoxyuridine and Ki-67, we found that removal of the adrenal glands increases proliferation rate. This increase in proliferation was, in particular, evident in those animals that displayed substantial cell loss. The accelerated cell-turnover after ADX was accompanied by reduced synaptic potentiation, both when recorded in vitro and in vivo. Corticosterone replacement in vivo (in adrenalectomized animals), at levels that activate the mineralocorticoid receptor, prevented ADX-induced proliferation, apoptosis, and restored synaptic potentiation to control levels. Importantly, corticosterone applied to slices from adrenalectomized rats also normalized synaptic potentiation, despite increased proliferation. This suggests that changes in cell proliferation and apoptotic cell death in the DG are not necessarily key factors determining the efficacy of synaptic potentiation.

Adrenalectomy↗
PubMed1992

5-hydroxytryptamine1B receptors block the GABAB synaptic potential in rat dopamine neurons.

Intracellular recordings were made from presumed dopamine-containing neurons in slices cut from the midbrain of the rat. Focal electrical stimulation produced a hyperpolarizing synaptic potential that was reduced by 75-95% by the GABAB-receptor antagonist 2-hydroxysaclofen (300 microM). 5-HT (3-100 microM) reduced the amplitude of the GABAB synaptic potential by 20-74%, with a 50% reduction at 10 microM, but did not reduce the amplitude of synaptic potentials mediated by GABAA receptors. 5-HT acted presynaptically because hyperpolarizations produced by exogenously administered GABA (1 mM) in picrotoxin (100 microM) were not affected by 5-HT (30 microM). (+/-)-Cyanopindolol (100 nM), a 5-HT1B antagonist, blocked the effect of 5-HT (10 microM); spiperone (1 microM), which is an antagonist at 5-HT1A and 5-HT2 receptors, had no effect. The amplitude of the GABAB synaptic potential was reduced by the 5-HT1B receptor agonists 1-[3-(trifluoromethyl)-phenyl]-piperazine (300 nM) and 7-trifluoromethyl-4-(4-methyl-1-piperazinyl)-pyrrolo[1,2-a]quinoxaline (1 microM), but not by the 5-HT1A agonist N,N-dipropyl-5-carboxamidotryptamine (1 microM) or the 5-HT2 agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane (10 microM). We conclude that 5-HT activates presynaptic 5-HT1B receptors that inhibit the release of GABA onto GABAB but not GABAA receptors.

Animals↗
PubMed2001

PI-3 kinase and IP3 are both necessary and sufficient to mediate NT3-induced synaptic potentiation.

Signaling mechanisms underlying neurotrophic regulation of synaptic transmission are not fully understood. Here we show that neurotrophin-3 (NT3)-induced potentiation of synaptic transmission at the neuromuscular synapses is blocked by inhibition of phosphoinositide-3 kinase, phospholipase C-gamma or the downstream IP3 receptors of phospholipase C-gamma, but not by inhibition of MAP kinase. However, neither stimulation of Ca2+ release from intracellular stores by photolysis of caged IP3, nor expression of a constitutively active phosphoinositide-3 kinase (PI3K*) in presynaptic motoneurons alone is sufficient to enhance transmission. Photo-uncaging of IP3 in neurons expressing PI3K* elicits a marked synaptic potentiation, mimicking the NT3 effect. These results reveal an involvement of PI3 kinase in transmitter release, and suggest that concomitant activation of PI3 kinase and IP3 receptors is both necessary and sufficient to mediate the NT3-induced synaptic potentiation.

Animals↗
PubMed1988

[Quantitative patterns of tubocurarine action on the synaptic potentials of frog muscle].

The dependence of amplitude of synaptic potentials (EPP and mEPP) upon the d-tubocurarine concentration was studied in the frog cutaneous pectoral muscle. In the presence of d-tubocurarine up to 5 x 10(-7) M, the amplitude of EPP and mEPP decreased to the extent which strictly followed competitive action of d-tubocurarine. At a higher concentration, the inhibition of synaptic potentials was stronger than would be expected assuming that d-tubocurarine can only act as a competitive antagonist.

Animals↗
PubMed1983

Effect of tetanus toxin on the excitatory and the inhibitory post-synaptic potentials in the cat motoneurone.

Tetanus toxin (100 mouse minimal lethal doses per kilogram) was injected into the medial gastrocnemius muscle of the cat. At various times thereafter, homonymous and heteronymous group Ia excitatory post-synaptic potentials (e.p.s.p.s), disynaptic reciprocal Ia inhibitory post-synaptic potentials (i.p.s.p.s) and post-synaptic potentials (p.s.p.s) produced by sural nerve stimulation were recorded in the medial gastrocnemius motoneurones. The duration of the after-hyperpolarization, the input resistance and the axonal conduction velocity of motoneurones were also measured. Homonymous Ia e.p.s.p.s remained normal until 72 h after toxin injection. However, 5 days after toxin injection, the amplitudes of Ia e.p.s.p.s. were significantly smaller than those in control animals (1.5 +/- 1.0 mV versus 5.6 +/- 2.7 mV; t test, P less than 0.001). Heteronymous Ia e.p.s.p.s produced by stimulation of the lateral gastrocnemius-soleus nerve 5 days after toxin injection were also significantly smaller than those in control animals (0.6 +/- 0.6 mV versus 2.5 +/- 1.5 mV; P less than 0.001). However, these heteronymous Ia e.p.s.p.s remained normal when the lateral gastrocnemius-soleus nerve was ligated and sectioned at the entry to those muscles just before the toxin injection. The ascending volleys, which are supposed to represent mainly the action potentials of the dorsal spinocerebellar tract and to be elicited monosynaptically by collaterals of group I afferents, were essentially the same in the left tetanic and right control sides up to 5 days after toxin injection. Ia i.p.s.p.s and the hyperpolarizing component of sural p.s.p.s could not be produced or were very small in motoneurones sampled later than 30 h after toxin injection. The duration of the after-hyperpolarization and the input resistance of motoneurones remained normal. Axonal conduction velocity of motoneurones measured 5 days after toxin injection was 89.4 +/- 12.7 m/s, and was significantly slower than that of control motoneurones (94.1 +/- 15.4 m/s) (P less than 0.005). Differences in the amplitude of group I incoming volleys between tetanic leg and contralateral control leg were not observed. These results suggest that tetanus toxin blocks excitatory synapses in the central nervous system as well as inhibitory synapses.

Action Potentials↗
PubMed1978

Synaptic potentials in sympathetic ganglia: are they mediated by cyclic nucleotides?

The hypothesis that cyclic nucleotides are intracellular second messengers mediating the generation of synaptic potentials was studied in the sympathetic ganglia of the bullfrog. Synaptic potentials and the effect of administering cyclic nucleotides and agents which affect cyclic nucleotide metabolism were recorded by the sucrose gap technique. The administration of adenosine 3',5'-monophosphate (cyclic AMP), guanosine 3',5'-monophosphate (cyclic GMP), or several of their derivatives produced little or no change in membrane potential. Prostaglandin E1 did not block the generation of postsynaptic potentials. Theophylline produced membrane effects that were different from those associated with postsynaptic potential generation; it also reduced the slow excitatory postsynaptic potential (EPSP) and potentiated the slow inhibitory postsynaptic potential (IPSP). The administration of papaverine, however, reduced both the slow EPSP and the slow IPSP. Although synaptic stimulation increases both cyclic GMP and cyclic AMP in these neurons, these results raise the possibility that these cyclic nucleotides may have functionla roles other than mediation of synaptic potentials.

Action Potentials↗
PubMed1970

Synaptic potentials recorded by the sucrose-gap method from the rabbit superior cervical ganglion.

1. Compound ganglionic potentials evoked by stimulation of the preganglionic nerves to the superior cervical ganglion of the rabbit were recorded by the sucrose-gap method.2. When the distal part of the ganglion was bathed in flowing isotonic sucrose solution or sodium-deficient solutions, ganglionic action potentials were no longer evoked, only large synaptic potentials.3. The compound synaptic potential, which remained unaltered for more than 1 h, originated in a population of cells at the interface between the Krebs and sucrose solutions. Hexamethonium reduced the size but did not alter the time course of the synaptic potential.4. It is suggested that a higher concentration of sodium ions is required for the generation of ganglionic action potentials than for either conduction in the postganglionic axons or production of synaptic potentials.5. When lithium replaced sodium in the solution bathing the distal part of the ganglion, the synaptic potential was greatly reduced in amplitude. Impulse propagation in the postganglionic axons was only slightly impaired when lithium replaced sodium in the solution bathing the axons.6. A quantitative assessment of the potency of the ganglion-blocking drugs nicotine, pentolinium, hexamethonium and pempidine was made by measuring the depression of the synaptic potentials produced by bathing the distal part of the ganglion in flowing isotonic sucrose solution. The concentrations which produced a 50% depression were 8.1 muM nicotine, 26.5 muM pentolinium, 111 muM hexamethonium and 22.2 muM pempidine.

Animals↗
PubMed1996

Synaptic potentials recorded from sea anemone muscle cells in situ.

Three pulse types, A,B, and C, can be recorded from column ring preparations of the sea anemone Calliactis parasitica (Couch). Lucifer Yellow injection confirmed that the recording sites are intracellular in endodermal myoepithelial cells. Type C pulses are spontaneously active depolarizing pulses, arising from a resting potential of around -60mV, and are usually < 5 mV in amplitude. When the cells were voltage-clamped these pulses reversed at around 0 mV membrane potential; therefore, we conclude that they are synaptic potentials. In some cells an increase in frequency of type C pulses accompanied contraction of the circular muscle field. Inward currents in these myoepithelial cells are carried by Ca2+, and although Na(+)-free solutions did not affect inward currents they did eliminate type C pulses, i.e., these synaptic potentials may result from activity of Na(+)-dependent nerve cells.

Animals↗
PubMed1984

Slow excitatory synaptic potentials recorded from neurones of guinea-pig submucous plexus.

Intracellular recordings made from neurones of guinea-pig submucous plexus revealed three types of synaptic input: cholinergic excitatory synaptic potentials (fast e.p.s.p.s) of 50-80 ms duration, inhibitory synaptic potentials (i.p.s.p.s) of 1 s duration, and non-cholinergic, non-adrenergic slow e.p.s.p.s which lasted for 15-20 s. A single stimulus was sufficient to elicit the slow e.p.s.p. in all neurones in which this synaptic input was present. Slow e.p.s.p.s were recorded in those neurones which also displayed i.p.s.p.s. Both the i.p.s.p. and the slow e.p.s.p. appeared in an all-or-none fashion and were not affected by alterations in the stimulus strength. The inhibitory as well as the slow excitatory synaptic potentials reversed close to the K+ equilibrium potential, indicating that the i.p.s.p. is due to an activation of K+ conductance while the slow e.p.s.p. is due to its inactivation. Evidence is presented which suggests the slow e.p.s.p. may be generated at a synapse located some distance from the soma, presumably at a dendritic location. Only those cells which showed slow e.p.s.p.s responded to substance P with a depolarization which mimicked the slow e.p.s.p.

Action Potentials↗
PubMed1987

Baclofen reduces post-synaptic potentials of rat cortical neurones by an action other than its hyperpolarizing action.

1. Intracellular recordings were obtained from neurones in layers 2 and 3 of the rat frontal neocortex in an in vitro slice preparation. Three distinct types of stimulation-evoked post-synaptic potentials were recorded in these neurones: excitatory post-synaptic potentials (e.p.s.p.s); bicuculline-sensitive, chloride-dependent inhibitory post-synaptic potentials (i.p.s.p.s) with times to peak of 20-25 ms (fast(f)-i.p.s.p.s); bicuculline-insensitive, potassium-dependent i.p.s.p.s with bicuculline-insensitive, potassium-dependent i.p.s.p.s with times to peak of 150-250 ms (long(l)-i.p.s.p.s). 2. The effects of baclofen were investigated on seventy-one neurones. Baclofen was applied by ionophoresis or pressure ejection from micropipettes or was added to the superfusion medium. 3. Baclofen depressed stimulation-evoked e.p.s.p.s in fifty-seven of the sixty neurones tested. This effect was associated with an increase in the stimulation intensity required to produce a synaptically evoked action potential for thirty-nine of forty-four neurones. 4. Baclofen depressed f-i.p.s.p.s in thirty-seven of the thirty-nine neurones tested and l-i.p.s.p.s in each one of the seventeen neurones tested. Reversal potential values for each type of i.p.s.p. were not changed by baclofen and its depressions of each were independent of membrane potential (Em). Baclofen reduced the magnitude and the duration of the conductance increases that were associated with f- and l-i.p.s.p.s. 5. Baclofen hyperpolarized forty of seventy-one neurones and produced outward currents in three of four neurones recorded in voltage clamp at holding potentials between -55 and -65 mV. These actions were associated with 10-58% reductions of neuronal input resistance (RN) and 10-20% increases in neuronal input conductance (gN), respectively. Baclofen decreased the direct excitability of twenty-three of twenty-seven neurones tested. Determinations of the reversal potential for baclofen-induced changes of Em indicate that baclofen increases the conductance of rat neocortical neurones to potassium ions. 6. The EC50 for each action of DL-baclofen was approximately 1 microM. L-Baclofen was greater than 100 times more potent than D-baclofen. 7. Concentrations of bicuculline that blocked f-i.p.s.p.s and responses to ionophoretically applied gamma-aminobutyric acid (GABA) had no effect on the depressions of e.p.s.p.s or the hyperpolarizations and decreases in RN that baclofen produced. 8. Baclofen did not reduce the duration of action potentials that were prolonged with intracellular injections of caesium ions or by superfusions with medium that contained 10 mM-tetraethylammonium (TEA).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1973

Properties of the depolarizing synaptic potential evoked by peripheral illumination in cones of the turtle retina.

1. Intracellular recordings of cone and horizontal cell responses to circles or annuli of light were made with the purpose of determining the properties of and the mechanisms underlying the horizontal-cell-mediated depolarization of cones which is evoked by surround illumination.2. A comparison of the responses of a cone and a near-by horizontal cell to a peripheral stimulus revealed a striking similarity in their time courses and amplitudes, indicating that a correlation exists between the depolarizing synaptic potential in the cone and the response of the horizontal cell.3. The depolarizing synaptic potential in cones was separated from the direct response of the cell to light by illuminating the periphery with an annulus during steady, bright illumination of the central cone. The synaptic potentials were graded with the intensity or area of peripheral illumination. In some cones a spike-like depolarization, which overshot the dark resting potential, occurred with bright illumination of the periphery.4. The effects of extrinsic current on the synaptic potential demonstrated that this response was generated by a change in membrane conductance consisting of two separate components with different time-dependences and reversal levels. The slower of the two components, which often outlasts the stimulus, represents an increase in membrane conductance.5. The progressive decline in the amplitude of the responses of horizontal cells under a large spot from centre to periphery was found to result in a diminished feed-back effect in cones near the edge of the spot. This leads to a Mach-band effect during the plateau phase of cone responses, suggesting that one function of the feed-back might be to enhance contrast discrimination.

Animals↗
PubMed2001

Differences in time course of ACh and GABA modulation of excitatory synaptic potentials in slices of rat hippocampus.

Activation of muscarinic receptors and GABA(B) receptors causes presynaptic inhibition of glutamatergic synaptic potentials at excitatory feedback connections in cortical structures. These effects may regulate dynamics in cortical structures, with presynaptic inhibition allowing extrinsic afferent input to dominate during encoding, while the absence of presynaptic inhibition allows stronger excitatory feedback during retrieval or consolidation. However, proposals for a functional role of such modulatory effects strongly depend on the time course of these modulatory effects; how rapidly can they turn off and on? In brain slice preparations of hippocampal region CA1, we have explored the time course of suppression of extracellularly recorded synaptic potentials after pressure pulse application of acetylcholine and GABA. Acetylcholine causes suppression of extracellular potentials with onset time constants between 1 and 2 s, and decay constants ranging between 10 and 20 s, even with very brief injection pulses. GABA causes suppression of extracellular potentials with onset time constants between 0.2 and 0.7 s, and decay time constants that decrease to values shorter than 2 s for very brief injection pulses. These techniques do not give an exact measure of the physiological time course in vivo, but they give a notion of the relative time course of the two modulators. The slow changes due to activation of muscarinic acetylcholine receptors may alter the dynamics of cortical circuits over longer intervals (e.g., between different stages of waking and sleep), setting dynamics appropriate for encoding versus consolidation processes. The faster changes in synaptic potentials caused by GABA could cause changes within each cycle of the theta rhythm, rapidly switching between encoding and retrieval dynamics during exploration.

Acetylcholine↗
PubMed2000

Changes in the distribution of synaptic potentials from bulbospinal neurones following axotomy in cat thoracic spinal cord.

1. Plasticity in functional connections of expiratory bulbospinal neurones was investigated by measurement of terminal potentials (TPs) and focal synaptic potentials (FSPs), recorded with spike-triggered averaging in the thoracic spinal cord of anaesthetized, paralysed cats. These measurements were made in normal cats and in those which had previously been subjected to spinal cord lesions that transected the axons of the bulbospinal neurones in the segment below that under investigation, either about 2 weeks or about 16 weeks previously. 2. In both groups of operated animals bulbospinal neurones with firing properties and conduction velocities similar to normal were present. The extracellular recordings that were averaged to reveal TPs and FSPs were made on two standard grids, each consisting of eight sites spaced 0.25 mm apart on two electrode tracks. One grid was positioned at a rostral and one at a caudal location within one segment (T7-T9). 3. Tn the normal animals TPs and FSPs were larger and/or more common at rostral sites than at caudal sites, by a factor of about 1.7. In both 2 week and 16 week animals, TPs and FSPs were observed, both showing normal tine courses and latencies. At rostral sites in 2 week and 16 week animals the amplitudes and/or the frequency of occurrence of TPs and FSPs were similar to normal, as was the case fir caudal sites in the 2 week animals. However, at caudal sites in the 16 week animals the FSPs were mole common and/or significantly larger than normal, with the increase particularly marked on the lateral track, being equivalent to a factor of about 2. A corresponding increase in the amplitude and/or frequency of occurrence of TPs at caudal lateral sites was also seen, but was not significant. 4. The results are interpreted as evidence for short-range sprouting of the bulbospinal axons and the formation by them of new connections in the caudal parts of the segments concerned.

Animals↗
PubMed1978

Dual effect of external calcium on the frequency of miniature synaptic potentials in frog sympathetic ganglion cells.

The effect of calcium on spontaneous transmitter release and on the release induced by tetanic stimulation and by raising the external potassium concentration ([K]0) was studied in sympathetic ganglion cells of Rana esculenta. 1. In standard Ringer's solution the frequency of miniature excitatory postsynaptic potentials (mepsp) ranged from 0.05--2.0 s-1 (0.05 +/- 0.09 s-1, n = 37) at room temperature. 2. At a [K]0 of 2.5 mM mepsp frequency was approximately linearly related to the logarithm of the external calcium concentration (log [Ca]0) (0.1 mM less than or equal to [Ca]0 less than or equal to 20 mM). 3. Duration and amplitude of the potentiation of transmitter release after tetanic preganglionic stimulation increased depending on [Ca]0. 4. Mepsp frequency was strongly dependent on [K]0 between 10 and 20 mM; the frequency being increased to about 40 times control level at a [K]0 of 20 mM. 5. Raising [Ca]0 up to 1.8 mM in high K solutions resulted in an increase in mepsp frequency followed by a decrease at higher [Ca]0. 6. These results are consistent with the idea that the effect of calcium on mepsp frequency depends on: (a) the driving force for calcium entry, (b) the effect of Ca ions on the potential gradient within the nerve membrane.

Animals↗