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At least 1,621 records · Page 90Linked to original sources
PubMed1988

Synaptic bases of cortically-induced rhythmical hypoglossal motoneuronal activity in the cat.

Intracellular recordings were made from hypoglossal motoneurons during cortically-induced fictive mastication in paralyzed encéphale isolé cats. Repetitive stimulation of the masticatory area of the cerebral cortex induced rhythmical tongue movements coordinated with jaw movements. After the animal was immobilized, the cortical stimulation still induced rhythmical burst activity in the hypoglossal nerve and the digastric nerve. The burst activities in the medial and lateral branches of the hypoglossal nerve alternated rhythmically, and were in and out of phase with the burst activities of the digastric nerve, respectively. All hypoglossal motoneurons showed rhythmical intracellular potentials during repetitive cortical stimulation. The rhythmical depolarizing potentials superimposed by spike bursts appeared in phase with rhythmical bursts in either the lateral or medial branch of the hypoglossal nerve. No hyperpolarization was present between consecutive depolarizing potentials. Synaptic activation noise increased coincidentally with the depolarizing potential, indicating that EPSPs were involved in the generation of the depolarizing potential. No evidence was obtained for the existence of IPSPs during the inter-depolarizing phase by intracellular current injection. It was concluded that rhythmical bombardment of excitatory impulses to hypoglossal motoneurons was responsible for the rhythmical activity induced by repetitive stimulation of the cortical masticatory area.

Animals↗
PubMed2004

Effects of naloxone on the long-term potentiation of EPSPs from the pathway of Schaffer collateral to CA1 region of hippocampus in aged rats with declined memory.

Morris water maze (MWM) was employed to distinguish the aged rats with declined memory to investigate the effect of naloxone on the synaptic plasticity of hippocampus in declined memory aged rats. After administration with naloxone for 7 days, LTP of excitatory post-synaptic potentials (EPSPs) from Schaffer collateral to CA1 region was recorded. The results showed that the maintenance of LTP of EPSPs from Schaffer collateral to CA1 subfield in isolate hippocampal brain slice was prolonged by naloxone with improved Morris water maze performance and reduced threshold of EPSPs. It is suggested that naloxone can improve learning and memory through enhancement of the synaptic plasticity of hippocampus in aged rats with declined memory.

Aging↗
PubMed2004

Bi-directional plasticity and age-dependent long-term depression at mouse CA3-CA1 hippocampal synapses.

Low-frequency stimulation (LFS) is used to induce long-term depression (LTD) and depotentiation at rodent CA3-CA1 hippocampal synapses. The relationship between the efficacy of LFS induction and postnatal age remains to be clearly defined in rat and had not been studied in mouse. The data presented here show that in acute mouse hippocampal slices LFS-induced LTD and depotentiation at CA3-CA1 synapses are: synapse specific; NMDA receptor-dependent; and metabotropic glutamate (mGlu) receptor type I/II independent. Furthermore LFS-induced LTD is highly age-dependent whilst long-term potentiation (LTP) and depotentiation are not. In slices from very young mice (P6-9) LFS induced a robust and stable LTD (-31.1 +/- 5.9%, n = 8, P < 0.01) of CA1 field excitatory post-synaptic potentials (fEPSPs), measured 55-60 min after conditioning. LFS also induced LTD in slices from mice aged P10-13 and P14-17 (-16.0 +/- 3.0%, n = 35, P < 0.001 and -17.9 +/- 5.5%, n = 12, P < 0.01, respectively). However, LTD was not expressed in slices from animals aged P18-21 ( -7.0 +/- 4.1%, n = 16, P > 0.05) or older.

Age Factors↗
PubMed1984

Intracellular study of effects of histamine on electrical behaviour of myenteric neurones in guinea-pig small intestine.

The actions of histamine on myenteric neurones were investigated with intracellular recording methods in guinea-pig small intestine. The actions of histamine at the ganglion cell soma were: membrane depolarization, increased input resistance, suppression of post-spike hyperpolarizing potentials, augmented excitability and repetitive spike discharge. Excitability was enhanced also at spike initiation sites remote from the cell body. Both H1, and H2, receptors were involved in the response to histamine. Dimaprit mimicked the responses to histamine in 80% and 2-methylhistamine in 50% of the trials. Cimetidine was an antagonist for histamine in 82% and for dimaprit in all of the trials. Pyrilamine blocked the actions of histamine in 59% of the cells and always blocked the action of 2-methylhistamine. Histamine mimicked slow synaptic excitation in the neurones, but was ruled out as a neurotransmitter for the slow excitatory post-synaptic potential (e.p.s.p.). Histamine either did not affect the responses to 5-hydroxytryptamine, substance P and acetylcholine or it potentiated the responses to these putative neurotransmitters for slow synaptic excitation. The results support the possibility that histamine released from mast cells by circulating peptidergic messengers, by neurotransmitters or during anaphylaxis could influence enteric nervous function.

Action Potentials↗
PubMed2005

Optical studies of nicotinic acetylcholine receptor subtypes in the guinea-pig enteric nervous system.

Nicotinic transmission in the enteric nervous system (ENS) is extensive, but the role of individual nicotinic acetylcholine receptor (nAChR) subtypes in the functional connectivity of its plexuses has been elusive. Using monoclonal antibodies (mAbs) against neuronal alpha3-, alpha4-, alpha3/alpha5-, beta2-, beta4- and alpha7-subunits, combined with radioimmunoassays and immunocytochemistry, we demonstrate that guinea-pig enteric ganglia contain all of these nAChR-subunits with the exception of alpha4, and so, differ from mammalian brain. This information alone, however, is insufficient to establish the functional role of the identified nAChR-subtypes within the enteric networks and, ultimately, their specific contributions to gastrointestinal physiology. We have used voltage-sensitive dyes and a high-speed CCD camera, in conjunction with specific antagonists to various nAChRs, to elucidate some of the distinct contributions of the individual subtypes to the behaviour of enteric networks. In the guinea-pig, the submucous plexus has the extraordinary advantage that it is virtually two-dimensional, permitting optical recording, with single cell resolution, of the electrical activity of all of its neurones. In this plexus, the block of alpha3beta2-, alpha3beta4- and/or alpha7-nAChRs always results in a decrease in the magnitude of the synaptic response. However, the magnitude of the fast excitatory post-synaptic potentials (epsps) evoked by electrical stimulation of a neighbouring ganglion varies from cell to cell, reflecting the differential expression of subunits already observed using mAbs, as well as the strengths of the activated synaptic inputs. At the same time, we observe that submucous neurones have a substantial mecamylamine (Mec)-insensitive (non-nicotinic) component to their fast epsps, which may point to the presence of purinergic or serotonergic fast epsps in this system. In the myenteric plexus, on the other hand, the antagonist-induced changes in the evoked synaptic response vary depending upon the location of the stimulating electrode with respect to the ganglion under study. The range of activity patterns that follows sequential pharmacological elimination of individual subtypes suggests that nAChRs may be capable of regulating the activity of both excitatory and inhibitory pathways, in a manner similar to that described in the central nervous system.

Animals↗
PubMed1995

Sub-nanomolar concentrations of ciguatoxin-1 excite preganglionic terminals in guinea pig sympathetic ganglia.

The actions of low concentrations of ciguatoxin-1 (CTX-1, 0.2-0.8 nM) in guinea-pig sympathetic ganglia have been analysed using intracellular recording techniques in vitro. The effects of CTX-1 were graded with concentration but sensitivity varied markedly between neurones in the same preparation. Other than an initial transient (approximately 10 min) depolarization of some ganglion cells accompanied by an increase in input resistance, passive electrical properties did not significantly differ from controls. Amplitude and threshold of action potentials evoked by depolarizing current and threshold, latency and form of the initial responses to nerve stimulation were also not affected. Exposure to CTX-1 generated marked increases in the frequency of spontaneous excitatory synaptic potentials which often occurred in bursts (15-66 Hz) of similar amplitudes. Single stimuli to incoming nerves produced repetitive synaptic responses arising from preganglionic, but not from peripheral afferent, axons. Following brief (< 5 min) exposure to CTX-1, these effects declined over 30 min but, after longer exposure (> 15 min), they persisted for several hours despite continuous washing. All activity generated by CTX-1 was significantly reduced or abolished by d-tubocurarine (10(-5)-10(-4) M), hexamethonium (10(-5) M), tetrodotoxin (10(-7)-10(-6) M), omega-conotoxin (10(-7) M), reduced Ca2+ (0.1 mM)/raised Mg2+ (10 mM), raised Ca2+ (6 mM) or raised Mg2+ (25 mM). The data suggest that CTX-1 activates preganglionic axons by modifying the voltage sensitivity of a subpopulation of Na+ channels. Effects on these unmyelinated axons occur at much lower concentrations than have been reported to affect myelinated ones. Many of the symptoms of ciguatera poisoning might be explained by activity in autonomic and perhaps other unmyelinated nerve terminals.

Animals↗
PubMed1982

Alteration of the electrophysiological activity in sympathetic ganglia infected with a neurotropic virus. I. Presynaptic origin of the spontaneous bioelectric activity.

The bioelectric activity of the rat superior cervical ganglion (SCG) infected with pseudorabies virus (PRV) was examined in vitro 30-38 h after inoculation. Simultaneous intra- and extracellular recordings on the internal (ICN) and external carotid nerves (ECN) revealed a synchronized spontaneous activity. This synchronization can be ascribed either to the functional organization of the ganglion or to the mechanism of initiation itself. In the infected ganglia two categories of cells were observed: cells displaying abnormal spontaneous discharges, and silent cells whose electrophysiological behavior was similar to control cells. Spontaneously active cells showed intermittent spiking and bursting activity. The discharge pattern was associated with the firing rate of the emitting cell: sporadically active cells emitted single spikes whereas highly active cells fired bursts of action potentials (APs). Long lasting intracellular recordings demonstrated that the cells undergo gradual changes evolving from sporadic on to high activity. Spontaneous APs usually rode on prepotentials similar to the excitatory postsynaptic potentials (EPSPs). A comparative study of spontaneous prepotentials and orthodromically evoked EPSPs in the same cell demonstrated that the spontaneous prepotentials are real synaptic potentials. No pace-maker potentials were observed. The passive and active electrical membrane properties of spontaneously active neurons were not different from those of silent cells or control cells impaled in uninfected ganglia. D-Tubocurarine abolished the spontaneous activity in the whole ganglion. Ortho- and antidromic electrical stimulations of suprathreshold intensity elicited an evoked response in neurons displaying spontaneous activity, followed by a delayed burst whose shape was similar to the spontaneous burst of the cell. Stimuli of subthreshold intensities induced this delayed burst independently from the evoked response. We conclude that the spontaneous bioelectrical activity is of presynaptic, but not necessarily of preganglionic origin. The possible existence of a cholinergic intraganglionic pathway revealed by the viral infection is discussed.

Action Potentials↗
PubMed1988

4-Aminopyridine induces a long-lasting depolarizing GABA-ergic potential in human neocortical and hippocampal neurons maintained in vitro.

Neocortical or hippocampal neurons were recorded intracellularly in slices obtained from human epileptogenic brain tissue excised during surgical treatment of epilepsy and perfused with medium containing 4-aminopyridine (4-AP, 50 microM). In addition to spontaneously occurring excitatory and inhibitory postsynaptic potentials, most of the neurons generated a long-lasting (up to 1.5 s) depolarization (LLD) which: (i) behaved as expected for a synaptic potential when the resting membrane potential was varied with intracellular injection of depolarizing and hyperpolarizing current; (ii) exerted a shunting inhibitory action on the generation of action potentials induced by intracellular depolarizing current pulses; and (iii) was blocked by bath application of bicuculline methiodide. It is concluded that like pyramidal or granule cells in the rat hippocampal slice, human neocortical and hippocampal cells possess in the presence of 4AP the ability to generate a LLD which is mediated through GABAA receptors presumably located into the dendrites.

4-Aminopyridine↗
PubMed1990

Hepoxilin A3 blocks the release of norepinephrine from rat hippocampal slices.

Hepoxilin A3 was previously shown to display neuromodulatory actions on rat hippocampal CA1 neurons, with hyperpolarization of the membrane potential, an increase in the amplitude and duration of the post-spike train after hyperpolarization and an increase in the inhibitory post synaptic potential. The present report describes new biochemical evidence of a presynaptic action of hepoxilin A3 in rat hippocampal slices prelabeled with [3H]-norepinephrine. Hepoxilin A3 on its own had a marginal effect on the release of label, but blocked release which was induced by 4-aminopyridine (4-AP). Prostaglandin E2 also behaved in a similar way. These results demonstrate that hepoxilins modulate neurotransmission in the mammalian CNS through both pre- and postsynaptic actions.

4-Aminopyridine↗
PubMed2002

Synchrony arising from a balanced synaptic plasticity in a network of heterogeneous neural oscillators.

We investigate the dynamics of a recurrent network of coupled heterogeneous neural oscillators with experimentally observed spike-timing-dependent synaptic plasticity. We show both theoretically and by computer simulations that, in a regime of a balance between synaptic potentiation and depression, the network of such oscillators converges to a stable synchronous state. The stability of this state is fostered by flexible synaptic weights which adjust themselves based on the relative timing of firing of pre- and postsynaptic oscillators.

Animals↗
PubMed1970

Effects of iontophoretically applied drugs on spinal interneurons of the lamprey.

1. Intracellular records were obtained from giant interneurones in the isolated spinal cord of the sea lamprey. The cells had a mean resting potential of about 75 mV and action potentials with overshoots of about 35 mV. Their input resistances, measured by passing polarizing currents through the recording pipette, were in the range 3-7 MOmega.2. Iontophoretic ejection of gamma-aminobutyric acid (GABA) from a micropipette placed near the surface of a cell resulted in a slight hyperpolarization, accompanied by a marked reduction in input resistance. The reversal point for the potential change was about 5 mV greater than the resting membrane potential.3. Iontophoretic application of L-glutamate to the cells produced a depolarization with a decrease in input resistance much smaller than that accompanying a GABA potential of similar amplitude. The action potential amplitude was reduced by L-glutamate application. The reversal potential could not be determined accurately but appeared to be near zero membrane potential.4. Glutamate application produced, in addition, a burst of inhibitory synaptic potentials in the cell, presumably by depolarizing either inhibitory presynaptic nerve terminals or nearby inhibitory cell bodies.5. Acetylcholine (ACh) produced no detectable change in membrane resistance or potential.6. Application of the three drugs to first-order sensory cells in the spinal cord had no effect on their membrane properties.

Acetylcholine↗
PubMed1984

The reversal potential of excitatory amino acid action on granule cells of the rat dentate gyrus.

The responses of granule cells to glutamate, aspartate, N-methyl-D-aspartate (NMDA), quisqualate and kainate applied by ionophoresis on to their dendrites in the middle molecular layer of the dentate gyrus were studied with intracellular electrodes using an in vitro hippocampal slice preparation. On passive depolarization 75% of the granule cells displayed anomalous rectification, which persisted in the presence of TTX and TEA but was eliminated by Co2+ or the intracellular injection of Cs+. Short ionophoretic applications of all the excitatory amino acids evoked dose-dependent depolarizations that were highly localized: movement of the ionophoretic electrode by as little as 10 microns could substantially change the size of the response. The depolarizations evoked by glutamate, asparatate, quisqualate and kainate were unaffected by TTX and Co2+. The depolarization evoked by NMDA was unaffected by TTX but markedly reduced by Co2+. Following intracellular injection of Cs+, neurones could be depolarized to +30 mV and the depolarizations produced by glutamate, quisqualate, NMDA and kainate reversed. The reversal potentials (E) were Eglutamate: -5.6 +/- 0.4 mV; ENMDA: 1.8 +/- 1.9 mV; Equisqualate: -3.9 +/- 1.9 mV; Ekainate: -4.6 +/- 2.0 mV. The excitatory post-synaptic potential (e.p.s.p.) evoked by stimulation of the medial perforant path could also be reversed and Ee.p.s.p. was -5.5 +/- 1.1 mV. The 6 mV difference between ENMDA and the equilibrium potential for the other exogenously applied excitatory amino acids and the statistically significant difference between ENMDA and Ee.p.s.p. (P less than 0.005; d.f.: 7) is consistent with our earlier hypothesis that both the transmitter released by the medial perforant path and exogenously applied glutamate are unlikely to interact with NMDA receptors.

Action Potentials↗
PubMed1975

Estimates of statistical release parameters from crayfish and frog neuromuscular junctions.

1. Transmitter release at crayfish and frog neuromuscular junctions was studied by recording synaptic potentials with extracellular or intracellular glass micro-electrodes. 2. The binomial release parameters n and p were calculated using the experimental observations for the mean number of quanta (m) released in a series of trials, the variance (var) of the quantum content distribution and the number of transmission failures (n-o). 3. In one series of experiments on frog neuromuscular junction, action potentials were blocked by tetrodotoxin. Transmitter release was limited to a circumscribed part of the nerve terminal by focal stimulation with a glass micro-electrode. Values for m were between 0-6 and 5-7 and calculated values for n ranged from 3 to 23. p was between 0-05 and 0-48. In a second series of experiments on frog neuromuscular junction transmitter release was evoked by conventional stimulation of the nerve trunk in Mg-Ringer. m was mostly between 20 and 60 and in the same experiments n was calculated to be between 70 and 125. Values for p ranged from 0-25 to 0-48. 4. It can be concluded from the present results that transmitter release at frog neuromuscular junction is described by binomial statistics as is the case for neuromuscular junction of crayfish. 5. In comparing the values for n for the two series of experiments on frog neuromuscular junction it appears that n is dependent on the length of the activated synaptic contact. The numbers for n calculated from frog neuromuscular junction are of the same order of magnitude as the number of 'active zones' seen in the corresponding length of the synaptic nerve terminal.

Action Potentials↗
PubMed1994

Major differences between long-term potentiation and ACPD-induced slow onset potentiation in hippocampus.

We examined the effects of a long-lasting application of the selective metabotropic glutamate receptor (mGluR) agonist 1S-3R, 1-amino cyclopentane-1,3-dicarboxylic acid (ACPD) on synaptic potentials recorded from the CA1 and CA3 subfields in hippocampal slices maintained in a superfusion slice chamber. In 25% of the slices, ACPD generated an slow onset potentiation (SOP) of population EPSPs (pEPSPs) in CA1. In contrast to long-term potentiation (LTP) induced by a tetanic train, SOP was accompanied by an increase in the magnitude of the presynaptic fiber volley. Potentiation of the isolated afferent volley suggests that the expression of SOP is due to a recruitment of additional presynaptic fibers by the test stimulus caused by the persistent block of K+ channels by ACPD.

Action Potentials↗
PubMed2002

Long-term potentiation in direct perforant path projections to the hippocampal CA3 region in vivo.

The perforant path constitutes the primary projection system relaying information from the neocortex to the hippocampal formation. Long-term synaptic potentiation (LTP) in the perforant path projections to the dentate gyrus is well characterized. However, surprisingly few studies have addressed the mechanisms underlying LTP induction in the direct perforant path projections to the hippocampus. Here we investigate the role of N-methyl-D-aspartate (NMDA) and opioid receptors in the induction of LTP in monosynaptic medial and lateral perforant path projections to the CA3 region in adult pentobarbital sodium-anesthetized rats. Similar to LTP observed at the medial perforant path-dentate gyrus synapse, medial perforant path-CA3 synapses display LTP that is blocked by both local and systemic administration of the competitive NMDA receptor antagonist (+/-)-3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid [(+/-)-CPP]. By contrast, LTP induced at the lateral perforant path-CA3 synapses is not blocked by either local or systemic administration of this NMDA receptor antagonist. The induction of LTP at lateral perforant path-CA3 synapses, which is blocked by the opioid receptor antagonist naloxone, is also blocked by the selective mu opioid receptor antagonist Cys(2)-Tyr(3)-Orn(5)-Pen(7)-amide (CTOP), but not the selective delta opioid receptor antagonist naltrindole (NTI). CTOP was without effect on the induction of medial perforant path-CA3 LTP. The selective sensitivity of lateral perforant path-CA3 LTP to mu-opioid receptor antagonists corresponds with the distribution of mu-opioid receptors within the stratum lacunosum-moleculare of area CA3 where perforant path projections to CA3 terminate. These data indicate that both lateral and medial perforant path projections to the CA3 region display LTP, and that LTP induction in medial and lateral perforant path-CA3 synapses are differentially sensitive to NMDA receptor and mu-opioid receptor antagonists. This suggests a role for opioid, but not NMDA receptors in the induction of LTP at lateral perforant path projections to the hippocampal formation.

Animals↗
PubMed1988

Enkephalins modulate excitatory synaptic transmission in the superficial dorsal horn by acting at mu-opioid receptor sites.

The effect of opioids on synaptic potentials of dorsal horn (DH) neurons has been investigated in a rat spinal cord DH slice-dorsal root ganglion (DRG) in vitro preparation. Conventional intracellular recording from DH and DRG neurons using 3 M potassium acetate-filled electrodes was employed. Dorsal roots were electrically isolated from the spinal cord slice and stimulated with pulses of different intensity and duration to evoke afferent action potentials monitored intracellularly from DRG neurons. Low-intensity single-shock stimulation of the dorsal roots (8-20 V pulses of 0.02-0.05 ms duration) activated large primary afferents and elicited excitatory postsynaptic potentials (EPSP) in all of the neurons tested. High-intensity stimulation of the dorsal roots (over 35 V pulses of 0.5 ms duration), sufficient to excite small myelinated and unmyelinated primary afferents resulted in a large and prolonged depolarization of DH neurons associated with firing of action potentials. Bath application (D-Ala2,N-Me-Phe4,Gly5-ol)-enkephalin (DAGO), (D-Ala2,D-Leu5)-enkephalinamide (DADLEA), or (D-Ala2,D-Met5)-enkephalinamide (DADMEA) produced dose-dependent, reversible hyperpolarization in about 75% of the neurons tested. The hyperpolarization was associated with a fall in neuronal input resistance. In addition, opioids depressed the synaptic transmission in all of the neurons examined. This depressant effect of opioids was independent from their effects on resting membrane potential. Delta specific receptor opioid agonists (D-Pen2.5)-enkephalin (DPDPE) and (D-Pen2,L-Pen5)-enkephalin (DPLPE), were completely ineffective in producing an effect on neuronal membrane or synaptic transmission. All opioid effects were antagonized by naloxone.

Animals↗
PubMed1986

N-methyl-D-aspartate receptor antagonists reduce synaptic excitation in the hippocampus.

The hypothesis that synaptic excitation in the CA1 region of the hippocampus is mediated in part by N-methyl-D-aspartate (NMDA) receptors was tested using intra- and extracellular recording techniques. Synaptic potentials elicited by stratum radiatum stimulation were examined in individual neurons before and after bath application of the NMDA receptor antagonist, DL-2-amino-5-phosphonovalerate (APV). This antagonist reduced both excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs). When IPSPs were suppressed by the addition of picrotoxin, EPSPs were seen in isolation. APV reduced these EPSPs but did not block synaptic transmission. This antagonist demonstrated anticonvulsant actions when tested against picrotoxin-induced epileptiform activity. These results suggest that, as in the spinal cord and neocortex, synaptic excitation in the CA1 region of the hippocampus is partially mediated by APV-sensitive NMDA receptors. The fact that synaptic activity is not blocked by NMDA antagonists indicates that EPSPs in CA1 neurons are not mediated solely by this receptor.

2-Amino-5-phosphonovalerate↗
PubMed1978

Quantal analysis of transmitter release at an inhibitory synapse in the central nervous system of the leech.

The quantal nature of transmitter release has been analysed at central inhibitory synapses in the leech nervous system between an interneurone (HN) and a motoneurone (HE) that regulate the heartbeat. 1. Ganglia were bathed in leech Ringer fluid containing 20 mM-Mg and 1.8 mM-Ca and the membrane of the presynaptic HN interneurone was hyperpolarized by current injection. Under these conditions successive inhibitory potentials in the HE motoneurone, evoked by impulses in the HN interneurone, showed striking fluctuations in amplitude. 2. Assuming a Poisson distribution of the i.p.s.p.s and estimating the number of failures from the amplitude histograms of the observed responses, the mean size of the quantal unit was estimated as 0.25 +/- 0.015 mV (S.E. of mean, n = 26). When m, the mean number of quanta released per trial, was varied by changing the membrane potential of the presynaptic HN cell (Nicholls & Wallace, 1978), the experimentally observed amplitude distributions could be predicted by the Poisson theory. 3. An independent estimate of the unit size was obtained by noise analysis. A long subthreshold depolarizing pulse applied to the presynaptic HN interneurone evoked a sustained hyperpolarization of the HE motoneurone, apparently caused by an increase in the rate of on-going release of quanta by the HN cell terminals. From the mean change in membrane potential and the increase in variance, the size of the unit was calculated as 0.21 +/- 0.039 mV (S.E. of mean, n = 11). For ten pairs of cells an estimate of unit amplitude was made both from the Poisson analysis and the analysis of variance, again with good agreement. For these cells the estimated unit sizes were 0.24 +/- 0.023 mV (S.E. of mean, n = 10) from the failures and 0.21 +/- 0.043 m V (S.E. of mean, n = 10) from the noise. 4. A similar analysis was made of the inhibitory synaptic potentials evoked in one HN interneurone by stimulation of its contralateral homologue. Transmission again appeared to be qualtal; the mean unit amplitude from Poisson analysis was 0.31 +/- 0.022 mV (S.E. of mean, n = 19) and from the noise 0.29 +/- 0.027 mV (S.E. of mean, n = 3). 5. We conclude that transmitter is released from the terminals of the HN interneurone in quantal units that evoke miniature i.p.s.p.s of about 0.25 mV in the post-synaptic cells. Furthermore, modulation of transmission proudced by variation in the presynaptic resting potential and during presynaptic inhibition results from changes in the mean number of quanta released by each impulse.

Animals↗