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PubMed1991

Apical dendritic depolarizations and field interactions evoked by stimulation of afferent inputs to rat hippocampal CA1 pyramidal cells.

The relationship between orthodromic extracellular field potentials and intradendritic depolarizations in apical dendrites of CA1 pyramidal neurons was investigated using the in vitro slice preparation of rat hippocampus. Orthodromic synaptic field potentials evoked by stimulation of afferent inputs in stratum radiatum or stratum oriens were used to measure extracellular voltage gradients generated over the pyramidal cell axis. Extracellular gradients were of opposite polarity over the region of pyramidal cell apical dendrites in stratum radiatum. The stratum radiatum-evoked gradient was negative towards the apical dendrites and the stratum oriens-evoked gradient negative towards the cell body layer, with gradients reaching values of up to 50 mV/mm over the apical dendritic axis. Intradendritic recordings obtained greater than 150 microns from stratum pyramidale directly measured the subthreshold apical dendritic excitatory postsynaptic potentials evoked by stratum radiatum or stratum oriens stimulation. These ground-referenced recordings were then compared to the transmembrane potential calculated by subtraction of the corresponding extradendritic field potential. Both stratum radiatum and stratum oriens stimulation evoked graded excitatory postsynaptic potentials that could be recorded in apical dendritic impalements up to 265 microns from stratum pyramidale. The calculated transmembrane potential of the stratum radiatum-evoked excitatory postsynaptic potential had a significantly greater rate of rise, peak amplitude, and rate of decay than that of the ground-referenced excitatory postsynaptic potential. In contrast, the rates of rise and decay of the transmembrane potential of the stratum oriens-evoked excitatory postsynaptic potential were reduced with respect to the ground-referenced recording. The peak amplitude of the stratum oriens-evoked transmembrane potential, however, varied according to the polarity of the corresponding extradendritic population spike response recorded in stratum radiatum. These data reveal that synaptic activation of either basal or apical dendrites of CA1 pyramidal cells evokes a depolarization that can be recorded over a substantial region of the apical dendritic arbor. Furthermore, extradendritic field potentials evoked by stimulation of these inputs produce opposite effects on the transmembrane potential of apical dendrites. The magnitude of the accompanying extracellular voltage gradients suggest that these shifts in transmembrane potential reflect ephaptic interactions at the apical dendritic level of pyramidal cells.

Animals↗

PubMed1998

Asymmetries in sensory pathways from skin to motoneurons on each side of the body determine the direction of an avoidance response in hatchling Xenopus tadpoles.

1. When swimming is initiated by tail stimulation in hatchling Xenopus tadpoles, the first trunk contraction is usually on the opposite side and directs the animal away from the stimulus. We have investigated how asymmetries in the skin sensory pathways mediate this response. 2. In alpha-bungarotoxin-immobilized tadpoles, intracellular recordings were made of responses to ipsilateral (ISS) and contralateral skin stimulation (CSS) in thirty-two presumed motoneurons. ISS evokes an inhibitory postsynaptic potential (IPSP) followed by an excitatory postsynaptic potential (EPSP) whereas CSS only evokes an EPSP. Blocking the short latency IPSP evoked by ISS with strychnine reduced the difference in spike latency on the two sides but spikes still occurred first to CSS. 3. Motoneuron EPSPs evoked by ISS and CSS were therefore recorded during microperfusion of strychnine to block the short latency IPSP. We found: (a) the CSS-EPSPs have lower threshold, larger amplitude at a given intensity of stimulus, faster rising phase, and shorter latencies than those of ISS-EPSPs; (b) the ISS-EPSP onset latencies were longer than CSS-EPSPs and became shorter as the stimulus intensity increased while those of CSS-EPSPs remained little changed. At high stimulus intensities, EPSPs caused by CSS and ISS became similar; and (c) onset latencies of ISS-EPSPs had higher variance than those of CSS-EPSPs. However, this difference was reduced as the stimulus intensity was increased. 4. Since motoneuron EPSP onset latencies varied with stimulus intensity, we proposed that the pathway from the opposite side had stronger synapses from afferents to sensory interneurons. To test this proposal we built a neuronal population model of the spinal pathway from skin afferents, via sensory interneurons to ipsilateral and contralateral motoneurons incorporating this asymmetry. Inhibition was omitted from the model. 5. Simulated motoneuron EPSPs in response to skin stimulation on each side of the body showed the major asymmetries found experimentally. If the distribution and axonal projections of the interneurons in the two sensory pathways were made the same these differences remained. However, if the synaptic strength from sensory afferents onto interneurons projecting to the two sides were made equal, the difference between the two sides were lost. 6. We propose that the sensory pathway to contralateral motoneurons has more effective excitation from afferents to sensory interneurons which leads to these motoneurons firing first. At higher stimulus strengths, when population recruitment can blur these subtle differences in excitation between the two sides, inhibition normally plays a significant role to ensure that most first responses are still contralateral.

Action Potentials↗

PubMed1998

An electrophysiological study of pterygopalatine ganglion neurons in the rabbit.

A preparation was developed to investigate the synaptic connections of the pterygopalatine ganglion (P.P.G.) neurons of the rabbit. Many neurons received synaptic inputs from more than one preganglionic fiber in the vidian nerve (preganglionic nerve) with a wide range of conduction velocities. It is assumed that P.P.G. neurons integrate synaptic inputs from the higher centers. In some neurons. nicotinic fast excitatory postsynaptic potentials (e.p.s.p.s) were evoked in response to stimulation of one posterior nasal nerve, and also an antidromic action potential occurred in response to stimulation of the other posterior nasal nerve. Fast e.p.s.p.s were recorded from a ganglion neuron in response to the cooling stimulation of the nasal mucosa. These results revealed that the ganglionic reflex are mediated through the nasal afferent fibers exists in the P.P.G. Moreover, the appearance of slow inhibitory postsynaptic potentials (slow i.p.s.p.s) and slow excitatory postsynaptic potentials (slow e.p.s.p.s) in response to repetitive stimuli of the vidian nerve may influence the synaptic transmissions of P.P.G. neurons. The P.P.G. plays a significant role as a complicated key point of signal transmissions from both the periphery and higher centers.

Animals↗

PubMed2000

Synaptic transmission in the neocortex during reversible cooling.

We studied the effects of reversible cooling on synaptic transmission in slices of rat visual cortex. Cooling had marked monotonic effects on the temporal properties of synaptic transmission. It increased the latency of excitatory postsynaptic potentials and prolonged their time-course. Effects were non-monotonic on other properties, such as amplitude of excitatory postsynaptic potentials and generation of spikes. The amplitude of excitatory postsynaptic potentials increased, decreased, or remain unchanged while cooling down to about 20 degrees C, but thereafter it declined gradually in all cells studied. The effect of moderate cooling on spike generation was increased excitability, most probably due to the ease with which a depolarized membrane potential could be brought to spike threshold by a sufficiently strong excitatory postsynaptic potential. Stimuli that were subthreshold above 30 degrees C could readily generate spikes at room temperature. Only at well below 10 degrees C could action potentials be completely suppressed. Paired-pulse facilitation was less at lower temperatures, indicating that synaptic dynamics are different at room temperature as compared with physiological temperatures. These results have important implications for extrapolating in vitro data obtained at room temperatures to higher temperatures. The data also emphasize that inactivation by cooling might be a useful tool for studying interactions between brain regions, but the data recorded within the cooled area do not allow reliable conclusions to be drawn about neural operations at normal temperatures.

Action Potentials↗

PubMed2000

Effects of DAGO on the rodent hippocampal evoked potentials using different perfusion solutions.

Opioid receptor agonists exert excitatory effects in the hippocampus by inhibiting GABA release. We report that the mu-opioid agonist, DAGO, increases the amplitude of the population spikes (PS) measured in the stratum pyramidale of the CA1 cell layer in mouse and rat hippocampal slices perfused with an artificial cerebrospinal fluid (ACSF), but not when perfused in Krebs solution. The GABAA agonist, 3-APS, induces inhibitory responses when perfused in either ACSF or Krebs. Also, the field excitatory postsynaptic potentials (EPSP) measured on stratum radiatum do not differ when the slice is perfused with either ACSF or Krebs. The increase in the amplitude of the PS induced by DAGO is not obtained when perfused in a modified. ACSF whose concentration of MgSO4 was lowered to its concentration in the Krebs solution (from 2.4 mM to 1.2 mM). Thus, changes in the concentration of MgSO4 seem to be responsible for the different responses induced by DAGO.

Analgesics↗

PubMed1997

Glutamate currents in morphologically identified human dentate granule cells in temporal lobe epilepsy.

Glutamate-receptor-mediated synaptic transmission was studied in morphologically identified hippocampal dentate granule cells (DGCs; n = 31) with the use of whole cell patch-clamp recording and intracellular injection of biocytin or Lucifer yellow in slices prepared from surgically removed medial temporal lobe specimens of epileptic patients (14 specimens from 14 patients). In the current-clamp recording, low-frequency stimulation of the perforant path generated depolarizing postsynaptic potentials that consisted of excitatory postsynaptic potentials and phase-inverted inhibitory postsynaptic potentials mediated by the gamma-aminobutyric acid-A (GABA(A)) receptor at a resting membrane potential of -62.7 +/- 2.0 (SE) mV. In the voltage-clamp recording, two glutamate conductances, a fast alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-receptor-mediated excitatory postsynaptic current (EPSC; AMPA EPSC) and a slowly developing N-methyl-D-aspartate (NMDA)-receptor-mediated EPSC (NMDA EPSC), were isolated in the presence of a GABA(A) receptor antagonist. NMDA EPSCs showed a voltage-dependent increase in conductance with depolarization by exhibiting an N-shaped current-voltage relationship. The slope conductance of the NMDA EPSC ranged from 1.1 to 9.4 nS in 31 DGCs, reaching up to twice the size of the AMPA conductance. This widely varying size of the NMDA conductance resulted in the generation of double-peaked EPSCs and a nonlinear increase of the slope conductance of up to 37.5 nS with positive membrane potentials, which resembled "paroxysmal currents," in a subpopulation of the neurons. In contrast, AMPA EPSCs, which were isolated in the presence of an NMDA receptor antagonist (2-amino-5-phosphonovaleric acid), showed voltage-independent linear changes in the current-voltage relationship and were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione. The AMPA conductance showed little variance, regardless of the size of the NMDA conductance of a given neuron. The average AMPA slope conductance was 5.28 +/- 0.65 (SE) nS in 31 human DGCs. This value was similar to AMPA EPSC conductances in normal rat DGCs (5.35 +/- 0.52 nS, mean +/- SE; n = 55). Dendritic morphology and spine density were quantified in the individual DGCs to assess epileptic pathology. Dendritic spine density showed an inverse correlation (r2 = 0.705) with a slower rise time and a longer half-width of the excitatory postsynaptic potentials mediated by the NMDA receptor. It is concluded that both AMPA and NMDA EPSCs contribute to human DGC synaptic transmission in epileptic hippocampus. However, a wide range of changes in the slope conductance of the NMDA EPSCs suggests that the NMDA-receptor-mediated conductance could be altered in human epileptic DGCs. These changes may influence the generation of chronic subthreshold epileptogenic synaptic activity and give rise to pathological excitation leading to epileptic seizures and dendritic pathology.

Animals↗

PubMed1990

Calcium released by photolysis of DM-nitrophen stimulates transmitter release at squid giant synapse.

1. Transmitter release at the squid giant synapse was stimulated by photolytic release of Ca2+ from the 'caged' Ca2+ compound DM-nitrophen (Kaplan & Ellis-Davies, 1988) inserted into presynaptic terminals. 2. Competing binding reactions cause the amount of Ca2+ released by DM-nitrophen photolysis to depend on the concentrations of DM-nitrophen, total Ca2+, Mg+, ATP and native cytoplasmic Ca2+ buffer. Measurements of presynaptic [Ca2+] changes by co-injection of the fluorescent indicator dye Fura-2 show that DM-nitrophen photolysis causes a transient rise in Ca2+ followed by decay within about 150 ms to an increased steady-state level. 3. Rapid photolysis of Ca2(+)-loaded nitrophen within the presynaptic terminal was followed in less than a millisecond by depolarization of the postsynaptic membrane. As with action potential-evoked excitatory postsynaptic potentials (EPSPs), the light-evoked response was partially and reversibly blocked by 1-3 mM-kainic acid which desensitizes postsynaptic glutamate receptors. 4. Release was similar in magnitude and rate to normal action potential-mediated EPSPs. 5. The release of transmitter by photolysis of Ca2(+)-loaded DM-nitrophen was not affected by removal of Ca2+ from the saline or addition of tetrodotoxin. Photolysis of DM-nitrophen injected into presynaptic terminals without added Ca2+ did not stimulate release of transmitter nor did it interfere with normal action potential-mediated release. 6. Stimulation of presynaptic action potentials in Ca2(+)-free saline during the light-evoked response did not elicit increased release of transmitter if the ganglion was bathed in Ca2(+)-free saline, i.e. in the absence of Ca2+ influx. Increasing the intensity of the light or stimulating presynaptic action potentials in Ca2(+)-containing saline increased the release of transmitter. Therefore the failure of presynaptic voltage change to increase transmitter release resulting from release of caged Ca2+ was not due to saturation or inhibition of the release mechanism by light-released Ca2+. 7. Decreasing the temperature of the preparation increased the delay to onset of the light-evoked response and reduced its amplitude and rate of rise to an extent similar to that observed for action potential-evoked EPSPs.

Acetates↗

PubMed2000

Seizures induce simultaneous GABAergic and glutamatergic transmission in the dentate gyrus-CA3 system.

Monosynaptic and polysynaptic responses of CA3 pyramidal cells (PC) to stimulation of the dentate gyrus (DG) are normally blocked by glutamate receptor antagonists (GluRAs). However, after kindled seizures, GluRAs block the monosynaptic excitatory postsynaptic potential (EPSP) and isolate a monosynaptic inhibitory postsynaptic potential (IPSP), suggesting that mossy fibers release GABA. However, kindling epilepsy induces neuronal sprouting, which can underlie this fast inhibitory response. To explore this possibility, the synaptic responses of PC to DG stimulation were analyzed in kindled epileptic rats, with and without seizures, and in nonepileptic rats, immediately after a single pentylenetetrazol (PTZ)-induced seizure, in which sprouting is unlikely to have occurred. Excitatory and inhibitory synaptic responses of PC to DG stimulation were blocked by GluRAs in control cells and in cells from kindled nonseizing rats, confirming that inhibitory potentials are disynaptically mediated. However, a fast IPSP could be evoked in kindled epileptic rats and in nonepileptic rats after a single PTZ-induced seizure. The same response was induced after rekindling the epileptic nonseizing rats. This IPSP has an onset latency that parallels that of the control EPSP and is not altered under low Ca(2+) medium or halothane perfusion. In addition, it was reversibly depressed by L(+)-2-amino-4-phosphonobutyric acid (L-AP4), which is known to inhibit transmitter release from mossy fibers. These results demonstrate that seizures, and not the synaptic rearrangement due to an underlying epileptic state, induce the emergence of fast inhibition in the DG-CA3 system, and suggest that the mossy fibers underlie this plastic change.

Amygdala↗

PubMedDate not supplied

Kindling-like state occurring on periodic increases in the extracellular K+ concentration in field CA1 in rat hippocampal slices.

Transient periodic increases in the extracellular K+ concentration (20 mM, 30 sec, 3-6 episodes) led to the appearance of a kindling-like state in local neuronal networks of field CA1 of rat hippocampal slices. A criterion for the appearance of this state was a reduction in the threshold for the generation of multiple population discharges and an increase in the total number of population spikes within discharges (epileptiform activity). This state correlated with potentiation of excitatory postsynaptic potentials (EPSP) (long-term increases in pyramidal neuron excitability), but not with potentiation of glutamatergic synaptic transmission in field CA1 of hippocampal slices. The role of the various Ca2+ channels in inducing and maintaining the kindling-like state in rat hippocampal sections, evoked by periodic increases in the extracellular K+ concentration, is discussed.

Animals↗

PubMed2001

Presynaptic effects of biogenic amines modulating synaptic transmission between identified sensory neurons and giant interneurons in the first instar cockroach.

Intracellular recording was used to investigate the modulatory effects of serotonin and octopamine on the identified synapses between filiform hair sensory afferents and giant interneurons in the first instar cockroach, Periplaneta americana. Serotonin at 10(-4) mol l(-1) to 10(-3) mol l(-1) reduced the amplitude of the lateral axon-to-ipsilateral giant interneuron 3 excitatory postsynaptic potentials. and octopamine at 10(-4) mol l(-1) increased their amplitude. Similar effects were seen on excitatory postsynaptic potentials in dorsal giant interneuron 6. Several lines of evidence suggest that both substances modulate the amplitude of excitatory postsynaptic potentials by acting presynaptically, rather than on the postsynaptic neuron. The fitting of simple binomial distributions to the postsynaptic potential amplitude histograms suggested that, for both serotonin and octopamine, the number of synaptic release sites was being modulated. Secondly, the amplitudes of miniature excitatory postsynaptic potentials recorded in the presence of tetrodotoxin were unaffected by either modulator. Finally, recordings from contralateral giant interneuron 3, which has two identifiable populations of synaptic inputs, showed that each modulator had a more pronounced effect on excitatory postsynaptic potentials evoked by the lateral axon than on those evoked by the medial axon. Immunocytochemistry confirmed that neuropilar processes containing serotonin are present in close proximity to these synapses.

Animals↗

PubMed2003

Timing of neural responses in cortical organotypic slices.

Timing is a fundamental part of sensory and motor processing. However, little is known about the neural mechanisms underlying timing in the range of tens to hundreds of milliseconds. Although many theoretical hypotheses have been put forth on the possible underpinnings of temporal processing, there is little cellular experimental data, particularly in vitro, as to the neural mechanisms that could potentially function as timers. We use organotypic cortical slices to show that reliably timed action potentials (or excitatory postsynaptic potentials) can be observed up to 300 ms after a single stimulus. There was no relationship between the latency of the late responses and distance from the stimulating electrode. Paired recordings and pharmacological manipulations suggest that the timed late responses are the result of the propagation of activity throughout functionally defined networks. These results show that cortical networks may be intrinsically able to process temporal information.

2-Amino-5-phosphonovalerate↗

PubMed1984

Influence of 11-hydroxy-delta-9-tetrahydrocannabinol on spinal motoneurons in cat.

Intracellular recording techniques were used on spinal motoneurons in the cat in order to define the synaptic pharmacology of 11-hydroxy-delta-9-tetrahydrocannabinol (11-hydroxy-delta-9-THC), the principal metabolite of delta-9-tetrahydrocannabinol (delta-9-THC). The 11-hydroxy derivative increased the amplitude of excitatory postsynaptic potentials; such an excitatory response did not appear to be the result of changes in afferent input. The increase in excitatory postsynaptic potentials, however, may be accounted for by a rise in membrane resistance. The cannabinoid also concomitantly produced synaptic depression, as indicated by a rise in the firing threshold for the motoneuron action potential. The responses to 11-hydroxy derivative suggest synaptic sites and mechanisms of action; for instance, the data indicate that the cannabinoid affected postsynaptic conductance. Finally, the similarity between the synaptic effects of the 11-hydroxy derivative and those of delta-9-THC suggest that the metabolite may contribute to the pharmacological properties of its parent compound.

Action Potentials↗

PubMed2002

Effects of temperature increase on the propagation of presynaptic action potentials in the pathway between the Schaffer collaterals and hippocampal CA1 neurons.

Effects of temperature increase on the neuronal activity of hippocampal CA2-CA1 regions were examined by using optical and electrophysiological recording techniques. Stimulation of the Schaffer collaterals at the CA2 region evoked depolarizing optical signals that spread toward the CA1 region at 32 degrees C. The optical signal recorded by 49 pixels was characterized by fast and slow components that were closely related to presynaptic action potentials and excitatory postsynaptic responses, respectively. The optical signal was depressed by temperature increase to 38-40 degrees C. The temperature increase to 38 degrees C produced a hyperpolarization and a depression of the excitatory postsynaptic potential (EPSP) in single hippocampal CA1 pyramidal neurons. The depression of the neuronal activity induced by temperature increase was attenuated by application of glucose (22 mM) or pyruvate (22 mM). Adenosine (200 microM) did not block the presynaptic action potential but strongly depressed the excitatory postsynaptic response. 8-Cyclopentyl-1,3-dimethylxanthine (8-CPT) (10 microM), an antagonist for adenosine A(1) receptors, attenuated the depression of the excitatory postsynaptic response but not the inhibition of the presynaptic action potential at 38 degrees C. These results suggest that adenosine mediates the high-temperature-induced depression of the excitatory synaptic transmission but not that of action potential propagation in rat CA1 neurons.

Action Potentials↗

PubMed1998

Depression of synaptic efficacy at intermolt in crayfish neuromuscular junctions by 20-hydroxyecdysone, a molting hormone.

This report demonstrates that ecdysteroids can reduce synaptic transmission at an intermolt stage of a crustacean tonic neuromuscular junction by acting at a presynaptic site. The steroid molting hormone, 20-hydroxyecdysone (20-HE), appears to act through a rapid, nongenomic mechanism that decreases the probability of synaptic vesicle release and reduces the number of release sites. Quantal analysis revealed that fewer vesicles were released for a given stimulus when 20-HE was present, and this in turn accounted for the reduced synaptic efficacy. Reduced synaptic efficacy produced smaller evoked postsynaptic currents and smaller excitatory postsynaptic potentials (EPSPs) across the muscle fiber membrane. The reduction in EPSPs was observed among muscle fibers that were innervated by high- or low-output terminals. The behavior of crustaceans/crayfish during the molt cycle, when 20-HE is high, may be explained by the reduction in synaptic transmission. Crustaceans become quiescent during the premolt periods as do insects. The effects of 20-HE can be reversed with the application of the crustacean neuromodulator serotonin, which enhances synaptic transmission.

Animals↗

PubMed1998

Gain control of NMDA-receptor currents by intracellular sodium.

The influx of Na+ is fundamental to electrical signalling in the nervous system and is essential for such basic signals as action potentials and excitatory postsynaptic potentials. During periods of bursting or high levels of discharge activity, large increases in intracellular Na+ concentration ([Na+]i) are produced in neuronal soma and dendrites. However, the intracellular signalling function of raised postsynaptic [Na+]i is unknown. Here we show that [Na+]i regulates the function of NMDA (N-methyl-D-aspartate) receptors, a principal subtype of glutamate receptor. NMDA-receptor-mediated whole-cell currents and NMDA-receptor single-channel activity were increased by raising [Na+]i and channel activity decreased upon lowering [Na+]i; therefore, the activity of NMDA channels tracks changes in [Na+]i. We found that the sensitivity of the channel to Na+ was set by a Src kinase that is associated with the channel. Raising [Na+]i selectively increased synaptic responses mediated by NMDA receptors, but not by non-NMDA receptors. Thus, the change in postsynaptic [Na+]i that occurs during neuronal activity is a signal for controlling the gain of excitatory synaptic transmission. This mechanism may be important for NMDA-receptor-dependent plasticity and toxicity in the central nervous system.

Animals↗

PubMed1997

A ventral pontine pathway promotes rhythmic activity in the medulla of neonate mice.

We have developed in new-born mice a ventral tilted-horizontal slice preparation for pontine stimulation and recording of spontaneous respiratory-like rhythmic trains of glutamatergic excitatory postsynaptic potentials (EPSPs) in medullary neurons. Electrical stimulations (10-50 Hz for 100-500 ms) of the caudal pontine reticular formation triggered a burst of EPSPs, recycling of the rhythmic activity and persistent increase of the rhythmic behaviour. These results identify a ventral pontine pathway that promotes rhythm generating mechanisms in the medulla and probably derives from a population of lateral reticular neurons identified in the embryonic hindbrain and eliminated after inactivation of the early developmental gene Krox-20.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1998

Post- and presynaptic effects of norepinephrine in guinea-pig colonic submucous plexus.

Intracellular recording techniques were used to investigate the effects of norepinephrine on submucous neurones in the guinea-pig distal colon. In 81% of the neurones, pressure microejection of norepinephrine produced a membrane hyperpolarization associated with a decrease in excitability and input resistance. Microejection of clonidine (1 microM) mimicked the norepinephrine-induced hyperpolarization, whereas both phentolamine (1 microM) and yohimbine (1 microM) reversibly suppressed it. Superfusion of norepinephrine (1 nM - 10 microM) hyperpolarized the cells in a concentration-dependent manner. Norepinephrine and clonidine (1 nM - 10 microM) caused a concentration-dependent presynaptic inhibition of stimulus-evoked cholinergic fast excitatory postsynaptic potential. Slow inhibitory post-synaptic potentials (sISPSs) were induced by focal electrical stimulation of the interganglionic fibre tracts in 43% of the neurones tested. Superfusion of both phentolamine (1 microM) and yohimbine (1 microM) reduced the sIPSPs while prazosin (1 microM) had no significant effect. We concluded that norepinephrine acted post- and presynaptically via alpha 2-adrenoreceptors to have an inhibitory effect on the guinea-pig colonic submucous. In addition, our study strongly supported the role of norepinephrine as a mediator of the sIPSPs. As a result, norepinephrine would primarily suppress information transfer within the neuronal circuits in guinea-pig colonic submucosal plexus.

Acetylcholine↗

PubMed2001

Comparison of the effects of neurokinin-3 receptor blockade on two forms of slow synaptic transmission in myenteric AH neurons.

AH neurons are intrinsic sensory neurons of the intestine that exhibit two types of slow synaptic event: slow excitatory postsynaptic potentials which increase their excitability for about 2-4 min, and sustained slow postsynaptic excitation which can persist for several hours, and may be involved in long-term changes in the sensitivity of the intestine to sensory stimuli. The effects of the neurokinin-3 tachykinin receptor antagonist, SR142801, on these two types of synaptic event in AH neurons of the myenteric ganglia of guinea-pig small intestine were compared. Slow excitatory postsynaptic potentials were evoked by stimulation of synaptic inputs at 10-20 Hz for 1s, and sustained slow postsynaptic excitation was evoked by stimulation of inputs at 1Hz for 4 min. SR142801 (1microM) reduced the amplitude of the slow excitatory postsynaptic potential to 26% of control, and also reduced the increase in input resistance and the extent of anode break excitation associated with the slow excitatory postsynaptic potential. In contrast, SR142801 did not reduce the increase in excitability, the increase in input resistance or the depolarisation that occur during the sustained slow postsynaptic excitation. SR142801 did not change the resting membrane potential or the resting input resistance. We conclude that tachykinins, acting through neurokinin-3 receptors, are involved in the generation of the slow excitatory postsynaptic potential, but not in the sustained slow postsynaptic excitation, and that the release of transmitters from synaptic inputs to AH neurons is frequency coded.

Action Potentials↗