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PubMed1999

Noradrenaline excites non-cholinergic laterodorsal tegmental neurons via two distinct mechanisms.

Cholinergic neurons of the laterodorsal tegmental nucleus have been hypothesized to play a critical role in the-generation and maintenance of rapid eye movement sleep. Less is known about the function of non-cholinergic laterodorsal tegmental nucleus neurons. As part of our ongoing studies of the brainstem circuitry controlling behavioral state, we have begun to investigate the functional properties of these neurons. In the course of these experiments, we have observed a novel response to the neurotransmitter noradrenaline. Whole-cell patch-clamp recordings of laterodorsal tegmental nucleus neurons were carried out in 21- to 35-day-old rat brain slices. A subpopulation of laterodorsal tegmental nucleus cells responded to a 30-s application of 50 microM noradrenaline with depolarization and a decrease in input resistance which lasted several minutes. Following return to resting membrane potential, these cells invariably exhibited barrages of excitatory postsynaptic potentials which lasted at least 12 min. These excitatory postsynaptic potentials were reversibly abolished by bath application of tetrodotoxin, as well as by the non-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione, but were insensitive to application of the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonopentanoic acid. To examine whether these neurons were cholinergic, the recorded cells were labeled with biocytin and tested for co-localization with reduced nicotinamide adenine dinucleotide phosphate-diaphorase, a marker for laterodorsal tegmental nucleus cholinergic neurons. In every instance, neurons with these properties were non-cholinergic. However, they were always located in close proximity to reduced nicotinamide adenine dinucleotide phosphate-diaphorase-positive laterodorsal tegmental nucleus cells. The present data indicate that noradrenaline, in addition to directly inhibiting cholinergic cells of the laterodorsal tegmental nucleus, also results in the direct and indirect excitation of non-cholinergic cells of the laterodorsal tegmental nucleus. The indirect excitation is long lasting and mediated by glutamatergic mechanisms. Our working hypothesis is that these non-cholinergic cells are local circuit inhibitory interneurons and that prolonged excitation of these neurons by noradrenaline may serve as a mechanism for inhibition of cholinergic laterodorsal tegmental nucleus cells during wakefulness, when noradrenaline tone is high.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1994

Arachidonic acid and diacylglycerol ACT synergistically through protein kinase C to persistently enhance synaptic transmission in the hippocampus.

In model membranes, arachidonic acid and diacylglycerol have been proposed to synergistically induce a membrane-inserted, constitutively active form of protein kinase C. We have investigated the effects of these lipid protein kinase C activators on synaptic efficacy in the Schaffer collateral input to CA1 hippocampal pyramidal cells. Arachidonic acid (5 microM) perfusion combined with repetitive afferent stimulation had no consistent effect on field excitatory postsynaptic potentials recorded in stratum radiatum, while treatment with a cell-permeable diglyceride, oleoyl-acetylglycerol (5 micrograms/ml), followed by stimulation, led to a short-term potentiation. By contrast, the combination of oleoyl-acetylglycerol and arachidonic acid gave rise to a long-lasting non-decremental potentiation of field excitatory postsynaptic potentials. The induction of potentiation was "activity dependent", as there was either no significant effect or there was a measurable depression when repetitive synaptic stimulation was omitted. Furthermore, consistent with a protein kinase C-dependent process, the potentiation was blocked by the kinase inhibitors H-7 and staurosporine. The results suggest that relatively low concentrations of arachidonic acid and diacylglycerol work synergistically through protein kinase C to persistently enhance synaptic transmission. This synergy has the makings of an associative (Hebbian) device for long-term potentiation induction operating at the second messenger level.

Animals↗

PubMed1990

Osmotic effects upon excitability in rat neocortical slices.

Acute osmotic disturbances can lead to profound neurological problems, yet there has been little experimentation at a cellular level to assess if neurophysiological changes are induced by altered osmolality. Using extra- and intracellular recording in the rat neocortical slice preparation, we examined pyramidal neurons of layers II-III under changing osmotic conditions. Single cell properties, field potentials, synaptic transmission and epileptiform discharges were studied in control saline (295 mOsm) and compared with corresponding data collected during exposure to osmolalities between 245 and 375 mOsm. Single cell properties (resting membrane potential, cell input resistance, action potential threshold and duration) did not change significantly, but neuronal interactions were considerably influenced by osmotic change within minutes. Hyposmolality increased the amplitude of evoked field potentials and of excitatory postsynaptic potentials recorded intracellularly. Hyperosmolality, induced with mannitol, decreased these parameters. Electrotonic coupling, as gauged by the degree of dye coupling and by cell input resistance, was not influenced by shifts in osmolality. The clinical finding that overhydration promotes seizure onset was examined in slices made epileptogenic in Mg2(+)-free saline. Hyposmolality increased the frequency and decreased the duration of interictal bursts, whereas raising osmolality with mannitol had opposite effects. None of the aforementioned effects occurred when osmolality was increased with a freely permeable substance such as dimethylsulfoxide, nor could they be ascribed to changes in saline Na+ or Ca2+ concentrations. The results are consistent with hyposmotic solutions reducing extracellular space by causing cells to swell. Theoretically, during population discharge, this should both concentrate K+ released extracellularly and possibly increase field (ephaptic) interactions. How lowered osmolality strengthens spontaneous and evoked excitatory synaptic transmission in neocortex is not yet clear. However, it may be an important mechanism underlying the increased seizure susceptibility of patients and experimental animals with lowered plasma osmolality. Conversely, suppression of excitatory postsynaptic potentials by osmotically active substances may be involved in the lowered seizure susceptibility observed clinically.

Action Potentials↗

PubMed1996

Enhancement of sensorimotor connections by conditioning-related stimulation in Aplysia depends upon postsynaptic Ca2+.

Classical conditioning of Aplysia's siphon-withdrawal reflex is thought to be due to a presynaptic mechanism-activity-dependent presynaptic facilitation of sensorimotor connections. Recent experiments with sensorimotor synapses in dissociated cell culture, however, provide an alternative cellular mechanism for classical conditioning-Hebbian long-term potentiation (LTP) of sensorimotor connections. Induction of Hebbian LTP of these connections is mediated by activation of N-methyl-D-aspartate-related receptors and requires the postsynaptic elevation of intracellular Ca2+. To determine whether the enhancement of sensorimotor synapses during classical conditioning in Aplysia-like LTP of sensorimotor synapses in culture-also depends upon the elevation of postsynaptic Ca2+, we carried out experiments involving the cellular analog of classical conditioning of siphon withdrawal. We examined changes in the strength of monosynaptic siphon sensorimotor connections in the abdominal ganglion of Aplysia following paired presentations of sensory neuron activation and tail nerve shock. This training regimen resulted in significant enhancement of the monosynaptic sensorimotor excitatory postsynaptic potential, as compared with the sensorimotor excitatory postsynaptic potential in preparations that received only test stimulation. Infusing the motor neuron with 1,2-bis(2-aminophenoxy)ethane-N,N-N',N'-tetraacetic acid, a specific chelator of intracellular Ca2+, prior to paired stimulation training blocked this synaptic enhancement. Our results implicate a postsynaptic, possibly Hebbian, mechanism in classical conditioning in Aplysia.

Animals↗

PubMed2002

Effects of a hydroxy-cinnamoyl conjugate of spermidine on arthropod neuromuscular junctions.

N1-coumaroyl spermidine is structurally similar to acylpolyamines found in spider and wasp venoms, which are known to block arthropod glutamate receptors. N1-coumaroyl spermidine reduced the amplitude of excitatory postsynaptic potentials recorded in crayfish muscle. This effect was dose dependent, with an IC50 value of 70 micromol l(-1). N1-coumaroyl spermidine reversibly reduced the amplitude of potentials elicited by iontophoretic application of L-glutamate, indicating a direct effect on postsynaptic glutamate receptors. Neither 1 mmol l(-1) spermidine nor 1 mmol l(-1) coumaric acid altered excitatory postsynaptic potential amplitude, indicating that blockage requires the conjugated phenolic polyamine. N1-coumaroyl spermine, a slightly longer phenolic polyamine, reduced excitatory postsynaptic potential amplitude with approximately the same potency as N1-coumaroyl spermidine. Thus, potency of blockage does not appear to be affected in this experimental preparation by small changes in length of the polyamine. N1-coumaroyl spermidine also reduced excitatory postsynaptic potentials in muscles of the insect Drosophila. The ability of N1-coumaroyl spermidine to attenuate synaptic transmission at insect neuromuscular synapses lends support to the notion that plant-derived phenolic polyamines might serve as natural insecticides.

Animals↗

PubMed1996

Accumulation and extrusion of permeant Ca2+ chelators in attenuation of synaptic transmission at hippocampal CA1 neurons.

The effects of extracellularly applied membrane-permeant Ca2+ chelators on field excitatory postsynaptic potentials were determined in the hippocampal CA1 region of rat brain slices. Field excitatory postsynaptic potentials in slices perfused with 0.05-50 microM bis-(-O-aminophenoxy)-ethane-N,N,N,N,-tetraacetic acid acetoxymethyl (BAPTA-AM) for 15 min were reversibly attenuated by 10-45% in a concentration-dependent manner. Attenuation occurred earlier at higher concentrations of BAPTA-AM, thus indicating that the rate of accumulation of BAPTA salt was concentration dependent. Antidromically evoked responses and presynaptic volleys were unaffected by BAPTA-AM. Attenuation of the field excitatory postsynaptic potentials by BAPTA-AM was temporarily eliminated by repetitive stimulation at 1 Hz, suggesting saturation of the chelator's Ca(2+)-binding capacity. The amplitude of field excitatory postsynaptic potentials was unaffected by similar applications of 5'5-dinitro-BAPTA-AM, a low Ca(2+)-affinity BAPTA analogue, and EGTA-AM (5 or 50 microM), a chelator with slow Ca(2+)-binding kinetics, suggesting a dependence of the BAPTA-AM effect on fast Ca2+ binding and high Ca2+ affinity. BAPTA-AM concentrations as low as 0.05 microM were effective provided application was prolonged to 40 min. Probenecid (1 mM), an anion transport inhibitor, accelerated the onset and significantly enhanced the BAPTA-mediated synaptic attenuation caused by low concentrations of BAPTA-AM. These data show that even very low extracellular concentrations of BAPTA-AM can profoundly affect synaptic transmission provided that sufficient chelator accumulates presynaptically. The effectiveness of BAPTA-AM can be increased by procedures which inhibit chelator extrusion.

Animals↗

PubMed1987

Morphology and synaptic connections of crossed corticostriatal neurons in the rat.

The neurons of origin of the bilateral corticostriatal projection arising from the medial agranular cortical field in rats were identified by antidromic activation from contralateral neostriatal stimulation. The same cells were tested for antidromic activation from the contralateral neocortex and for orthodromic responses to stimulation of neocortex of the contralateral hemisphere or ipsilateral rostral thalamus. The neurons were then stained by intracellular injection of horseradish peroxidase. The laminar distribution of these neurons was compared to that of cortical cells stained retrogradely after injection of wheat germ agglutinin/HRP in the ipsilateral or contralateral neostriatum. The morphological features of physiologically identified corticostriatal neurons, their laminar organization, and their responses to stimulation were examined and compared with crossed corticocortical and brainstem-projecting cells. Crossed corticostriatal cells of the medial agranular cortical field were medium-sized pyramidal neurons found in the superficial part of layer V and in the deep part of layer III. Their basilar dendritic fields and initial intracortical axon collateral arborizations were coextensive with the layer defined by the distribution of corticostriatal neurons. The apical dendrites were thin and sparsely branched but consistently reached layer I, where they made a small arborization. These morphological features were shared by cortical neurons projecting to contralateral neocortex but not responding antidromically to stimulation of contralateral neostriatum, but they were not shared by brainstem-projecting cortical cells. Orthodromic responses to contralateral cortical stimulation consisted of brief excitatory postsynaptic potentials that were followed by powerful and longer-lasting inhibitory postsynaptic potentials. Corticostriatal cells also exhibited small excitatory postsynaptic potentials in response to thalamic stimulation. Many crossed corticostriatal neurons were also commissural corticocortical neurons. The results of reciprocal collision tests showed that this was due to the existence of two separate axonal branches, one projecting to contralateral neocortex and one to contralateral neostriatum. Intracellular staining of these neurons revealed ipsilateral axonal projections to the neostriatum and cortex.

Animals↗

PubMed1988

Morphine induces a spontaneous and evoked bursting activity in rat cortical neurons by adding a postsynaptic active mechanism to the synaptic input: an intracellular study in vivo.

The action of morphine on spontaneous and stimulus-evoked postsynaptic potentials was investigated in rat cortical neurons recorded intracellularly in vivo. Iontophoretically applied, morphine increased supra-threshold evoked depolarizing postsynaptic potentials inducing bursts of spikes, but only slightly increased weak (subthreshold) potentials. Spontaneous excitatory postsynaptic potentials were affected in a similar way, but their frequency did not change. Inhibitory postsynaptic potentials were only subsequently modified. Membrane hyperpolarization, induced by negative current injection, counteracts the morphine-induced burst generation. We suggest that the action of this alkaloid on threshold postsynaptic events involves a voltage-dependent mechanism, which may be triggered by synaptic currents.

Action Potentials↗

PubMed1990

[A quantum analysis of the long-term posttetanic changes in the minimal postsynaptic potentials in surviving hippocampal slices].

Excitatory postsynaptic potentials (EPSPs) were recorded in guinea pig hippocampal slices (area CA1) from 13 neurons after single or double-pulse stimulation of stratum radiatum (the Schaffer collaterals) and stratum oriens. Amplitudes of 23 EPSPs (9 neurons, 12 pathways) grew 5 to 55 min after 10 tetanic stimulations of the Schaffer collaterals. This increase has been considered as a long-term potentiation (LTP). A statistical analysis was carried out by four methods of the quantal hypothesis based on the binomial distribution. It revealed an increase in the mean quantal content (m) during LTP. An increase in the quantal size was also observed in the majority of the cases but it showed only a weak correlation with the LTP magnitude and for some methods it was statistically significant only for the periods later than 15 min after tetanic stimulation. A well expressed increase in m demonstrated by various methods corresponds to data of the previous in vivo studies and favours the presynaptic location of mechanisms of the LTP maintenance.

Animals↗

PubMed1986

[Effect of thiamine on various types of synaptic junctions].

Thiamine (1.10(-14) -- 1.10(-4) mol/l) reversibly increased the frequency of miniature excitatory postsynaptic potentials, amplitude and quantal content of excitatory postsynaptic potentials in crayfish glutaminergic synapse. Thiamine also increased spontaneous electrical activity and amplitude of synaptic potentials in guinea-pig taenia coli. In synaptosomes from the rat brain thiamine produced depolarization of nerve endings. The role of thiamine in the regulation of synaptic transmission and mechanism of its action are discussed.

Animals↗

PubMed1985

Synaptic transmission in the rabbit inferior mesenteric ganglion.

Electrical properties, cholinergic neurotransmission and non-cholinergic neurotransmission in the rabbit inferior mesenteric ganglion (IMG) in vitro were examined with intracellular recording techniques. A single ganglionic neuron received an average of 42 nicotinic cholinergic synaptic inputs. An atropine-sensitive slow excitatory postsynaptic potential not followed by a non-cholinergic late slow excitatory postsynaptic potential (LS-EPSP) was observed in 7% of the cells. In 63% of the cells a LS-EPSP insensitive to antagonism of nicotinic and muscarinic receptors was observed following repetitive nerve stimulation. The involvement of substance P (SP) in the genesis of the LS-EPSP was tested by applications of SP, applications of SP antagonists and applications of capsaicin. Neither SP, SP antagonists nor capsaicin affected the LS-EPSP. These findings distinguish the LS-EPSP in the rabbit IMG from its counterpart in the guinea pig IMG where SP has been proposed as the mediator of the LS-EPSP. A late slow inhibitory postsynaptic potential was observed in 13% of the cells. This hyperpolarization followed repetitive nerve stimulation and was insensitive to blockade of cholinergic receptors. There is a marked convergence of subthreshold fast excitatory postsynaptic potentials (F-EPSPs) of both central and peripheral origin onto these cells. The LS-EPSP could provide a mechanism for increasing the likelihood of temporal and/or spatial summation of these fast synaptic inputs, thereby increasing the probability of action potential generation in the ganglion cells.

Action Potentials↗

PubMed1996

Conditions required for polysynaptic excitation of dentate granule cells by area CA3 pyramidal cells in rat hippocampal slices.

Under control conditions, stimulation of area CA3 pyramidal cells in slices can produce inhibitory postsynaptic potentials in granule cells by a polysynaptic pathway that is likely to involve hilar neurons [Muller W. and Misgeld U. (1990) J. Neurophysiol. 64, 46-56; Muller W. and Misgeld U. (1991) J. Neurophysiol. 65, 141-147; Scharfman H. E. (1993) Neurosci. Lett. 156, 61-66; Scharfman H. F. (1994) Neurosci. Lett. 168, 29-33]. When slices are disinhibited, excitatory postsynaptic potentials occur after the same stimulus [Sharfman H. E. (1994) J. Neurosci. 14, 6041-6057]. The excitatory postsynaptic potentials are likely to be mediated by pyramidal cells that innervate hilar mossy cells, which in turn innervate granule cells. [Scharfman H. F. (1994) J. Neurosci 14, 6041-6057]. These pathways are potentially important, because they could provide positive or negative feedback from area CA3 to the dentate gyrus. However, it is not clear when the CA3-mossy cell-granule cell excitatory pathway operates, because to date it has only been described in detail when GABA(A) receptors are blocked throughout the entire slice [Scharfman H. E. (1994) J. Neurosci 14, 6041-6057]. Furthermore, the monosynaptic excitatory synaptic connections between these cells have only been observed in the presence of bicuculline [Scharfman H. F. (1994) J. Neurophysiol. 72, 2167-2180; Scharfman H. E. (1995) J. Neurophysiol. 74, 179-194]. Yet in vivo data suggest that a CA3-mossy cell-granule cell excitatory pathway may be active under some physiological conditions, because granule cells discharge in association with sharp wave population bursts of CA3 [Ylinen A., et al. (1995) Hippocampus 5, 78-90]. To address whether the CA3-mossy cell-granule cell pathway occurs without global disinhibition of the slice, and where in the network disinhibition may be required, the effects of area CA3 stimulation on granule cells was examined after focal application of the GABAA receptor antagonist bicuculline to restricted areas of hippocampal slices. A micropipette containing 1 mM bicuculline was placed transiently either (i) in the area CA3 cell layer, (ii) the granule cell layer, (iii) the hilus, or (iv) more than one site in succession. If a small segment of the CA3 pyramidal cell layer or the hilus was disinhibited, or bicuculline was applied to both regions, area CA3 stimulation still evoked inhibitory postsynaptic potentials in granule cells. In fact, inhibitory postsynaptic potentials were enhanced under these conditions, probably because excitation of inhibitory cells was increased. When bicuculline was applied just to the area near an impaled granule cell, all inhibitory postsynaptic potentials evoked in that cell were blocked, but no underlying excitatory postsynaptic potential was uncovered. If bicuculline was applied focally to either area CA3 or the hilus and the impaled granule cell, CA3 stimulation subsequently evoked excitatory postsynaptic potentials in that granule cell, presumably because excitatory neurons innervating granule cells were disinhibited while the effects of inhibitory cells on granule cells were blocked. Excitatory postsynaptic potentials were produced without bicuculline application in three of seven cells, simply by stimulating the fimbria repetitively. Thus, if bicuculline is applied to different sites in the slice, different effects occur on the inhibitory postsynaptic potentials of granule cells that are evoked by a fimbria stimulus. If bicuculline is applied to both the granule cell soma and either area CA3 or the hilus, inhibitory postsynaptic potentials are reduced, and reveal that excitatory postsynaptic potentials can be produced by the same stimulus. (ABSTRACT TRUNCATED)

Animals↗

PubMed1999

Interaction between intracellular tetanization and pairing-induced long-term synaptic plasticity in the rat visual cortex.

Long-term changes in synaptic transmission in slices of rat visual cortex were induced either by pairing the excitatory postsynaptic potentials with postsynaptic depolarization or by intracellular tetanization without synaptic stimulation. Changes in the excitatory postsynaptic potential amplitude induced by any of the protocols applied in isolation persisted for longer than 1 h. Pairing-induced long-term potentiation was input specific. We studied the interaction between intracellular tetanization and pairing-induced plasticity by applying the two protocols one after the other at 10-min intervals. The pairing procedure applied after intracellular tetanization did not lead to any further potentiation, but to a depotentiation of the potentiated inputs. A second pairing protocol applied 10 min later led to further depotentiation, while previously unaffected inputs became weakly depressed. If intracellular tetanization was applied after the pairing procedure, the synaptic responses did not change immediately, but a slow return of the excitatory postsynaptic potential amplitude to the control level could be observed. Therefore, intracellular tetanization is not capable of inducing further potentiation after pairing, and pairing cannot further potentiate the inputs which have already been potentiated by intracellular tetanization. The maintenance of long-term potentiation induced by any of the protocols was impaired by successive application of another procedure. These results suggest a similarity of the mechanisms of synaptic changes induced by the two protocols and demonstrate that the direction of synaptic gain change depends on the history of the synapse.

Action Potentials↗

PubMed2000

Neuropeptide Y reduces epileptiform discharges and excitatory synaptic transmission in rat frontal cortex in vitro.

Neuropeptide Y reduced spontaneous and stimulation-evoked epileptiform discharges in rat frontal cortex slices perfused with a magnesium-free solution and with the GABA(A) receptor antagonist picrotoxin. To investigate the mechanism of that action, effects of neuropeptide Y on intrinsic membrane properties and synaptic responses of layer II/III cortical neurons were studied using intracellular recording. Neuropeptide Y (1 microM) had no detectable effect on the membrane properties of neurons. The evoked synaptic potentials were attenuated by neuropeptide Y. Moreover, the pharmacologically isolated excitatory postsynaptic potentials, mediated by N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors, were reversibly depressed by neuropeptide Y. The most pronounced inhibitory effect of neuropeptide Y was observed on late polysynaptic excitatory postsynaptic potentials. To assess a putative postsynaptic action of neuropeptide Y, N-methyl-D-aspartate was locally applied in the presence of tetrodotoxin. The N-methyl-D-aspartate-evoked depolarizations were unaffected by neuropeptide Y, which suggests that the depression of excitatory postsynaptic potentials was due to an action at sites presynaptic to the recorded neurons. These data show that neuropeptide Y attenuates epileptiform discharges and the glutamate receptor-mediated synaptic transmission in the rat frontal cortex. The above results indicate that neuropeptide Y may regulate neuronal excitability within the cortex, and that neuropeptide Y receptors are potential targets for an anticonvulsant therapy.

Animals↗

PubMed2003

Analysis of purinergic and cholinergic fast synaptic transmission to identified myenteric neurons.

Types and projections of neurons that received cholinergic, purinergic and other fast excitatory synaptic inputs in myenteric ganglia of the guinea-pig distal colon were identified using combined electrophysiological recording, application of selective antagonists, marker dye filling via the recording microelectrode, and immunohistochemical characterisation. Fast synaptic inputs were recorded from all major subtypes of uniaxonal neurons including Dogiel type I neurons, filamentous interneurons, circular muscle motor neurons and longitudinal muscle motor neurons. Fast excitatory postsynaptic potentials were completely blocked by the nicotinic receptor antagonists hexamethonium or mecamylamine in 62% of neurons tested and were partially inhibited in the remaining neurons. The P2 purine receptor antagonist, pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid, reduced the amplitudes of fast excitatory postsynaptic potentials in 20% of myenteric neurons. The 5-hydroxytryptamine(3) receptor antagonist granisetron reduced the amplitude of fast excitatory postsynaptic potentials in only one of 15 neurons tested. In five of five neurons tested, the combination of a nicotinic antagonist, pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid, granisetron and 6-cyano-7-nitroquinoxaline-2,3-dione did not completely block the fast excitatory postsynaptic potentials. Immunohistochemical studies of the neurons that had been identified electrophysiologically and morphologically imply that P2X(2) receptors may mediate fast transmission in some neurons, and that other P2X receptor subtypes may also be involved in fast synaptic transmission to myenteric neurons of the guinea-pig distal colon. Neurons with nicotinic and pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid-sensitive fast excitatory postsynaptic potentials were present in both ascending and descending pathways in the distal colon. Thus, neither cholinergic nor mixed cholinergic/purinergic synaptic responses are confined to a particular class of neuron. The results indicate that acetylcholine and ATP are the major fast excitatory neurotransmitters in guinea-pig distal colon myenteric ganglia.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1983

The effect of transection and cold block of the spinal cord on synaptic transmission between Ia afferents and motoneurones.

Composite excitatory postsynaptic potentials were elicited in lumbar motoneurones by Ia afferents from muscles of the triceps surae group. These excitatory postsynaptic potentials were examined in the same cell before, during and after interruption of descending spinal pathways. After transection or cold block of the spinal cord at T12-T13, the amplitude of composite excitatory postsynaptic potentials showed no significant change for a period of up to seven hours after transection. However, there was a reduction in amplitude of the monosynaptic reflex in the extensor motoneurones which may be due to an observed hyperpolarization and reduction in membrane time constant in these neurones. The reduction in amplitude of the monosynaptic reflex observed in spinal shock can be attributed to the effects of these changes, rather than to a decrease in the size of the monosynaptic excitatory postsynaptic potential.

Afferent Pathways↗

PubMed1992

Vasoactive intestinal polypeptide modulates neuronal excitability in hippocampal slices of the rat.

Vasoactive intestinal polypeptide added at submicromolar concentrations to the perfusion fluid of rat hippocampal slices and slice cultures enhanced the excitability of CA1 and CA3 pyramidal cells in several ways. Specifically, cells were depolarized and the Ca(2+)- and cyclic AMP-dependent potassium conductance was blocked as demonstrated by reduction of the long-lasting afterhyperpolarization and the accommodation of firing. This was also found in tetrodotoxin-containing medium. In low Ca(2+)-high Mg2+ medium (in synaptic isolation) the firing rate was increased. Synaptic transmission was potentiated: extracellularly registered excitatory postsynaptic potentials and population spikes in response to stratum radiatum stimulation and intracellularly recorded excitatory postsynaptic potential-inhibitory postsynaptic potential sequences were enhanced. These results are in keeping with the known stimulation of adenylate cyclase by vasoactive intestinal polypeptide.

Animals↗

PubMed1979

Avermectin B1a irreversibly blocks postsynaptic potentials at the lobster neuromuscular junction by reducing muscle membrane resistance.

Avermectin B1a, a macrocyclic lactone with broad spectrum anthelmintic activity, affects neuromuscular transmission in the lobster stretcher muscle. Perfusion of the muscle with 1-10 microgram of the drug per ml eliminates inhibitory postsynaptic potentials within a few minutes. Intracellularly recorded excitatory postsynaptic potentials are gradually reduced in amplitude over 20-30 min, and their falling phases become faster; there is no effect, however, on extracellularly recorded excitatory potentials. Avermectin B1a reduced the input resistance of the muscle fibers with a time course similar to that of the reduction of excitatory potentials. Washing for up to 2 hr with drug-free solution fails to reverse the drug's effects. However, perfusion with 20 microgram of picrotoxin per ml results in recovery of the excitatory potentials and input resistance. Avermectin B1a also blocks the firing of the crayfish stretch receptor neuron, and this block is also reversed by picrotoxin. We hypothesize that the reduction in excitatory postsynaptic potentials after avermectin B1a treatment is caused solely by reduction in membrane resistance; additional experiments suggest that the reduction in membrane resistance is due to the opening of membrane Cl- channels, perhaps including those regulated by gamma-aminobutyric acid at the inhibitory synapse.

Animals↗