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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↗

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↗

PubMed1989

Interaction of telenzepine with muscarinic receptors in mammalian sympathetic ganglia.

The interaction of the antimuscarinic drug telenzepine with muscarinic receptors was studied in rabbit and rat isolated superior cervical sympathetic ganglia. Radioligand binding demonstrated two muscarinic receptor sites in rabbit ganglia, with the characteristics of M1- and M2-receptors. Telenzepine bound to the M1 sites with a KI of 0.94 nmol/l and to the M2 sites with a KI of 17.8 nmol/l; the corresponding values for pirenzepine were 18.6 and 588 nmol/l; for AF-DX 116 the values were 891 and 33 nmol/l respectively. [3H]Telenzepine dissociated from the M1-receptors with a half time of 46 min at 37 degrees C. Electrophysiological experiments demonstrated that telenzepine reduced the amplitude of the extracellularly recorded slow excitatory postsynaptic potential and the slow inhibitory postsynaptic potential (ED50: 38 and 253 nmol/l respectively). In rat ganglia, application of muscarine or the M1-receptor agonist McN-A-343 increased the amplitude of submaximal population action potentials. This facilitation of synaptic transmission was potently blocked by telenzepine and pirenzepine but only weakly by AF-DX 116 (ED50: ca. 30, 150 and 20 mumol/l, respectively). It is concluded that telenzepine blocks the generation of the slow excitatory postsynaptic potential and the excitatory action of muscarine and McN-A-343 via an action on muscarinic M1-receptors.

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↗

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↗

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↗

PubMed1987

[Effect of trimebutine on cholinergic transmission in neurons of the inferior mesenteric ganglion of the rabbit].

We analyzed the effects of trimebutine on the synaptic activity of neurons of the rabbit inferior mesenteric ganglion, using intracellular recording techniques. The synaptic activity was produced by subthreshold stimuli (0.5 Hz) applied individually, on lumbar splanchnic and lumbar colonic nerves. These stimuli triggered cholinergic responses corresponding to fast excitatory postsynaptic potentials. In 8 of 20 neurones tested trimebutine (10(-6) g/ml) produced an inhibition of excitatory postsynaptic potentials, without any change in the resting membrane potential. In 6 of 20 neurons tested, trimebutine produced, successively, an early facilitation followed by a late inhibition of excitatory postsynaptic potentials. Both effects occurred without change in the resting membrane potential. The inhibitory and facilitatory effects of trimebutine were accompanied, by an increase and a decrease in the number of failures of nerve stimulation respectively. These results indicate that inhibitory and facilitatory effects of trimebutine correspond respectively to a decrease and an increase in the amount of acetylcholine released from presynaptic nerve terminals originating from the spinal cord and the distal colon.

Acetylcholine↗

PubMed1992

Synaptic mechanisms in sympathetic preganglionic neurons.

Intracellular recordings from sympathetic preganglionic neurons (SPNs) in adult cat and neonatal rat spinal cord slices reveal four types of synaptic potentials, namely, excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and slow EPSPs in both preparations, and a slow IPSP in cat SPNs. Pharmacological studies show that glutamate or a related excitatory amino acid and glycine are the probable mediators of EPSPs and IPSPs. There may be heterogenous mediators of slow EPSPs; substance P, serotonin, norepinephrine, and epinephrine are all probable mediators of slow EPSPs in subpopulations of SPNs. In the case of slow IPSPs, norepinephrine appears to be the likely transmitter. Finally, stimulation of ventral roots elicits a synaptic potential that appears to be caused by glutamate released from afferent fibers in the ventral roots. Our results indicate that a multitude of synaptic mechanisms exist in the rat SPNs by means of which inputs arising from sensory and supraspinal neurons are processed in a timely and orderly manner, thus ensuring highly organized but differentiated outputs to multiple peripheral target cells.

Animals↗

PubMed1990

Mu opioid receptor activation reduces inhibitory postsynaptic potentials in hippocampal CA3 pyramidal cells of rat and guinea pig.

Using intracellular recording techniques, we characterized synaptic responses of CA3 pyramidal cells to mu and kappa agonists in hippocampal slices from rats and guinea pigs. In rat CA3 pyramidal cells, the mu selective agonist (N-MePhe3,D-Pro4)-morphiceptin (PLO17) inhibited both the early and the late inhibitory postsynaptic potentials (IPSPs) and increased excitatory postsynaptic potential (EPSP) amplitudes. Voltage clamp analysis of synaptic currents indicated that the excitatory postsynaptic current were not increased by PLO17, showing that the apparent increase in EPSPs was a result of a decrease in the underlying IPSP. The kappa agonists trans-(+)-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzeneacetamide methanesulfonate and dynorphin A (1-17) had no effect on EPSPs or IPSP conductances measured in rat pyramidal cells. Maximal inhibition of IPSPs by PLO17 resulted in a bursting response to stimulation in rat but not guinea pig CA3 pyramidal cells. In guinea pig CA3 pyramidal cells, PLO17 also inhibited IPSP conductances but did not affect EPSP amplitudes. In contrast to the lack of effect in rat pyramidal cells, trans-(+)-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzeneacetamide methanesulfonate (100 nM) inhibited the late IPSP conductance without influencing the EPSP or the early IPSP conductance of guinea pig pyramidal cells. Dynorphin A (1-17) (0.01-10 microM) did not affect resting membrane properties or evoked synaptic conductances in either preparation. Mu receptor activationin the CA3 of rats and guinea pigs results in the inhibition of inhibitory synaptic input to pyramidal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

[A quantal analysis of the long-term potentiation of the total postsynaptic neuronal potentials in surviving hippocampal slices].

Excitatory postsynaptic potentials (EPSPs) from 14 neurons have been recorded in hippocampal slices (area CA1) of guinea pigs after stimulation of stratum radiatum (Schaffer collaterals) and stratum oriens. An increase of EPSP amplitudes observed in 7 neurons (9 pathways) recorded 15-45 min after titanic stimulation of Schaffer collaterals is considered as a long-term potentiation (LTP). A statistical analysis in the frame of two methods of the quantal hypothesis (histogram and variance methods) has shown an increase in the mean quantal content (m) during LTP. An increase in the quantal size found only by the histogram method is considered to be less reliable because comparatively strong dependence of the histogram method on the noise level. An increase in m revealed by two methods corresponds to the previous in vivo studies and favours a presynaptic location of mechanisms responsible for the growth of the synaptic efficacy during LTP.

Animals↗

PubMed1991

Frequency potentiation in granule cells in vivo at theta frequency perforant path stimulation.

The effect of frequency potentiation on the postsynaptic potential in granule cells was studied stimulating the perforant path in curarized and urethanized rats. At stimulation frequencies between 2.0-5.0 Hz, synaptic efficacy in eliciting an orthodromic action potential increased despite the hyperpolarization of the transmembrane potential. The excitatory postsynaptic potential (EPSP) slope and duration also increased while the inhibitory postsynaptic potential (IPSP) was reduced. Stimulation frequencies greater than 5.0 Hz produced similar changes in the transmembrane potential and EPSP-IPSP sequence, but they did not increase synaptic efficacy. The frequency potentiation at frequencies into the theta band suggest that this potentiation participates in theta rhythm genesis in this structure which, in turn, suggests that the fascia dentata could work as a band-pass filter. In 12.5% of cases postpotentiation was also observed.

Action Potentials↗

PubMed1989

Tongue-muscle-controlling motoneurons in the Japanese toad: neural inputs from the thalamus.

The anuran tongue is an effector organ specialized for snapping up prey during visually guided prey-catching behavior. As a step toward elucidating the control mechanisms of the tongue movement and overall organization of visually guided behavior, properties of neural inputs from the thalamus (of which electrical stimulation elicited a behavior very similar to the visually guided predator-avoidance behavior under freely behaving conditions) were investigated in paralyzed Japanese toads. Tongue-muscle-controlling motoneurons (tongue-protractor motoneurons (PMNs) and tongue-retractor motoneurons (RMNs)) were identified antidromically, and synaptic inputs in response to electrical stimuli applied to various points in the thalamus (mainly the posterocentral thalamic nucleus) were examined. Hyperpolarizing potentials were evoked in both PMNs and RMNs in response to single electrical stimuli applied to the thalamus contralateral or ipsilateral to the recording side. Since these potentials reversed to depolarizing ones after injecting Cl- ions into the cell interior, these hyperpolarizing potentials were concluded to be the usual fast type of inhibitory postsynaptic potentials (IPSPs). On the other hand, depolarizing potentials which were superimposed on the underlying IPSPs were evoked when repetitive electrical stimuli were applied to the thalamus. The amplitude of these depolarizing potentials was decreased when depolarizing currents were injected intracellularly, while it was increased when hyperpolarizing currents were injected, indicating that these depolarizing potentials are excitatory postsynaptic potentials (EPSPs).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1987

Antagonist discrimination of two muscarinic responses elicited by applied agonists and orthodromic stimuli in superior cervical ganglion of rabbit.

Pirenzepine and gallamine selectively and differentially antagonized two muscarinic responses, in the superior cervical ganglion of the rabbit, whether elicited by the muscarinic agonist methacholine or by orthodromic stimulation. Methacholine elicited a biphasic ganglionic response, consisting of hyperpolarizing and depolarizing components that were the agonist-induced equivalents of the slow-inhibitory and slow-excitatory postsynaptic potentials elicited by orthodromic stimulation. Superfusion of ganglia with pirenzepine resulted in a concentration-dependent suppression of depolarization induced by methacholine with no suppressant action on ganglionic hyperpolarization. In contrast, superfusion of ganglia with gallamine resulted in a concentration-dependent suppression of ganglionic hyperpolarization and the slow-inhibitory postsynaptic potential. These effects occurred without appreciable suppression of ganglionic depolarization or the slow-excitatory postsynaptic potential. The action of gallamine was specific for muscarinic hyperpolarization. Hyperpolarizations produced by superfusion with dopamine or norepinephrine were unaffected by gallamine, at concentrations that suppressed the muscarinic slow-inhibitory post-synaptic potential. Incubation with anti-cholinesterases produced a parallel shift, to the right, of concentration-response curves for suppression by gallamine of the slow-inhibitory postsynaptic potential. This was presumably the consequence of an increase in the acetylcholine available for interaction with the muscarinic receptor. The evidence suggests that the ability of gallamine and pirenzepine to suppress selectively the slow-inhibitory and slow-excitatory postsynaptic potentials, as previously demonstrated, is through an action at muscarinic receptors. Furthermore, the data suggest that these pharmacological agents produce their effects by interaction at different muscarinic recognition sites.

Animals↗