Correlations between membrane potential and inhibitory post-synaptic potential in spinal motor neurones.
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Animals↗
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[Proceedings: 237. Synaptic potentials in C1-free solution (author's transl)].
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Animals↗
Non-fibrillar beta-amyloid abates spike-timing-dependent synaptic potentiation at excitatory synapses in layer 2/3 of the neocortex by targeting postsynaptic AMPA receptors.
Cognitive decline in Alzheimer's disease (AD) stems from the progressive dysfunction of synaptic connections within cortical neuronal microcircuits. Recently, soluble amyloid beta protein oligomers (Abeta(ol)s) have been identified as critical triggers for early synaptic disorganization. However, it remains unknown whether a deficit of Hebbian-related synaptic plasticity occurs during the early phase of AD. Therefore, we studied whether age-dependent Abeta accumulation affects the induction of spike-timing-dependent synaptic potentiation at excitatory synapses on neocortical layer 2/3 (L2/3) pyramidal cells in the APPswe/PS1dE9 transgenic mouse model of AD. Synaptic potentiation at excitatory synapses onto L2/3 pyramidal cells was significantly reduced at the onset of Abeta pathology and was virtually absent in mice with advanced Abeta burden. A decreased alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/N-methyl-D-aspartate (NMDA) receptor-mediated current ratio implicated postsynaptic mechanisms underlying Abeta synaptotoxicity. The integral role of Abeta(ol)s in these processes was verified by showing that pretreatment of cortical slices with Abeta((25-35)ol)s disrupted spike-timing-dependent synaptic potentiation at unitary connections between L2/3 pyramidal cells, and reduced the amplitude of miniature excitatory postsynaptic currents therein. A robust decrement of AMPA, but not NMDA, receptor-mediated currents in nucleated patches from L2/3 pyramidal cells confirmed that Abeta(ol)s perturb basal glutamatergic synaptic transmission by affecting postsynaptic AMPA receptors. Inhibition of AMPA receptor desensitization by cyclothiazide significantly increased the amplitude of excitatory postsynaptic potentials evoked by afferent stimulation, and rescued synaptic plasticity even in mice with pronounced Abeta pathology. We propose that soluble Abeta(ol)s trigger the diminution of synaptic plasticity in neocortical pyramidal cell networks during early stages of AD pathogenesis by preferentially targeting postsynaptic AMPA receptors.
Action Potentials↗
Synaptic potentials effect the release of transmitter from locust nonspiking interneurons.
An excitatory synaptic potential in a local nonspiking interneuron of a locust is able to effect the release of chemical transmitter. The consequence is that a discrete inhibitory synaptic potential is evoked in an identified postsynaptic motoneuron. These local interactions between interneurons and motoneurons are of behavioral significance in that they ensure the correct operation of a resistance reflex.
Action Potentials↗
Characterization of the anoxia-induced long-term synaptic potentiation in area CA1 of the rat hippocampus.
1. The purpose of the present study was to characterize the mechanisms underlying the anoxia-induced long-term potentiation (LTP) of glutamatergic synaptic transmission in the CA1 region of rat hippocampus by use of intracellular recordings in vitro. 2. In response to superfusion of an anoxic medium equilibrated with 95% N2 - 5% CO2, the initial slope (measured within 3 ms from the onset of the synaptic response) of the excitatory postsynaptic potential (e.p.s.p.) generated in the hippocampal CA1 neurones by stimulation of Schaffer collateral-commissural afferent pathway was significantly decreased by 91.3 +/- 4.9% (n = 10) within 10 min of the anoxic episode. The reduction of the initial slope of the e.p.s.p. was accompanied by a transient membrane hyperpolarization followed by a sustained depolarization (10.8 +/- 1.7 mV, n = 10), along with a reduction in membrane input resistance (69.3 +/- 4.8% of control, n = 10). On return to reoxygenated medium, the e.p.s.p. slope returned to the control value within 8-10 min and was subsequently and progessively potentiated to reach a plateau (195.6 +/- 14.7% of control, n = 10) 15-20 min after return to control ACSF. This anoxic episode-induced persistent potentiation of synaptic transmission lasted for more than 1 h and was termed anoxic LTP. 3. The anoxic episode induced a persistent potentiation of the initial slopes of both pharmacologically isolated alpha-amino-3-hydroxy-5-methyl-4-isoxazola-propionate (AMPA) receptor-mediated e.p.s.p. (e.p.s.p.AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated e.p.s.p. (e.p.s.p.NMDA) with a similar time course and magnitude. The sensitivity of postsynaptic neurones to NMDA (10 microM), but not to AMPA (10 microM) was also persistently potentiated following the anoxic episode. In addition, the anoxia-induced LTP of the initial slope of e.p.s.p.AMPA was accompanied by a decrease in the magnitude of paired-pulse facilitation (PPF; from 106.8 +/- 17.6 to 46.6 +/- 18.4%, n = 6), a phenomenon which was associated with presynaptic transmitter release mechanisms. 4. The induction of the anoxic LTP is dependent on the extracellular Ca2+ concentration. The induction of the anoxic LTP was completely abolished when the external Ca2+ was removed and substituted with equimolar Mg2+. Moreover, the anoxic LTP was completely abolished in neurones intracellularly recorded with Ca2+ chelator bis-(O-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA, 500 mM). 5. Occlusion experiments were performed to examine whether the sustained enhancement of the initial slope of the e.p.s.p. produced by tetanic stimulation and the anoxic episode share common cellular mechanisms. Three episodes of tetanic stimulation were delivered to saturate the LTP, following which a long period (15 min) of anoxia failed to cause a further potentiation of the initial slope of the e.p.s.p. Similarly, prior induction of anoxic LTP also significantly attenuated the subsequent synaptic potentiation induced by a high-frequency tetanic stimulation (100 Hz for 1 s duration). These data imply that these two forms of synaptic plasticity may share a common cellular mechanism. 6. These results provide strong evidence that the generation of the anoxia-induced LTP of glutamatergic synaptic transmission in the CA1 region of rat hippocampus probably involves both of the presynaptic and postsynaptic loci. The mechanisms underlying the persistent potentiation are likely to be attributable to an enhancement of presynaptic glutamate release and a selective upregulation of postsynaptic NMDA receptor-mediated synaptic response through the Ca2+-dependent processes.
Animals↗
Modulation of intracortical synaptic potentials by presynaptic somatic membrane potential.
Traditionally, neuronal operations in the cerebral cortex have been viewed as occurring through the interaction of synaptic potentials in the dendrite and soma, followed by the initiation of an action potential, typically in the axon. Propagation of this action potential to the synaptic terminals is widely believed to be the only form of rapid communication of information between the soma and axonal synapses, and hence to postsynaptic neurons. Here we show that the voltage fluctuations associated with dendrosomatic synaptic activity propagate significant distances along the axon, and that modest changes in the somatic membrane potential of the presynaptic neuron modulate the amplitude and duration of axonal action potentials and, through a Ca2+-dependent mechanism, the average amplitude of the postsynaptic potential evoked by these spikes. These results indicate that synaptic activity in the dendrite and soma controls not only the pattern of action potentials generated, but also the amplitude of the synaptic potentials that these action potentials initiate in local cortical circuits, resulting in synaptic transmission that is a mixture of triggered and graded (analogue) signals.
Action Potentials↗
Excitatory, inhibitory and biphasic synaptic potentials mediated by an identified dopamine-containing neurone.
1. A giant dopamine-containing cell, situated in the left pedal ganglion of the water snail Planorbis corneus, was identified in isolated living preparations of the central nervous system. Spectrophotofluorimetric analysis confirms that the cell contains dopamine, whereas noradrenaline appears to be absent. The cell is unique in being a repeatedly identifiable dopamine-containing neurone. 2. Stimulation of the giant dopamine-containing cell resulted in excitatory, inhibitory or biphasic (depolarizing-hyperpolarizing) synaptic potentials in a number of follower neurones. The duration of the e.p.s.p.s and i.p.s.p.s was 0-3-5 sec; they ranged from barely detectable responses to ones 7 mV in amplitude in different cells. The depolarizing phase of a biphasic synaptic potential (b.p.s.p.) was usually less than 1 mV in amplitude (max. 3mV) and lasted 40-400 msec. The latency of i.p.s.p.s was long (70-120 msec) compared with that of e.p.s.p.s and b.p.s.p.s (20 msec). Abolition of the depolarizing phase of b.p.s.ps. by tubocurarine left a long-latency (70-120 msec) i.p.s.p. All responses showed summation and marked facilitation. 3. Evidence is presented that the post-synaptic potentials are produced by direct connections from the giant cell and result from a release of dopamine. Of eight putative transmitter substances tested on these different groups of neurones, only dopamine produced a potential change which in each case was of the same polarity as the post-synaptic potential when this was monophasic. However, generally applied dopamine produced only a hyperpolarization in follower cells showing b.p.s.p.s. This result is probably partly due to rapid desensitization of the receptors mediating the depolarization and also to a masking of the depolarization by the more effective hyperpolarizing response. 4. Erogometrine and 6-hydroxydopamine specifically antagonized the i.p.s.p.s and dopamine receptors mediating inhibition. Neither the e.p.s.p.s nor the excitatory dopamine response were blocked by high concentrations of hexamethonium. Hexamethonium was also ineffective in blocking the depolarizing phase of a b.p.s.p., which was, however, selectively eliminated by tubocurarine. 5. It is suggested that dopamine is the transmitter released from the giant cell and that it can mediate excitatory, inhibitory or biphasic responses in different follower neurones.
Acetylcholine↗
A non-adrenergic, non-cholinergic slow inhibitory post-synaptic potential in neurones of the guinea-pig submucous plexus.
1. Intracellular recordings were made from neurones in the submucous plexus of guinea-pig ileum and caecum. The responses to electrical stimulation of fibre strands entering the nodes of the plexus were studied. 2. Stimuli comprising trains of pulses (20 Hz, 1-5 s) produced nicotinic excitatory post-synaptic potentials (fast e.p.s.p.s), an adrenergic inhibitory post-synaptic potential (i.p.s.p.), a slow excitatory post-synaptic potential (slow e.p.s.p.) and a fourth, hitherto unnoticed, slow hyperpolarization which followed the slow e.p.s.p. All these responses were abolished by tetrodotoxin or solutions containing a low calcium concentration. 3. The slow hyperpolarization (slow i.p.s.p.) was examined in the presence of blockers of the nicotinic and adrenergic responses, and in conditions in which the slow e.p.s.p. was prevented by desensitizing concentrations of substance P or vasoactive intestinal polypeptide. The slow i.p.s.p. was unaffected by prazosin (0.1-1 microM), propranolol (0.1-1 microM), atropine (1 microM) or naloxone (1 microM). 4. The amplitude and duration of the slow i.p.s.p. increased with increasing numbers of stimulus pulses; it had an amplitude of 17 mV and a duration of 70 s when evoked by a stimulus of 20 Hz for 3 s. 5. The slow i.p.s.p. was associated with a decrease in the input resistance of the cell. It reversed polarity at -90 mV in 4.7 mM-potassium and the extrapolated reversal potential in 0.47 mM-potassium was -145 mV; these findings indicate that the slow i.p.s.p. results from an increase in membrane potassium conductance. 6. The slow i.p.s.p. could still be recorded from submucous plexus neurones in segments of ileum which had been extrinsically denervated 6-11 days previously.(ABSTRACT TRUNCATED AT 250 WORDS)
Action Potentials↗
Presynaptic depolarization facilitates neurotrophin-induced synaptic potentiation.
Neurotrophins have been proposed to participate in activity-dependent modifications of neuronal connectivity and synaptic efficacy. Preferential strengthening of active inputs requires restriction of putative neurotrophin-mediated synaptic potentiation to active synapses. Here we report that potentiation of synaptic efficacy by brain-derived neurotrophic factor (BDNF) is greatly facilitated by presynaptic depolarization at developing neuromuscular synapses. Brief depolarization in the presence of low-level BDNF results in a marked potentiation of both evoked and spontaneous synaptic transmission, whereas exposure to either BDNF or depolarization alone is without effect. This potentiation depends on the relative timing of depolarization and reflects an enhancement of transmitter secretion from the presynaptic neuron. Thus synapses made by active inputs may be selectively strengthened by secreted neurotrophins as part of activity-dependent refinement of developing connections or of mature synapses.
Action Potentials↗
Influence of stretch-evoked synaptic potentials on firing probability of cat spinal motoneurones.
Shapes of post-synaptic potentials (p.s.p.s) in cat motoneurones were compared with the time course of correlated changes in firing probability during repetitive firing. Excitatory and inhibitory post-synaptic potentials (e.p.s.p.s. and i.p.s.p.s) were evoked by brief triangular stretches of the triceps surae-plantaris muscles. Depolarizing current was injected through the recording micro-electrode to evoke repetitive firing and the post-stimulus time histogram of motoneurone spikes was obtained. E.p.s.p.s (n = 80) of different sizes (30-1040 microV) and rise times (1.1-8.2 ms) were investigated in fifty-nine motoneurones. The majority of the e.p.s.p.s were recorded in triceps surae-plantaris motoneurones with high levels of synaptic noise (estimated peak-to-peak fluctuations of 1.5-3.5 mV). This noise was generated by keeping the triceps surae-plantaris muscles stretched to a near maximal degree. The remaining e.p.s.p.s were recorded in motoneurones to other hind-limb muscles with a low level of synaptic noise. The height of the primary peak of the correlogram with respect to base-line firing rate increased in proportion to both amplitude and rising slope of the e.p.s.p.s. Using normalization procedures or using e.p.s.p.s of constant amplitude but different slopes and vice versa, the relative peak height increased with e.p.s.p. peak derivative with a slope of around 6/mV per millisecond and with e.p.s.p peak amplitude with a slope of about 1/mV. The shape of the correlogram (peak and trough) seemed well described by a linear combination of the shape of the e.p.s.p. derivative and that of the e.p.s.p. itself. The relative e.p.s.p. contribution (e.p.s.p.:e.p.s.p. derivative ratio) varied with e.p.s.p. amplitude and noise level, being largest (mostly 0.25-1.0) for small e.p.s.p.s (100-300 microV) in high levels of synaptic noise and smaller (0-0.25) for larger e.p.s.p.s and for e.p.s.p.s in a low noise background. In conformity with the above finding, a leaky integration of the correlograms gave time courses that in most cases closely resembled the shape of the e.p.s.p.s. The time constant of the leaky circuit (= inverse value of e.p.s.p.:e.p.s.p. derivative ratio) varied with e.p.s.p. amplitude and noise level in the same manner as obtained by direct fitting of e.p.s.p. and e.p.s.p. derivative shape to correlogram shape. Stretch-evoked i.p.s.p.s (n = 10) of small amplitude (90-360 microV as measured close to firing level) were investigated in pre-tibial flexor motoneurones with low levels of synaptic noise. These i.p.s.p.s generated correlogram troughs closely resembling, albeit somewhat wider than, the shape of the i.p.s.p. derivatives.(ABSTRACT TRUNCATED AT 400 WORDS)
Action Potentials↗
Effect of lactate on the synaptic potential, energy metabolism, calcium homeostasis and extracellular glutamate concentration in the dentate gyrus of the hippocampus from guinea-pig.
Towards understanding the role of glycolysis on synaptic function, we examined the effect of lactate on synaptic potential, energy metabolism, Ca(2+) homeostasis and extracellular glutamate in the dentate gyrus of guinea-pig hippocampus. Postsynaptic population spikes were recorded from the granule cell layer of the dentate gyrus in guinea-pig hippocampal slices after replacing glucose with lactate in the perfusion medium. Population spikes were not maintained and spontaneously recovered around 35min after the replacement of glucose with lactate. However, ATP levels of the dentate gyrus remained unchanged while those during the glucose-free condition decreased to 73% of the initial levels at 60min. Intracellular Ca(2+) was measured with the calcium indicator dye fura-2 AM, and the population spike was recorded simultaneously. Ca(2+) levels increased concomitantly with the early decay of synaptic potentials, and recovered partially with the spontaneous recovery of synaptic potentials. The time course of decay of population spikes and the increase of Ca(2+) levels during lactate replacement were similar to those during glucose deprivation. Increase in Ca(2+) levels during lactate replacement was completely blocked by the ryanodine receptor/calcium release channel antagonist dantrolene. Glutamate was released more significantly in the medium during lactate replacement than with normal Ringer solution, and less than that during glucose deprivation. Addition of the N-methyl-D-aspartate blocker, D-(-)-2-amino-5-phosphonovaleric acid, and the L-type calcium channel blocker, nimodipine, but not dantrolene blocked spontaneous recovery of population spikes. The results indicate that lactate can maintain energy levels in hippocampal slices, but cannot maintain ion homeostasis in granule cells of the dentate gyrus. Glycolysis plays an important role in maintaining ion homeostasis, and activation of N-methyl-D-aspartate and L-type calcium channels is necessary for support of synaptic function by lactate utilization.
2-Amino-5-phosphonovalerate↗
Jaw-tongue reflex: afferents, central pathways, and synaptic potentials in hypoglossal motoneurons in the cat.
The tongue position is reflexively controlled by the jaw position (the jaw-tongue reflex). The purpose of this study was to clarify the mechanism of this reflex in terms of afferents, central pathways, and synaptic potentials in hypoglossal motoneurons in the cat. Intracellular recordings from hypoglossal motoneurons revealed that electrical stimulation of the temporalis muscle nerve evoked excitatory and inhibitory post-synaptic potentials in hypoglossal motoneurons. The threshold of temporalis muscle nerve stimulation for evoking the synaptic potentials was higher than 2.0 times the nerve threshold. The amplitude of the potentials increased with stimulus intensity up to 5.0 times the nerve threshold. Punctate light pressure applied to the temporalis muscle induced a tonic depolarizing potential in hypoglossal motoneurons on which action potentials as well as depolarizing synaptic activation noise were superimposed. On the other hand, electrical stimulation of the temporalis muscle during jaw-opening could slightly inhibit the electromyographic activities in the genioglossus and styloglossus muscles. Lesions including the Probst's tract at the level caudal to the trigeminal motor nucleus abolished both excitation and inhibition in hypoglossal motoneurons induced by tonic depression of the lower jaw, but exerted no effects on either the tonic stretch reflex or the trigemino-hypoglossal reflex. In contrast, lesions including the trigeminal spinal tract produced no changes in either excitation or inhibition of hypoglossal motoneurons induced by temporalis muscle afferents, whereas the excitation of hypoglossal motoneurons was abolished by the lesions. We conclude that the group II muscle spindle afferents from the temporalis muscle are primarily responsible for evoking the jaw-tongue reflex.
Afferent Pathways↗
Mediators of slow synaptic potentials in the myenteric plexus of the guinea-pig ileum.
1. Intracellular recordings were made from neurones in the myenteric plexus of the ileum isolated from adult guinea-pigs.2. Three synaptic potentials were evoked in different myenteric neurones by focal stimulation of the ganglion surface at a distance of up to 100 mum from the cell body from which the recording was made. These were the fast cholinergic excitatory post-synaptic potential (e.p.s.p.), the slow e.p.s.p. and the slow inhibitory post-synaptic potential (i.p.s.p.).3. 5-hydroxytryptamine and substance P were applied to the neurones by superfusion (10 nm-1 mum) or by electrophoresis within 5 mum of the neurone cell body. 5-HT depolarized, hyperpolarized or had no effect on approximately equal numbers of neurones, whereas substance P depolarized 90% of neurones.4. Many neurones with a depolarizing slow e.p.s.p. were hyperpolarized by superfusion or electrophoretic application of 5-HT.5. Superfusion with 5-HT reversibly depressed the fast e.p.s.p., slow e.p.s.p. and slow i.p.s.p. Superfusion with substance P depressed the slow e.p.s.p.6. Methysergide (10-30 mum) reduced the amplitude of the fast e.p.s.p., the slow e.p.s.p. and the slow i.p.s.p.7. Chymotrypsin (200 mug/ml.) reversibly reduced the amplitude of the slow e.p.s.p., but had no effect on membrane potential, the action potential or the fast e.p.s.p. Chymotrypsin reduced or abolished the depolarization caused by electrophoretic application of substance P, but had no effect on the depolarization or hyperpolarization caused by 5HT.8. The results provide evidence that 5-HT is not the transmitter which mediates the slow e.p.s.p. in myenteric neurones. The slow e.p.s.p. may be caused by substance P or another similar peptide.
Animals↗
Intracellular tetraethylammonium ions enhance group Ia excitatory post-synaptic potentials evoked in cat motoneurones.
Single fibre group Ia excitatory post-synaptic potentials (e.p.s.p.s) were recorded in cat spinal motoneurones after the neurones were injected with tetraethylammonium (TEA) ions. TEA injection increased the peak amplitude of most e.p.s.p.s. The time course of e.p.s.p.s generated at the soma was unaffected, but the time course of e.p.s.p.s generated in the dendrites was prolonged. The membrane time constant did not change after TEA injection. Somatic e.p.s.p.s were voltage clamped after TEA was injected. The reversal potential for these e.p.s.p.s was more positive than for e.p.s.p.s unaffected by TEA. Composite e.p.s.p.s added linearly, or greater than linearly, whereas in motoneurones without TEA they added linearly or less than linearly. The enhanced amplitude and prolonged time course observed in dendritic e.p.s.p.s after TEA injection was reduced by small hyperpolarizing currents. Greater than linear summation of composite e.p.s.p.s was converted to linear summation by small hyperpolarizing currents. The increase in somatic e.p.s.p.s was attributed to a more positive reversal potential for the e.p.s.p.s. We suggest that TEA decreases the relative permeability of K+ in the subsynaptic channels. We propose that in the presence of TEA, dendritic depolarization activates an inward current which amplifies and prolongs synaptic potentials spreading towards the soma.
Action Potentials↗
Electrotonic profile and passive propagation of synaptic potentials in three subpopulations of hippocampal CA1 interneurons.
To elucidate the role of dendritic morphology in signal transfer, the passive propagation of somatic and dendritic potentials was compared in multi-compartment models of three interneuron subpopulations in the CA1 region. Nine calbindin-, 15 calretinin- and 10 parvalbumin-containing cells were modelled incorporating the detailed geometry, the currents of the action potentials in the soma, and the AMPA, N-methyl-D-aspartate and GABA-B receptor-mediated postsynaptic currents in the dendrites. The cable properties show characteristic differences among the subpopulations. The morphotonic length of calbindin and calretinin cell dendrites is larger than of parvalbumin cells. Thus parvalbumin cells are more compact than calbindin or calretinin cells unless the ratio of their axial and membrane resistivities exceeds the ratios of the other two cell types by more than 33%. In calbindin cells, the distal parts of the extremely long dendrites that invade the alveus are virtually isolated from the soma for passively propagating signals. The synaptic potentials evoked at a given morphotonic distance from the soma show larger differences locally on the dendrites than on the soma in all subpopulations. Both the somatic and dendritic amplitude ratios are the smallest in PV cells. In calbindin cells the somatic amplitude of synaptic potentials evoked at the same morphotonic distance from the soma is similar regardless of the number of branchpoints along their path. In calretinin and parvalbumin cells, from dendrites with long primary segments synaptic potentials reach the soma with larger amplitude than from dendrites that are branching close to the soma. The dendrites with the larger impact on somatic membrane potential are usually the dendrites that enter the stratum lacunosum-moleculare. These results indicate that dendritic morphology plays a role in changing the effectiveness of synaptic potentials evoked at different dendritic locations, and in this way is likely to be an important factor in determining the integrative properties of the different neuron populations.
Animals↗
Synaptic potentials induced by postganglionic stimulations in cat bladder parasympathetic neurones.
Intracellular recording techniques were used to examine and compare synaptic potentials evoked by stimulating pre- and postganglionic nerve trunks in cat bladder parasympathetic ganglia. In the 76 ganglion cells examined, two types of responses were recorded on stimulating the postganglionic nerve: an antidromic action potential (type PostNS1; n = 30) or a fast excitatory postsynaptic potential (f-EPSP; type PostNS2; n = 46) which resulted in an orthodromic-like action potential. In some of the cells exhibiting a PostNS1 response (n = 19), a fast depolarization was superimposed on the antidromic spike. This depolarization was due to the synaptic activation of nicotinic receptors. In many of the cells exhibiting either PostNS1 or PostNS2 responses, repetitive stimulation of the postganglionic nerve induced a slow hyperpolarization. Applying nicotinic (hexamethonium, 0.5-1 mM) receptor muscarinic (atropine, 1 microM), alpha-adrenergic (phentolamine, 1 microM) and purinergic (caffeine, 0.5-1 mM) receptor antagonists completely inhibited the tetanus-induced slow hyperpolarization in some cells (n = 5). In other cells (n = 15), a slow hyperpolarization persisted in the presence of these antagonists. These results indicate that stimulation of the postganglionic nerve trunk of cat bladder parasympathetic ganglia can elicit not only an antidromic action potential, but also synaptic potentials which are mediated by the activation of cholinergic (nicotinic and muscarinic), noradrenergic and purinergic receptors, as well as non-cholinergic, non-alpha-adrenergic and non-purinergic synaptic potential.
Animals↗
Activation of quisqualate metabotropic receptors reduces glutamate and GABA-mediated synaptic potentials in the rat striatum.
The role of quisqualate (QUIS) metabotropic receptors in the synaptic transmission in the striatum was investigated using the cortico-striatal slice preparation. Low concentrations (1-30 microM) of trans-1-amino-cyclopentyl-1,3- dicarboxylic acid (t-ACPD), a selective agonist of QUIS metabotropic receptors, decreased glutamate-mediated synaptic potentials (EPSPs) evoked in the striatum by the stimulation of cortico-striatal fibers. This agonist decreased also GABA-mediated depolarizing synaptic potentials evoked by intrastriatal stimulation in the presence of 6-cyano-7-nitro-quinoxaline-2,3- dione (CNQX); this effect was less potent than the action of t-ACPD on glutamate-mediated potentials. Low concentrations of t-ACPD did not affect the intrinsic membrane properties of striatal neurons and their postsynaptic responses to exogenous glutamate and GABA. Higher concentrations (50-100 microM) to t-ACPD caused membrane depolarizations and inward currents in several neurons. Our data suggest that low concentrations of t-ACPD selectively reduce synaptic transmission while higher concentrations of this agonist may cause a direct excitatory action on striatal neurons.
6-Cyano-7-nitroquinoxaline-2,3-dione↗
Temperature dependence of intrinsic membrane properties and synaptic potentials in hippocampal CA1 neurons in vitro.
The temperature dependence of intrinsic membrane conductances and synaptic potentials in guinea pig hippocampal CA1 pyramidal neurons were examined in vitro as they were cooled from 37 degrees C to between 33 and 27 degrees C. Cooling reversibly increased resting input resistance in a voltage-independent manner (Q10 = 0.58 to 0.75). The amplitude and duration of orthodromically evoked action potentials were increased by cooling (Q10 = 0.87 and 0.52 to 0.53, respectively), whereas the maximum rates of rise and fall were reduced (Q10 = 1.27 to 1.49 and 2.19 to 2.44, respectively). The amplitude and duration of the afterhyperpolarization which follows a directly evoked train of action potentials were substantially increased at low temperatures. It is possible to attribute this increase to an augmentation of Ca2+ influx during the train and also to a slowing of Ca2+ removal from the cytoplasm. Spike frequency adaptation during prolonged depolarizing pulses was enhanced at low temperatures. In addition, there was a decrement in spike amplitude during the train of action potentials. These observations all suggest an increase in Ca2+-activated K+ conductance at low temperature. A late, slow, hyperpolarizing synaptic potential in response to orthodromic stimulation became apparent at low temperature. This potential had an apparent reversal potential more negative than the early inhibitory postsynaptic potential, suggesting that it was mediated by a K+ conductance, possibly activated by Ca2+ influx. We conclude that reductions in temperature of as little as 5 to 10 degrees C from normal can significantly alter the intrinsic and synaptic physiology of hippocampal neurons and should, therefore, be considered an important variable in in vitro brain slice experiments.
Action Potentials↗