Modulation of synaptic potentials at central and peripheral synapses.
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Synaptic potentiation in the hippocampal CA1 region induced by application of N-methyl-D-aspartate.
The effect of local pressure application of N-methyl-D-aspartate (NMDA) in the synaptic layer of CA1 pyramidal cells was investigated in the guinea pig hippocampal slice preparation using extracellular recording technique. Application of NMDA produced a transient depression and a subsequent 30-60 min potentiation of the field excitatory postsynaptic potential (EPSP) seen as an increase of the initial slope and amplitude of the EPSP. The increase in amplitude was consistently greater than that of the initial slope. Prior tetanization that caused saturation of long-term potentiation prevented the generation of an NMDA-induced potentiation of the initial slope for more than 1-2 h, but not the generation of an increase of the amplitude.
Animals↗
Effect of adrenalectomy on membrane properties and synaptic potentials in rat dentate granule cells.
Adrenalectomy is known to accelerate both neurogenesis and cell death of granule cells located in the suprapyramidal blade of the rat dentate gyrus. Three days after adrenalectomy, some granule cells have already died by apoptosis while newly formed cells are not yet incorporated in the cell layer, resulting in a temporary loss of granule cells. Concomitantly, the field response to stimulation of perforant path afferents is reduced. While the temporary cell loss is likely to attenuate synaptic field responses, adrenalectomy-induced changes in properties of the surviving cells may also contribute to the reduction in field response amplitude. To address this possibility, we here investigated the membrane properties and synaptic responses of dentate granule cells, 3 days after adrenalectomy. We found that passive and most of the active membrane properties of granule cells in adrenalectomized rats were not significantly different from the cell properties in sham-operated controls. However, intracellularly recorded synaptic responses from surviving granule cells were markedly reduced after adrenalectomy. The N-methyl-D-aspartate (NMDA)- and the non-NMDA receptor-mediated components were reduced to a similar extent, suggesting that the attenuation of synaptic transmission after adrenalectomy could be partly of presynaptic origin. The data indicate that the earlier observed attenuation of synaptic field responses after adrenalectomy may be partly due to a diminished glutamatergic input to the dentate gyrus and not exclusively to a loss of granule cells participating in the synaptic circuit.
Action Potentials↗
Adenosine A1 receptor-mediated depression of corticostriatal and thalamostriatal glutamatergic synaptic potentials in vitro.
Electrophysiological recordings in rat brain slices have been used to study the actions of adenosine on striatal neurons and striatal excitatory amino acid neurotransmission originating in the cortex or the thalamus. Adenosine had no effects on membrane properties of striatal neurons. Adenosine and the A1 agonist N6-Cyclopentyl adenosine reduced EPSPs of both cortical and thalamic origin by more than 50%. Depression of EPSPs was associated with an increase in paired-pulse facilitation, suggesting a presynaptic locus of action. EPSP depression was blocked by the A1 antagonist, 8-Cyclopentyl-1,3-dipropyl xanthine. The A2 agonist 5'-(N-cyclopropyl)-carboxamidoadenosine had no effect on excitatory amino acid neurotransmission. The A1 antagonist alone enhanced the synaptic component of the evoked field potential (23 +/- 12%). These results indicate that endogenous adenosine, acting via A1 receptors, limits striatal glutamatergic neurotransmission, serving a modulatory and neuroprotective role.
Adenosine↗
Impairment in short-term but enhanced long-term synaptic potentiation and ERK activation in adult hippocampal area CA1 following developmental thyroid hormone insufficiency.
Thyroid hormones are critical for the development and maturation of the central nervous system. Insufficiency of thyroid hormones during development impairs performance on tasks of learning and memory that rely upon the hippocampus and impairs synaptic function in young hypothyroid animals. The present study was designed to determine if perturbations in synaptic function persist in adult euthyroid animals exposed developmentally to insufficient levels of hormone. Pre- and postnatal thyroid hormone insufficiency was induced by administration of 3 or 10 ppm propylthiouracil (PTU) to pregnant and lactating dams via the drinking water from gestation day (GD) 6 until postnatal day (PN) 30. This regimen produced a graded level of hormonal insufficiency in the dam and the offspring. Population spike and population excitatory postsynaptic potentials (EPSP) were recorded at the pyramidal cell layer and the stratum radiatum, respectively, in area CA1 of hippocampal slices from adult male offspring. PTU exposure increased baseline synaptic transmission, reduced paired-pulse facilitation, and increased the magnitude of the population spike long-term potentiation (LTP). Phosphorylation of the extracellular signal-regulated kinases (ERK1 and ERK2) was increased as a function of LTP stimulation in slices from PTU-exposed adult animals. On the other hand, no differences in the basal levels of synaptic proteins implicated in synaptic plasticity (total ERK, synapsin, growth-associated protein-43, and neurogranin) were detected. These results reinforce previous findings of persistent changes in synaptic function and, importantly extend these observations to moderate levels of thyroid hormone insufficiency that do not induce significant toxicity to the dams or the offspring. Such alterations in hippocampal synaptic function may contribute to persistent behavioral deficits associated with developmental hypothyroidism.
Animals↗
Theta-frequency synaptic potentiation in CA1 in vitro distinguishes cognitively impaired from unimpaired aged Fischer 344 rats.
Hippocampal-dependent learning and memory deficits have been well documented in aging rodents. The results of several recent studies have suggested that these deficits arise from weakened synaptic plasticity within the hippocampus. In the present study, we examined the relationship between hippocampal long-term potentiation (LTP) in vitro and spatial learning in aged (24-26 months) Fischer 344 rats. We found that LTP induced in the CA1 region using theta-frequency stimulation (5 Hz) is selectively impaired in slices from a subpopulation of aged rats that had shown poor spatial learning in the Morris water maze. LTP at 5 Hz in aged rats that did not show learning deficits was similar to that seen in young (4-6 months) controls. We also found that 5 Hz LTP amplitude strongly correlated with individual learning performance among aged rats. The difference in 5 Hz LTP magnitude among aged rats was not attributable to an altered response to 5 Hz stimulation or to differences in the NMDA receptor-mediated field EPSP. In addition, no performance-related differences in LTP were seen when LTP was induced with 30 or 70 Hz stimulation protocols. Finally, both 5 Hz LTP and spatial learning in learning-impaired rats were enhanced with the selective muscarinic M2 antagonist BIBN-99 (5,11-dihydro-8-chloro-11-[[4-[3-[(2,2-dimethyl-1-oxopentyl)ethylamino]propyl]-1-piperidinyl]acetyl]-6H-pyrido[2,3-b][1,4]benzodiazepin-6-one). These findings reinforce the idea that distinct types of hippocampal LTP offer mechanistic insight into age-associated cognitive decline.
Age Factors↗
Acetylcholine and norepinephrine mediate slow synaptic potentials in normal and epileptic neocortex.
Slow excitatory postsynaptic potentials (EPSPs) were identified in rat neocortical slices. Such potentials, resistant to blockade of glutamate and gamma-aminobutyric acid-A (GABAA) receptors, were partially antagonized by muscarinic or beta-adrenergic antagonists separately, and completely blocked when these agents were added in combination. Slow EPSPs were enhanced by a cholinesterase inhibitor or catecholamine reuptake blockers. Spontaneous epileptic discharges induced by picrotoxin also triggered slow EPSPs. Such potentials were pharmacologically identical to those induced by electrical stimulation under normal conditions. A non-conventional mechanism for synaptic transmission is postulated to account for triggering of slow EPSPs by epileptic discharges.
Acetylcholine↗
The effects of repetitive low frequency stimulation on control and "potentiated" synaptic responses in the hippocampus.
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Novel synaptic potentials in cerebellar Purkinje cells: probable mediation by metabotropic glutamate receptors.
Glutamate receptors of both the ionotropic (ion channel-linked) and metabotropic (enzyme-linked) categories are abundantly expressed by Purkinje cells in the cerebellum but the functional significance of the latter receptors is unknown. We have tested the possibility that they are activated by the parallel fibre input by recording from Purkinje cells within a biplanar cerebellar slice preparation using the grease-gap technique. Under conditions where ionotropic (NMDA and non-NMDA) glutamate and GABA receptors were blocked pharmacologically, electrical stimulation of parallel fibres gave rise to two very slow potentials. The first peaked about 400 msec from the start of stimulation and was depolarising. It was not evident with single stimuli but reached maximum amplitude after 6 shocks delivered at 50 Hz. The wave was abolished when the slices were perfused with Ca(2+)-free solution or with drugs that inhibit synaptic transmission, but it was resistant to blockade of GABAB receptors, acetylcholine receptors and adrenergic receptors. Next came a slow hyperpolarising potential that peaked about 30 sec after stimulation and which was also Ca(2+)-dependent. The sequence of potentials was replicated by perfusion of an exogenous agonist acting selectively on metabotropic glutamate receptors. We conclude that parallel fibre-to-Purkinje cell synaptic transmission involves not only fast signals generated through ionotropic non-NMDA receptors but also much slower potentials that are likely to be mediated by metabotropic glutamate receptors. These potentials are likely to be significant both for shorter-term (seconds to minutes) Purkinje cell excitability as well as for the induction of longer-term synaptic plasticity.
2-Amino-5-phosphonovalerate↗
Excitatory GABAergic synaptic potentials in the mesencephalic trigeminal nucleus of adult rat in vitro.
The mesencephalic trigeminal nucleus (MesV) contains the somata of primary afferent neurons innervating masticatory muscle spindles and the periodontal membrane. MesV afferent somata are unique in receiving synaptic inputs. Intracellular recordings in coronal pontine slices from adult rats were made from MesV neurons identified by having Cs-sensitive inward rectification and pseudounipolar morphology. Stimuli near the MesV evoked either a cluster of action potentials superimposed on a postsynaptic potential (PSP) or an antidromic spike at resting membrane potential (RMP). Membrane hyperpolarization revealed that each cluster of action potentials consisted of an antidromic spike and a subsequent PSP. Evoked PSPs in slices and miniature postsynaptic currents (mPSCs) recorded using whole-cell patch in dissociated MesV neurons were resistant to glutamate antagonists and strychnine but were reversibly abolished by 40 microM bicuculline. Superfusion of 1-10 mM GABA decreased input resistance and depolarized the membrane. Reversal potentials for evoked PSPs and GABA-induced depolarizations were similar and close to that for mPSCs which matched the Cl- equilibrium potential. Thus activation of synapses on MesV somata evokes GABAergic PSPs that generate action potentials at RMP in the adult. These data also indicate that primary afferent MesV neurons can act as interneurons in the central control of mastication.
Action Potentials↗
Motor map expansion following repeated cortical and limbic seizures is related to synaptic potentiation.
The effect of experimentally induced seizure activity on the functional reorganization of motor maps has not previously been investigated. Furthermore, while the functional reorganization of motor maps has been thought to involve increases in synaptic communication, there has yet to be a test of this hypothesis. Here we show that repeated seizure activity (kindling), that is accompanied by increased synaptic strength within adult rat motor cortex, results in a doubling of the caudal forelimb motor area. We measured neo-cortical evoked potentials in the right hemisphere prior to 25 days of electrical kindling of the medial frontal corpus callosum or amygdala and re-measured them either 1 or 21 days following the last kindling session. Then, using high resolution intracortical microstimulation (ICMS), the caudal forelimb area in the left hemisphere was mapped. This is the first report of any procedure causing a motor representation to double in size. Furthermore, this expansion was related to the enhanced area of a neocortical polysynaptic field potential and not the motor convulsions per se. Moreover, both the motor map and field potential enhancements were persistent in nature and could be driven from either cortical or limbic sites. The data have implications for human populations with epilepsy.
Animals↗
Long-lasting facilitation of a synaptic potential following tetanization in the in vitro hippocampal slice.
Field potentials evoked by stimulation of afferent fibers in stratum radiatum were recorded in the CA1 region of the hippocampal slice maintained in vitro. Stimulation rates of 3-50/sec produced a large increase in amplitude of the population spike in CA1. This increase was maintained for several hours after the tetanization. The facilitation phenomenon appeared to be specific to the synapse of stratum radiatum afferents onto CA1 pyramidal cells since: (1) stimulation outside the radiatum layer did not produce the effect, (2) antidromic field potentials recorded in CA3 were unchanged, (3) EPSP threshold in CA1 was unchanged, and (4) alveus tetanization did not produce a facilitatory effect.
Animals↗
Post-synaptic potentials recorded from afferent nerve fibres of the posterior semicircular canal in the frog.
Glass microelectrode recordings were made from single fibres of the posterior ampullary nerve in the isolated labyrinth of the frog (Rana esculenta). Potentials were recorded both at rest and during rotatory stimulation of the canal. At rest, the tracings revealed an intense background of small, largely summated potentials (0.5-10 mV amplitude, 3-6 msec duration), which underlay the discharge of spikes in all the impaled units. The frequency of the subthreshold events was related to the frequency of the propagated spikes, the latter ranging from 0 to 40/sec. Stimulation modulated the frequency of both spikes and subthreshold potentials, whose summation during excitation led to a positive shift of the fibre membrane potential. The small potentials proved to be dependent on Ca2+ and Mg2+ levels in the bath. Antidromic-stimulation of the posterior ampullary nerve indicated that the observed events do not represent an artifact due to extracellular field interference related to spike activity in the neighbouring fibres. Tetrodotoxin (10(-7)-10(-6) g/ml) applied externally to the preparation or previously perfused through the frog vessels abolishes the propagated spikes but left unaffected the small potentials which, even under drug treatment, were normally modulated by the stimulus. The subthreshold potentials thus appear to be EPSPs generated at the cyto-neural junction between the hair cells and the endings of the ampullary nerve fibres.
Action Potentials↗
Changes in excitatory and inhibitory synaptic potentials leading to epileptogenic activity.
The effects of the epileptogenic agent, penicillin, on excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) were studied in the hippocampal in vitro slice preparation. The actions of penicillin were compared to those of bicuculline, an antagonist of gamma-aminobutyric acid. Neither substance enhanced monosynaptic EPSP amplitude in CA1 pyramidal cells, but both penicillin and bicuculline depressed IPSPs. Large depolarizations that gave rise to cellular bursting activity did develop after addition of penicillin or bicuculline to the bathing medium. There was also an increase in the incidence of fast prepotentials of 'd-spikes.' These observations are interpreted according to the hypothesis that penicillin and bicuculline block cellular IPSPs, and consequently allow remote intrinsic excitatory events to invade the cell soma and trigger action potentials.
Animals↗
Facilitation of monosynaptic excitatory synaptic potentials in spinal motoneurones evoked by internuncial impulses.
1. Descending tracts and primary afferent fibres were chronically degenerated in the lumbosacral cord of the cat, and attempts were made to evoke monosynaptic e.p.s.p.s in motoneurones by stimulation of interneurones with a pair of fine electrodes inserted into the cord.2. The reversal potential of monosynaptic e.p.s.p.s so produced was more negative than that measured for monosynaptic e.p.s.p.s produced by afferent impulses.3. Monosynaptic e.p.s.p.s evoked in motoneurones by internuncial impulses showed a significantly greater facilitation than those produced by afferent impulses.4. Monosynaptic e.p.s.p.s in a motoneurone produced by supramaximal intraspinal stimuli often revealed a fluctuation in amplitude. In such cases, when two successive stimuli were applied at a short interval, the mean amplitude of the second e.p.s.p.s was greater than that of the first e.p.s.p.s. This facilitation was associated with a decrease in the coefficient of variation of the e.p.s.p. amplitude fluctuation.5. The degree of facilitation of monosynaptic e.p.s.p.s evoked by internuncial impulses was not related to the amount of transmitter released by the preceding impulses.6. It is concluded that facilitation of monosynaptic e.p.s.p.s evoked by both afferent and internuncial impulses is based on the same mechanism and that the degree of facilitation of e.p.s.p.s is entirely determined by the nature of presynaptic elements.
Animals↗
[Analysis of the components of synaptic potentials induced by corticofugal spikes in the rubrospinal neurons of the cat].
EPSPs of rubrospinal neurons evoked by stimulation of the sensorimotor cortex were studied in nembutalized cats by means of intracellular recordings. Participation of the corticospinal input in the genesis of EPSPs mentioned was revealed by selective activation of corticospinal fibres on the level of medullary pyramids as well as by studying peculiarities of their interaction with the effects of cortical stimulation. It was shown that both predominantly slow conducting corticospinal and corticorubral neurons participate in the genesis of the first two components of the complex EPSPs. Problems of cellular composition and mechanisms of corticofugal influences on the red nucleus neurons are discussed.
Animals↗
Connections between EEG activity and post-synaptic potentials of spinal motoneurones during convulsions.
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The speed of passive dendritic conduction of synaptic potentials in a model montoneurone.
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