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PubMed2005

The tipsy terminal: presynaptic effects of ethanol.

Considerable evidence suggests that the synapse is the most sensitive CNS element for ethanol effects. Although most alcohol research has focussed on the postsynaptic sites of ethanol action, especially regarding interactions with the glutamatergic and GABAergic receptors, few such studies have directly addressed the possible presynaptic loci of ethanol action, and even fewer describe effects on synaptic terminals. Nonetheless, there is burgeoning evidence that presynaptic terminals play a major role in ethanol effects. The methods used to verify such ethanol actions range from electrophysiological analysis of paired-pulse facilitation (PPF) and spontaneous and miniature synaptic potentials to direct recording of ion channel activity and transmitter/messenger release from acutely isolated synaptic terminals, and microscopic observation of vesicular release, with a focus predominantly on GABAergic, glutamatergic, and peptidergic synapses. The combined data suggest that acute ethanol administration can both increase and decrease the release of these transmitters from synaptic terminals, and more recent results suggest that prolonged or chronic ethanol treatment (CET) can also alter the function of presynaptic terminals. These new findings suggest that future analyses of synaptic effects of ethanol should attempt to ascertain the role of presynaptic terminals and their involvement in alcohol's behavioral actions. Other future directions should include an assessment of ethanol's effects on presynaptic signal transduction linkages and on the molecular machinery of transmitter release and exocytosis in general. Such studies could lead to the formulation of new treatment strategies for alcohol intoxication, alcohol abuse, and alcoholism.

Animals↗
PubMed1994

Dynamic neuromodulation of synaptic strength intrinsic to a central pattern generator circuit.

Motor circuits are often thought to be physically separate from their neuromodulatory systems. We report here a counter example, where neurons within a circuit appear to modulate synaptic properties of that same circuit during its normal operation. The dorsal swim interneurons (DSIs) are members of the central pattern generator circuit for escape swimming in the mollusc Tritonia diomedea. However, DSI stimulation also rapidly enhances the synaptic potentials evoked by another neuron in the same circuit onto its follower cells. This modulatory action appears to be mediated by serotonin (5-hydroxytryptamine); the DSIs are serotonin-immunoreactive, and bath-application of serotonin mimics and occludes the effect of DSIs. These results indicate that during the escape swim, circuit connection strengths are dynamically controlled by the activity of neurons within the circuit itself. This 'intrinsic neuromodulation' may be important for the animal's initial decision to swim, the generation of the swim motor programme itself, and certain types of learning.

Animals↗
PubMed2002

Direct cortical input modulates plasticity and spiking in CA1 pyramidal neurons.

The hippocampus is necessary for the acquisition and retrieval of declarative memories. The best-characterized sensory input to the hippocampus is the perforant path projection from layer II of entorhinal cortex (EC) to the dentate gyrus. Signals are then processed sequentially in the hippocampal CA fields before returning to the cortex via CA1 pyramidal neuron spikes. There is another EC input-the temporoammonic (TA) pathway-consisting of axons from layer III EC neurons that make synaptic contacts on the distal dendrites of CA1 neurons. Here we show that this pathway modulates both the plasticity and the output of the rat hippocampal formation. Bursts of TA activity can, depending on their timing, either increase or decrease the probability of Schaffer-collateral (SC)-evoked CA1 spikes. TA bursts can also significantly reduce the magnitude of synaptic potentiation at SC-CA1 synapses. The TA-CA1 synapse itself exhibits both long-term depression (LTD) and long-term potentiation (LTP). This capacity for bi-directional plasticity can, in turn, regulate the TA modulation of CA1 activity: LTP or LTD of the TA pathway either enhances or diminishes the gating of CA1 spikes and plasticity inhibition, respectively.

Action Potentials↗
PubMed2003

Regulation of neuritogenesis and synaptic transmission by msec7-1, a guanine nucleotide exchange factor, in cultured Aplysia neurons.

msec7-1, a mammalian homologue of yeast sec7p, is known as a GDP/GTP exchange factor (GEF) for the ADP ribosylation factor (ARF) family of small GTPases. Here, we report that msec7-1 overexpression in cultured Aplysia neurons leads to an extensive neuritogenesis in a GEF activity-dependent manner through the modulation of the actin cytoskeleton. Similarly, the overexpression of ARNO, another mammalin GEF, produces extensive neuritogenesis in Aplysia neurons. In addition, msec7-1 overexpression increases the number of varicosities with an altered size and shape in a GEF activity-dependent manner. The overexpression of msec7-1 in pre-synaptic sensory neurons co-cultured with post-synaptic target motor neurons leads to an increase in the amplitude of the excitatory post-synaptic potential through its GEF activity. Our results demonstrate that msec7-1 regulates neuritogenesis and synaptic transmission.

Animals↗
PubMed1994

Interactive and discontinuous long-lasting potentiation in the dentate gyrus.

Non-overlapping applications of l-isoproterenol, a beta-adrenergic agonist, and the neuropeptide cholecystokinin 8-S produce long-lasting potentiation of evoked action potentials in the dentate gyrus. There is no corresponding modification of excitatory post-synaptic potentials. This effect, referred to as interactive long-lasting potentiation, is pharmacologically similar to the long-lasting potentiation produced by discontinuous or non-overlapping applications of l-isoproterenol. Metoprolol or propranolol, both beta-adrenergic antagonists, prevent interactive long-lasting potentiation, but D-amino-5-phosphonopentanoic acid, an N-methyl-D-aspartate receptor antagonist, does not. Cholecystokinin 8-S and beta-adrenergic receptors may activate a common intermediate in the interactive paradigm.

2-Amino-5-phosphonovalerate↗
PubMed1994

Anoxia induced functional inactivation of neonatal respiratory neurones in vitro.

In the isolated brain stem-spinal cord preparation of neonatal rats, respiratory (C4) activity persisted at reduced frequency during tissue anoxia. In seven biphasic expiratory (Bi-E) and in 12 of 22 inspiratory (Insp) neurones, recorded with the 'blind' patch-clamp technique, anoxia evoked a persistent hyperpolarization by up to 16 mV whereas membrane potential of the remaining Insp neurones depolarized slightly or remained unaffected. Respiration-related synaptic potentials and action potential discharges were blocked in all Bi-E and in about 50% of the Insp neurones, whereas rhythmic activity persisted in the other cells. The results indicate that a major population of neonatal respiratory neurones is functionally inactivated during anoxia. This mechanism might contribute to the anoxia tolerance of the immature brain.

Animals↗
PubMed1973

The formation of synapses in reinnervated and cross-reinnervated adult avian muscle.

1. A study has been made of the formation of synapses in spontaneously reinnervated and cross-reinnervated anterior latissimus dorsi (ALD) and posterior latissimus dorsi (PLD) muscles of adult fowls.2. Denervated ALD and PLD muscle fibres have a uniform and high sensitivity to iontophoretically applied acetylcholine (ACh). During early reinnervation the sensitivity distribution to ACh of the ALD muscle fibres begins to return to normal before synaptic potentials can be evoked. The normal ACh sensitivity distribution of PLD muscle fibres is also restored after reinnervation. After cross-reinnervation of the ALD and PLD muscles the ACh sensitivity distribution of many of the muscle fibres is again restored to normal.3. Reinnervating and cross-reinnervating ALD nerve terminals showed a greater than normal degree of facilitation of transmitter release when a test impulse was applied at various intervals after a conditioning impulse. Cross-reinnervating PLD nerve terminals showed facilitation of transmitter release rather than the normal depression in a conditioning-test impulse sequence.4. The distribution of nerve terminals over the surface of spontaneously reinnervated and cross-reinnervated ALD and PLD muscle fibres has been determined from an examination of the sensitivity distribution to applied ACh, the graded versus all-or-none nature of the evoked potential and the distribution of cholinesterase stained synapses.5. The results suggest that the innervation pattern of individual ALD and PLD muscle fibres is restored both after spontaneous reinnervation and cross-reinnervation.

Acetylcholine↗
PubMed1982

On the quantal release of endogenous glutamate from the crayfish neuromuscular junction.

1. The abdominal slow flexor muscle was isolated from the crayfish (Cambarus clarkii) and placed in 150 microliters. Harreveld solution. The concentrations of glutamate and aspartate in this solution were measured by mass fragmentography. 2. Application of black widow spider venom (BWSV) produced a marked increase in the frequency of miniature excitatory post-synaptic potentials (m.e.p.s.p.s). During the high frequency discharge of m.e.p.s.p.s, the glutamate content in the solution was significantly increased. There was an approximately linear relationship between the increase in the glutamate efflux produced by BWSV and the variance of the membrane potential fluctuation during high frequency discharge of m.e.p.s.p.s. 3. In most cases, the efflux of aspartate during control rest periods was smaller than that of glutamate. During the discharge of m.e.p.s.p.s produced by BWSV, the increase in the aspartate efflux was very small compared to glutamate. 4. Nerve stimulation caused a significant increase in the efflux of glutamate, but the change in the aspartate efflux was very small and not significant. 5. Application of methylene blue increased the frequency of m.e.p.s.p.s and glutamate efflux, but little, if any, increase was found in aspartate efflux. 6. It is concluded that glutamate is preferentially released from nerve terminals in a quantal fashion.

Animals↗
PubMed1987

Electrophysiological properties of ependymal cells (radial glia) in dorsal cortex of the turtle, Pseudemys scripta.

1. We have investigated the electrophysiological properties of ependymal cells in the isolated dorsal cortex of the turtle, Pseudemys scripta. The cell bodies of these radial glia form an epithelium at the ventricular surface, and each cell sends one or more branching processes through the cortex to the pial surface. Very few non-ependymal glia exist in the dorsal cortex. 2. Ependymal cells had high resting membrane potentials (-90 mV), very fast time constants and a lack of intrinsic excitability or synaptic potentials. 3. Changes in the K+ concentration ([K+]) of the bathing solution caused near-Nernstian changes of ependymal membrane potentials. When local neuronal pathways were activated, ependymal cells slowly depolarized while extracellular voltage shifted negatively. Simultaneous measurements of extracellular [K+] ([K+]o) near the impaled ependymal cell body showed that these slow depolarizations were fully accounted for by activity-dependent increases in [K+]o. Similar measurements during focal pressure applications of solutions with high [K+] suggested that intrasomatic recordings reflect predominantly the [K+]o adjacent to the cell body, and not the intracortical process. 4. Intracellular injections of the fluorescent dye Lucifer Yellow CH, and simultaneous recordings from neighbouring cells, indicated that ependymal cells are chemically and electrically coupled to one another. Increasing the ambient CO2 level from 5 to 40% depolarized cells, increased their input resistance, and abolished interglial dye coupling. 5. The physiological properties of ependymal cells are very similar to those of a variety of glial cell types in a range of vertebrate and invertebrate species. In the absence of other types of glia, radial glia may function as the sole cellular mediators of K+ redistribution (i.e. K+ spatial buffering) following neural activity, as well as the generators of slow extracellular potentials.

Action Potentials↗
PubMed1991

Paroxysmal inhibitory potentials mediated by GABAB receptors in partially disinhibited rat hippocampal slice cultures.

1. Intracellular recording techniques were used to study synaptic potentials in CA3 pyramidal cells elicited with mossy fibre stimulation in partially disinhibited hippocampal slice cultures. Two experimental protocols were used: (1) high concentrations (20-40 microM) of the A-type gamma-aminobutyric acid (GABAA) receptor antagonist bicuculline plus low concentrations (2-4 microM) of the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), or (2) low concentrations (1-2.5 microM) of bicuculline alone. 2. Under the first condition, stimulation of mossy fibre afferents evoked epileptic bursts alternating with a response consisting of an excitatory postsynaptic potential (EPSP) followed by an unusually large and long-lasting hyperpolarizing potential with a maximal amplitude in the range of -30 mV from the resting membrane potential. 3. This paroxysmal inhibitory potential (PIP) had a reversal potential near that of potassium. The amplitude of the PIP was not dependent on action potentials superimposed on the preceding EPSP, and was present in cells recorded with microelectrodes containing the Ca2+ chelator EGTA. These data suggest that the PIP is not a Ca(2+)-activated K+ potential. 4. The PIP was prolonged by the GABA-uptake blocker nipecotic acid, was reduced by hyperpolarizing interneurons with the opioid agonist FK 33-824, and was abolished by the GABAB-receptor antagonist CGP 35 348. These data indicate that the PIP is mediated by the activation of GABAB receptors following GABA release from interneurons. 5. The NMDA-receptor antagonist D-2-amino-5-phosphonovalerate (D-APV) strongly reduced the amplitude of the PIP, but had no effect on the GABAB receptor-mediated inhibitory postsynaptic potential (IPSP) under control conditions. 6. Under the first condition, regular stimulation elicited a cyclical pattern of evoked responses. There was either an alternation between an epileptic burst and a PIP or, at shorter interstimulus intervals, a sequence of gradually increasing PIPs followed by an epileptic burst, which then reset the cycle. 7. Under the second condition, in low concentrations of bicuculline alone, the early GABAA-mediated IPSP was little affected, but the late GABAB-mediated IPSP was greatly enhanced. These enhanced late IPSPs were comparable in amplitude and duration to the PIPs seen under the first conditions, could exhibit cyclical behaviour, and were reduced by D-APV. 8. Application of CGP 35 348 abolished the late IPSP under control conditions, but had no effect on hippocampal excitability. In contrast, CGP 35 348 blocked the PIP elicited in low bicuculline, and consequently led to intense epileptic discharge.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1991

Postsynaptic potentials mediated by excitatory and inhibitory amino acids in interneurons of stratum pyramidale of the CA1 region of rat hippocampal slices in vitro.

1. Because interneurons of stratum pyramidale partly mediate the feed-forward inhibition of pyramidal cells, intracellular postsynaptic potentials (PSPs) evoked by activation of afferent fibers were examined in 32 nonpyramidal cells of stratum pyramidale of the CA1 region of rat hippocampal slices. 2. Electrical stimulation of stratum radiatum at the CA1-CA3 border elicited, in interneurons, PSPs that were composed of four components: a fast excitatory postsynaptic potential (EPSP), an early inhibitory postsynaptic potential (IPSPA), a late IPSPB, and in some cells a delayed, slower EPSP. These synaptic potentials summated and elicited single action potentials in 57% of cells (17/30) and burst of action potentials (2-10) in the remaining 43%. 3. The fast EPSP was observed in all cells, and the mean stimulation intensity at its threshold was 53.4 microA. Its amplitude increased with membrane hyperpolarization, and it was associated with a 45.4% decrease in cellular input resistance. The fast EPSP always elicited an action potential at short latencies (3.6-6.4 ms poststimulation). It was reversibly reduced by 6-cyano-7-nitroquinoxaline-2,3- dione (CNQX), a blocker of non-N-methyl-D-aspartate (non-NMDA) excitatory amino acid receptors. 4. The IPSPA was observed in 28/32 cells, and the mean intensity of stimulation was 57.6 microA at its threshold. The mean latency of its peak amplitude was 17.4 ms. The mean equilibrium potential (Erev) was -72.8 mV, and it was associated with a 38.9% decrease in cellular input resistance. IPSPA was blocked by the GABAA antagonist bicuculline. 5. The IPSPB was seen in 29/32 cells, and the mean intensity of stimulation at its threshold was 80.3 microA. Its latency to peak was 130.6 ms, its Erev was -107.6 mV, and it was associated with a small (7.6%) decrease in cellular input resistance. IPSPB was blocked by the GABAB antagonist phaclofen. 6. In 11/32 cells a slower EPSP was also observed. Its mean latency to peak was 53.3 ms, and the mean intensity of stimulation at its threshold was 89.4 microA. In two cells its amplitude decreased with membrane hyperpolarization, and its was associated with a 6.8% increase in cellular input resistance. In 8 of 13 cells showing burst responses, this slow EPSP was present. 7. Both EPSPs and IPSPs were sensitive to repetitive stimulation. The amplitude of the fast EPSP was potentiated during paired-pulse stimulation at interstimulus intervals between 30 and 200 ms and occasionally depressed at intervals of 10-20 ms.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1993

Anoxic depression of excitatory and inhibitory postsynaptic potentials in rat neocortical slices.

1. The effects of brief anoxia (4-6 min replacement of O2 by N2) on synaptic potentials evoked from layer IV and/or the white matter were studied in pyramidal neurons of layers II-III from rat neocortical slices. 2. The early and late components of excitatory postsynaptic potentials (EPSPs) showed differential sensitivity to anoxia: within 2 min the late EPSP (lEPSP) disappeared, whereas the amplitude of the early EPSP (eEPSP) decreased by 70% at 5 min of anoxia. Recovery was complete within 4-11 min. 3. Both fast and slow inhibitory postsynaptic potentials (IPSPs) were extremely sensitive to lack of O2 and were abolished earlier than the lEPSP evoked by the same stimulus. As well, recovery of the IPSPs was always more delayed than that of the EPSPs. 4. A transient increase in excitability during early anoxia and/or midrecovery, manifested as enhanced probability of spiking in 25% of neurons, is attributed to the higher sensitivity of IPSPs compared with EPSPs. 5. The anoxic-induced depression of the lEPSP and IPSPs, which are generated close to the soma, is not due to depolarization-induced occlusion; however, occlusion may cause an attenuation of the eEPSP at dendritic sites. 6. The depression of the EPSPs is not a result of a decreased transmembrane Na+ gradient after inactivation of Na-K-adenosine triphosphatase (Na-K-ATPase). Although ouabain induced a depolarization similar to that of anoxia, it did not affect EPSP amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

The effect of calcium and magnesium on the spontaneous release of transmitter at insect motor nerve terminals.

1. The effect of the extracellular calcium and magnesium concentrations and calcium ionophore, X-537A, on the frequency of miniature excitatory post-synaptic potentials (MEPSPs) was studied in cockroach leg muscle fibres. 2. The frequency of MEPSPs increased as the calcium concentration was increased from 0.1 to 10 mM. In the presence of 10 mM magnesium, however, raising the calcium concentration from 0.1 to 1 mM slightly depressed the frequency. In saline containing elevated potassium (20.8 mM), increasing the calcium concentration produced a much higher frequency than that in the normal potassium saline (10.8 mM) in the absence of magnesium. Raising the extracellular potassium concentration was without effect unless the bathing solution contained calcium. 3. The frequency of the miniature potentials was reduced as the magnesium concentration was raised from 0 to 10 mM, depending on the presence of calcium ions. On the contrary, a slightly increased frequency was observed in the low calcium saline as the magnesium concentration was raised from 1 to 10 mM. The reciprocal relationship between calcium and magnesium and the time course of the effect suggest that both ions act at the same surface sites in the presynaptic membrane. 4. X-537A elicited a transient increase in frequency followed by a fall of the frequency to a very low rate. Further application of the ionophore was without effect. The effect of X-537A on the spontaneous release of transmitter at the insect neuromuscular junction was comparable with that on the spontaneous acetylcholine release in vertebrate neuromuscular junctions.

Animals↗
PubMed1978

[Convergence of reticulo-, vestibulo- and rubrospinal influences on motor neurons of the cervical region of the cat spinal cord].

Intracellular recording of synaptic potentials of 93 cervical motoneurons was performed in cats under stimulation of medial longitudinal fasciculus, Deiters vestibular nucleus and red nucleus. Under stimulation of medial longitudinal fasciculus and Deiters nucleus in motoneurons of the forelimb muscles distal groups excitatory reactions were predominant and in motoneurons of proximal extensors inhibitory reactions prevailed. When stimulating the red nucleus excitatory and inhibitory reactions were recorded almost in equal number of cells independently of functional significance of corresponding muscles. Monosynaptic EPSPs were recorded in 1/5 of motoneurons under stimulation of the medial longitudinal fasciculus and only in several cases during stimulation of vestibular and red nuclei. In the other cases stimulation of the structures investigated caused polysynaptic reactions in motoneurons which arose after a series of 2-3 stimuli. In 62% of motoneurons when stimulating different structures under study the reactions were of the same direction. The mutual facilitation of reactions was revealed under stimulation of different inputs. The data obtained show that interaction of influences of the studied structures occurs to a considerable extent at the level of spinal interneurons.

Animals↗
PubMed1997

A role for adenosine A2 receptors in the induction of long-term potentiation in the CA1 region of rat hippocampus.

Although reductions in neurotransmission have been reported in response to agonist-mediated adenosine A1 receptor activation, the implications of A2 receptor activation on synaptic transmission have not been well explored. We examined the role adenosine A2 receptors play in the efficacy of neurotransmission between the Schaffer collateral-CA1 pathway in the rat transverse hippocampal slice. A2 receptor blockade in the presence of complete A1 receptor inhibition led to a reversible reduction of the field excitatory post-synaptic potential (EPSP) slope in response to low-frequency test pulses (0.033 Hz) indicating that A2 receptors can enhance synaptic transmission. A2 receptor blockade by the A2 antagonist, DMPX (3,7-dimethyl-1-propargylxanthine) prevented the induction of tetanus-induced long-term potentiation (LTP) of the EPSP. In contrast, no such effect on LTP induction was observed during A1 receptor blockade. We also examined the effects of DMPX on the induction of LTP during continued A1 receptor blockade with CPT. Under this condition, LTP was significantly reduced when compared to LTP induced in the presence of CPT alone. A similar result was found using the highly polar A2 antagonist 8-SPT (8-(p-sulfophenyl)theophylline) suggesting that the effects of DMPX on LTP were not due to a direct action on an intracellular intermediate. DMPX had no effect on LTP expression if applied 45 min following the tetanus indicating that A2 receptors play no significant role in the maintenance phase of LTP. Selective A2a receptor activation did not alter the field EPSP. Similarly, selective blockade of the A2a receptor did not interfere with tetanus-induced LTP. Increases in neuronal firing rates can result in elevations in the concentration of extracellular adenosine. Together, these results suggest that the A2 receptors may play an important role in the induction although not the maintenance of hippocampal LTP and that the effect is likely to be mediated by the A2b receptor.

Adenosine↗
PubMed1999

Activation of intrinsic hippocampal theta oscillations by acetylcholine in rat septo-hippocampal cocultures.

1. Oscillatory electro-encephalographic activity at theta frequencies (4-15 Hz) can be recorded from the hippocampus in vivo and depends on intact septal projections. The hypothesis that these oscillations are imposed on the hippocampus by rhythmically active septal inputs was tested using dual intracellular recordings from CA1 and CA3 pyramidal cells in septo-hippocampal cocultures. 2. Septo-hippocampal cocultures displayed spontaneous oscillatory synaptic activity at theta frequencies. In CA3 cells, EPSP/IPSP sequences predominated, whereas only EPSPs were apparent in CA1 cells. Synaptic potentials in CA3 cells preceded those in CA1 cells by 5-10 ms. 3. Oscillatory synaptic activity was blocked in cocultures by the muscarinic antagonist atropine (0.1 microM), facilitated but unchanged in frequency upon application of the acetylcholinesterase inhibitor neostigmine (1 microM), and not seen in hippocampal monocultures. 4. The muscarinic agonist methacholine (5-20 nM) induced oscillatory synaptic activity at 4-15 Hz in hippocampal monocultures, which was identical to that occurring spontaneously in septo-hippocampal cocultures. 5. Synaptic theta activity was observed in cocultures of septal tissue with subdissected hippocampal slices containing area CA3 alone, but not in septo-CA1 cocultures. 6. We conclude that oscillatory synaptic activity at theta frequencies, with similar characteristics to theta activity in vivo, can be generated by the hippocampal network in response to activation of muscarinic receptors by synaptically released acetylcholine from septal afferents. Furthermore, the oscillatory activity is determined by mechanisms intrinsic to the hippocampal circuitry, particularly area CA3. Rhythmic septal input is not required.

Acetylcholine↗
PubMed2000

Cellular abnormalities and synaptic plasticity in seizure disorders of the immature nervous system.

The nervous system has an enhanced capacity to generate seizures during a restricted phase of postnatal development. Studies in animals and particularly in in vitro brain slices from hippocampus and neocortex have been instrumental in furthering an understanding of the underlying processes. Developmental alterations in glutaminergic excitatory synaptic transmission appear to play a key role in the enhanced seizure susceptible of rodents during the second and third week of life. Prior to this period, the number of excitatory synapses is relatively low. The scarcity of connections and the inability of the existing synapses to release glutamate when activated at high frequencies likely contribute importantly to the resistance of neonates to seizures. However, at the beginning of week 2, a dramatic outgrowth of excitatory synapses occurs, and these synapses are able to faithfully follow activation at high frequencies. These changes, coupled with the prolonged nature of synaptic potentials in early life, likely contribute to the ease of seizure generation. After this time, seizure susceptibility declines, patterns of local synaptic connectivity remodel, and some synapses are pruned. Concurrently, the duration of excitatory postsynaptic potentials shortens due at least in part to a switch in the subunit composition of postsynaptic receptors. Other studies have examined the mechanisms underlying chronic epilepsy initiated in early life. Models of both cortical dysplasia and recurrent early-life seizures suggest that alterations in the normal development of excitatory synaptic transmission can contribute importantly to chronic epileptic conditions. In the recurrent early-life seizure model, abnormal use-dependent selection of subpopulations of excitatory synapses may play a role. In experimental cortical dysplasia, alterations in the molecular composition of postsynaptic receptor are observed that favor subunit combinations characteristic of infancy.

Age Factors↗
PubMed1984

Extracellular fields influence transmembrane potentials and synchronization of hippocampal neuronal activity.

The influence of extracellular fields on the transmembrane potential (TMP) of CA1 pyramidal neurons was investigated following both ortho- and antidromic stimulation in the in vitro hippocampal slice preparation. A short latency negative deflection on the intracellular potential coincided with the falling phase of the extracellular population spike. Subtraction of extracellular field potentials from ground referenced intracellular records revealed a sharp depolarizing wave of the TMP superimposed upon the underlying synaptic potential. This graded depolarization was capable of discharging CA1 cells and displayed a parallel shift in latency and amplitude with the extracellular population spike. A similar depolarizing wave was associated with the antidromically evoked population spike which persisted following blockade of synaptic activity. Finally, multiple population spike activity similar to that observed during epileptiform discharge was associated with repetitive depolarizing waves of the TMP. These data suggest that extracellular field potentials can ephaptically discharge CA1 neurons and may play a role in recruitment and synchronization of neuronal activity in the hippocampus.

Animals↗