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PubMed1994

Patterns of excitatory and inhibitory synaptic transmission in the rat neostriatum as revealed by 4-AP.

1. Synaptic potentials induced by 4-aminopyridine (4-AP) were recorded intracellularly from rat neostriatal neurons in an in vitro slice preparation. EC50 for this 4-AP action was approximately 120 microM. The threshold for activation of synaptic potentials was 5 microM. 2. 4-AP-induced synaptic potentials appeared stochastically. Most were blocked by 1 microM tetrodotoxin or 400 microM Cd2+. Therefore they reflect a release of neurotransmitters dependent on both Ca2+ entry to the terminals and action potential firing. 3. Bicuculline (BIC) (< or = 10 microM), a gamma-aminobuturic acid-A (GABAA) antagonist, blocked about half of the 4-AP-induced synaptic potentials. This suggests that intrinsic inhibitory connections within the neostriatum are activated by 4-AP administration. 4. 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; < or = 10 microM) plus D-2-amino-5-phosphonovaleric acid (D-APV; < or = 100 microM) blocked most of the BIC-resistant 4-AP-induced synaptic potentials. This suggests that 4-AP induced release of glutamate (GLU) from extrinsic glutamatergic afferents. As most glutamatergic afferents are extrinsic, these afferents then would be able to fire spikes and release transmitter for several hours after they are cut from their somata. 5. If CNQX plus D-APV were administered before BIC, neostriatal neurons responded in different ways. In one half of the neurons, all induced synaptic potentials were blocked. This suggests that most GABAergic intrinsic connections between neostriatal neurons are activated indirectly by 4-AP. 4-AP would first activate extrinsic glutamatergic afferents and these in turn would activate GABAergic intrinsic neurons and connections. 6. In the remaining half of the recorded neurons, administration of CNQX plus D-APV blocked most, but not all of the 4-AP-induced synaptic potentials. The synaptic potentials that remained had a characteristic pattern: they were high amplitude, rhythmic, bursts of synaptic potentials. They were blocked by BIC (5 microM) but not by mecamylamine (> 10 microM). This suggests that these bursts of synaptic potentials were GABAergic and generated by intrinsic neurons. Therefore these neurons would not innervate all neostriatal neurons equally but just a subset of them. 7. Records from an identified aspiny neostriatal interneuron, obtained from the same preparation, are shown. This interneuron fired in bursts and its morphologically and physiologically similar to the recently described, fast spiking, parvalbumin immunoreactive, GABAergic, aspiny interneuron is functional in the slice preparation.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗
PubMed1992

High-frequency EEG activity at the start of seizures.

Frequencies above 35-40 Hz are poorly visualized on conventional EEG scalp recordings. We investigated frequency components up to 150 Hz in digitally recorded EEGs of seizures in five patients with implanted subdural grids, as part of their evaluation for epilepsy surgery. Amplifier bandpass was set from 0.1 to 300 Hz, and EEG was digitized at 2,000 samples per second. Seizures with electrodecremental patterns at the start showed a significant increase in spectral power above 35 Hz, with a twofold increase in the 40-50-Hz range, and up to a fivefold increase in the 80-120-Hz portion of the spectrum. Activity above 40 Hz could represent summed action potentials, harmonics of synaptic potentials or transient sharp components of synaptic potentials. High-frequency increases were largely localized to the region of the seizure focus. Grid sites remote from the focus did not show significant energy in the EEG band above 40 Hz at baseline, nor at time of seizure onset. Our findings suggest that high-frequency recordings may be of use in localizing seizure foci.

Adolescent↗
PubMed1968

A direct synaptic connexion between the left and right giant cells in Aplysia.

1. In Aplysia fasciata, intrasomatic stimulation of the giant cell (RGC) of the right upper quadrant of the abdominal ganglia is followed after a constant delay by the appearance of a synaptic potential recorded in the giant cell (LGC) of the left pleural ganglion.2. The synaptic potential recorded in the LGC soma has a biphasic form (hence biphasic post-synaptic potential or BPSP) consisting of a fast depolarizing phase of about 200-800 muV amplitude and 0.15-0.25 sec duration, followed by a slow hyperpolarizing phase of about 200-800 muV amplitude and 1-3 sec duration.3. During repetitive stimulation summation results in an over-all hyperpolarization at low frequencies (less than 5/sec) and an over-all depolarization for higher frequencies. Very high frequencies (25/sec) of stimulation of the RGC may elicit a spike in the LGC.4. Stimulation with two shocks showed increasing effects with shorter intervals on both the depolarizing and hyperpolarizing phase. These effects were progressive and there was no falling out of one of the two phases as might be expected if the BPSP was a composite of an inhibitory post-synaptic potential (IPSP) and an excitatory post-synaptic potential (EPSP).5. The effects of artificially imposed polarization of the LGC through a second micro-electrode suggest that the BPSP results from a chemical transmission mechanism for both its depolarizing and hyperpolarizing phases but electrical transmission cannot be excluded.6. Curare has no effect on the BPSP and thus excludes a cholinergic transmission mechanism. Chloride ions injected into the LGC soma do not appear to modify the BPSP and hence it is concluded that the hyperpolarizing phase is different from IPSPs of the same cell.7. No synaptic potential is recorded in the RGC following stimulation of the LGC, except in a single preparation in which the RGC soma was situated in the right pleural ganglion. In this case the synaptic potential recorded in both giant cells following stimulation of the other, was biphasic in form.8. It is concluded that the BPSP is a unitary monosynaptic potential which is a characteristic feature of the organization of these two giant cells.

Abdomen↗
PubMed1988

Intrinsic and extrinsic inhibitory synaptic inputs to submucous neurones of the guinea-pig small intestine.

1. The sources of inhibitory synaptic inputs to neurones in submucous ganglia of the guinea-pig small intestine were examined by making lesions to cause selective degeneration of nerve terminals of sympathetic or intrinsic origin. Intracellular recordings were used to evaluate the effects of lesions on the inhibitory inputs. Immunohistochemical techniques were used to identify the neurochemical classes of the impaled neurones and to confirm the efficacy of the lesions. 2. The neurones from which recordings were taken were filled with the fluorescent dye Lucifer Yellow. The preparations were then fixed and processed for immunohistochemistry. 3. Thirty-one neurones reactive for vasoactive intestinal polypeptide (VIP) were examined in control submucous ganglia and all exhibited inhibitory synaptic potentials. In preparations extrinsically denervated by severing the mesenteric nerves, twenty-seven of twenty-eight VIP-reactive neurones had inhibitory synaptic potentials. This indicates that these neurones receive inhibitory synaptic inputs from intrinsic neurones. However, significantly more stimuli were required to evoke a detectable inhibitory synaptic potential in extrinsically denervated preparations than in normal intestine. 4. Extrinsic denervations were combined with removal of the myenteric plexus so that nerve terminals arising from both cell bodies in extrinsic ganglia and in the myenteric plexus degenerated. Under these conditions no inhibitory synaptic potentials could be recorded in any of the nine VIP-reactive neurones studied. 5. The conductance change underlying the intrinsic inhibitory synaptic potentials appeared to be similar to that underlying the responses in normal intestine. 6. The time courses of the intrinsic inhibitory synaptic potentials differed from those of the control responses. The responses to short trains of stimuli were significantly briefer and the responses to long trains significantly more prolonged in the extrinsically denervated preparations than in normal preparations. 7. The intrinsic inhibitory synaptic potentials were not significantly affected by phentolamine (0.2 microM), guanethidine (1 microM) or naloxone (1 microM), although the first two drugs markedly depressed control inhibitory synaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1993

Induction of hippocampal long-term potentiation by alpha-tocopherol.

Long-term potentiation (LTP) of synaptic transmission in the hippocampus is thought to be one of the cellular mechanisms underlying learning and memory. Recent evidence in literature suggests the involvement of free radicals in impeding LTP maintenance. In the present study, the effects of alpha-tocopherol, a major lipid-soluble antioxidant which could prevent lipid peroxidation, were examined on the excitatory post-synaptic potentials (EPSPs) of CA1 neurons in guinea pig hippocampal slices. alpha-Tocopherol phosphate disodium salt (0.2 mM applied for 5 min) induced a slowly developing long-lasting increase of the EPSP, without significantly changing the membrane potential, the input resistance and the ability to generate action potentials. No significant changes in the fast and the slow inhibitory post-synaptic potentials (IPSPs) were observed during the alpha-tocopherol-induced LTP of the EPSP. 2-Amino-5-phosphonovalerate (APV) did not block the induction of this LTP. L-Ascorbic acid (Na salt, 3-10 mM), a water-soluble antioxidant, failed to produce any significant enhancement in the EPSP. These results indicate that alpha-tocopherol can induce LTP of the EPSP in guinea pig hippocampal CA1 neurons. The activation of N-methyl-D-aspartate (NMDA) receptors does not appear to be necessary for this action of alpha-tocopherol. Whether the LTP-inducing action of this agent is related to its antioxidant property is unclear.

Animals↗
PubMed2002

Protein kinase C mediates potentiation of synaptic transmission by phorbol ester at parallel fibers in the dorsal cochlear nucleus.

Many cells in the outer two layers of the dorsal cochlear nucleus (DCN) express high levels of the phospholipid-activated, calcium dependent kinase, protein kinase C (PKC), an enzyme that can phosphorylate numerous proteins involved in neurotransmission and postsynaptic signaling. We investigated the effects of stimulating PKC with phorbol esters (phorbol 12-13 diacetate; PDAc) on parallel fiber synaptic transmission in brain slices of the guinea pig DCN. Phorbol esters increased the amplitude of the postsynaptic components of the field potential, including the excitatory post-synaptic field potential (fEPSP) and the population spike following electric stimulation of parallel fibers. Phorbol esters simultaneously decreased paired-pulse facilitation, suggesting that transmitter release mechanisms were affected. Potentiation of synaptic transmission and diminished paired-pulse potentiation were also observed in intracellular recordings of DCN neurons. The effects of phorbol esters were antagonized by the specific PKC blockers bisindolylmaleimide and calphostin C. Although modulation of the synaptic potentials appears to be mediated by presynaptic PKC, the differential effects of PDAc on the fEPSP and the population spike also suggest the involvement of postsynaptic PKC and postsynaptic targets. These experiments demonstrate that protein kinase C is capable of profoundly modulating synaptic transmission at parallel fiber synapses in the DCN.

Acoustic Stimulation↗
PubMed1988

Electrical properties of motoneurons in the spinal cord of rat embryos.

Electrical properties of immature motoneurons were studied in vitro using isolated segments of spinal cords of rat embryos aged 14-21 days of gestation. Stable resting potentials and evoked synaptic potentials were recorded for more than 9 hr, indicating that motoneurons remain viable for many hours. Motoneurons are electrically excitable at 14 days of gestation and from the onset of excitability the action potentials are Na+-dependent but slow rising long-duration Ca2+-dependent action potentials can be evoked if K+ conductance is reduced. Thus, during embryonic development the regenerative potential inward current is Na+-and Ca2+-dependent. During motoneurons' differentiation there are some changes in their electrical properties: resting membrane potential increases, input resistance decreases, input capacitance increases, threshold for action potential decreases, and maximum rate of rise of action potential increases. Afferent motoneuron contacts are formed at 16-18 days of gestation when excitatory synaptic potentials can first be evoked in response to dorsal root stimulation. The changes in input capacitance and threshold for action potential occur at the onset of functional afferent motoneuron contacts, but it is not known whether these changes are autonomous or are influenced by the newly formed sensory inputs.

Action Potentials↗
PubMed1988

Long-term potentiation of synaptic transmission in kitten visual cortex.

1. Potentiation of synaptic transmission in visual cortex (areas 17 and 18) of kittens was investigated by extracellular recording of field potentials (FPs) and cortical units in cortical slices and whole-animal preparations. Responses to test stimulation (0.05 Hz) of the white matter (WM), lateral geniculate nucleus (LGN), and optic chiasm (OC) were documented before and after conditioning stimulation (2 Hz for 1 h). 2. In slice preparations of area 17, the FPs were always depressed during conditioning stimulation and were usually potentiated immediately after conditioning stimulation. Long-term potentiation (LTP) of FPs developed rapidly during the initial 1-2 h and continued to increase slowly for several hours after conditioning. 3. LTP of FPs was age dependent: LTP occurred most frequently (43/53) at the ages of 21-34 days, less frequently (4/7 and 5/11) at 14-20 and 35-41 days, and never (0/5 and 0/5) at 7-13 and 42-49 days. LTP age relationship determined as a ratio of the amplitudes of FPs after conditioning to that before conditioning was greater at 21-34 days (mean potentiation, 2.4 +/- 0.6) than at 14-20 or 35-41 days (1.7 +/- 0.5). 4. LTP was also documented by the shortening in latencies of orthodromic responses of cortical units sampled from 10 pairs of conditioned and unconditioned control slices. Unit responses were classified into mono- and polysynaptic groups according to the central delay, defined as the time required for their activation after the arrival of afferent impulses. The monosynaptic central delays were 0.22 ms shorter in conditioned (0.60 +/- 0.17 ms, n = 56) than in control slices (0.82 +/- 0.22 ms, n = 57); similarly, polysynaptic central delays were 0.66 ms smaller (1.70 +/- 0.43 ms, n = 51; and 2.36 +/- 0.79 ms, n = 51). Both differences were statistically significant (P less than 0.001). 5. There were laminar differences in LTP of mono- and polysynaptic transmission. LTP of monosynaptic transmission occurred throughout layers II-V (central delays shortened about 0.2 ms), whereas LTP of polysynaptic transmission was greatest in layer II (1.17 ms), moderate in layer III (0.66 ms), and slight in layer IV (0.3 ms). The time course of shortening in orthodromic latency in five polysynaptic units agreed with the time course of LTP of FP. 6. Location of synapses involved in LTP of synaptic transmission was studied by current source-density (CSD) analysis in slice preparations of area 17 during test stimulation of WM. CSD analysis demonstrated two components of current sinks (early and late), probably representing mono- and polysynaptic transmission.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Electrophysiological and morphological classification of myenteric neurons in the proximal colon of the guinea-pig.

Intracellular recordings were made from myenteric neurons in the proximal colon of the guinea-pig. The electrical behaviour of the neurons in response to intracellular depolarizing current pulses, and to internodal strand stimulation, was recorded. The intracellular electrode contained the intracellular marker biocytin which was injected into impaled neurons for subsequent histochemistry. Proximal colon myenteric neurons displayed electrophysiological properties similar to myenteric neurons in the small intestine, and were classified as either AH- or S-neurons. AH-neurons were characterized by the presence of a slow afterhyperpolarization following an action potential. Internodal strand stimulation evoked slow excitatory synaptic potentials in five out of six AH-neurons tested, but did not evoke fast excitatory synaptic potentials in 26 AH-neurons tested. S-neurons lacked a slow afterhyperpolarization, but internodal strand stimulation evoked fast excitatory synaptic potentials in all 113 neurons and slow excitatory synaptic potentials in seven out of 17 tested. A subpopulation of AH-neurons displayed a rhythmic oscillation in membrane potential which could be triggered by an action potential. S-neurons could be subdivided into those that fired tonically and those that fired phasically in response to long depolarizing current pulses. About 80% of the AH-neurons were immunoreactive for calbindin, as were 10% of S-neurons. A further 17% of S-neurons, but no AH neurons, were calretinin immunoreactive. Morphological analysis of filled neurons revealed eight distinct classes. Neurons electrophysiologically classified as AH typically had a large, oval soma and several long tapering processes. Processes of AH-neurons branched into many adjacent ganglia. Almost all S-neurons were uniaxonal and many axons ended in an expansion bulb in the myenteric plexus. S-neurons typically had broad, lamellar processes, or short, spiny processes. Roughly equal proportions of S-neurons had oral or anal projection. However, almost all S-neurons that were immunoreactive for calbindin or calretinin projected orally. The results indicate that myenteric neurons in the proximal colon of the guinea-pig are electrophysiologically similar to myenteric neurons in the small intestine, but there are a greater number of morphological and chemical categories.

Action Potentials↗
PubMed1993

Glycine-induced changes in synaptic efficacy in hippocampal slices involve changes in AMPA receptors.

Brief applications of high glycine concentrations to hippocampal slices have been shown to produce long-lasting changes in synaptic efficacy. In the present study, we show that glycine application transiently and reversibly increases the amplitude and prolongs the duration of synaptic potentials mediated by N-methyl-D-aspartate (NMDA) receptors. The long-lasting changes in synaptic potentials mediated by AMPA receptors are correlated with changes in the binding of [3H]alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid ([3H]AMPA) to membranes prepared from glycine-treated slices. The changes in binding properties of AMPA receptors in adult slices are due to an increase in affinity of the agonist for the receptor. Furthermore, glycine-induced increases in [3H]AMPA binding and in synaptic potentials in adult hippocampal slices are markedly reduced in the presence of low extracellular calcium or of the phospholipase inhibitor bromophenacylbromide. Finally, glycine-induced potentiation of synaptic potentials is associated with an increased potency of the glutamate receptor antagonist, 6,7-dinitroquinoxaline (DNQX), to inhibit synaptic potentials. The results indicate that glycine-induced changes in synaptic efficacy are likely triggered by the activation of NMDA receptors and expressed by changes in the properties of AMPA receptors. As similar events underly long-term potentiation (LTP), this phenomenon might provide important clues to elucidate the molecular mechanisms involved in LTP maintenance.

Animals↗
PubMed1979

Localization of synaptic input on dendrites of a lamprey spinal cord neurone from physiological measurements of membrane properties.

1. Composite excitatory post-synaptic potentials (e.p.s.p.s) resulting from electrotonic and chemical synaptic junctions were recorded from eighteen interneurones following stimulation of the I2 burster axon in the isolated lamprey spinal cord. 2. In each cell, the half-width of the electrotonic e.p.s.p. was measured and used, together with the cable parameters estimated for the same neurone, to locate the position of synaptic contact made by the I2 axon on the dendrites of the interneurone. The synaptic location ranged from 0.05 to 1.35 space constants with a mean of 0.46. 3. The synaptic potential was simulated using the Rall model of the neurone. When compared with the experimentally recorded e.p.s.p. with the same half-width, the rise-time of the simulated synaptic potential was found to be faster. By changing the value of synaptic distance and/or synaptic current duration the half-width, rise-time, and decay of the simulated synaptic potential fit closely the experimental e.p.s.p. The range of synaptic distance estimated from the simulation decreased considerably (0.2--0.7 space constants; mean 0.52). 4. Direct comparison of synaptic location estimated from histological tracings of dendritic trees from these same cells injected with horseradish peroxidase compared favourably with synaptic location estimated from the simulations. 5. These results support the hypothesis that functionally similar presynaptic axons make synaptic connexions at the same electrotonic distance from the soma on functionally similar post-synaptic cells. This occurs in the face of large variations in physical distance for these same synaptic contacts.

Animals↗
PubMed1995

Synaptic excitation in the thoracic spinal cord from expiratory bulbospinal neurones in the cat.

1. Synaptic actions in the thoracic spinal cord of individual expiratory bulbospinal neurones were studied in anaesthetized cats by the use of two techniques: (i) the monosynaptic connections to motoneurones were assessed by cross-correlations between the discharges of the neurones and efferent discharges in the internal intercostal nerves of several segments bilaterally; and (ii) distributions of terminal and focal synaptic potentials were measured by extracellular spike-triggered averaging in the thoracic ventral horn. 2. Monosynaptic connections were identified by both the durations and timings of observed cross-correlation peaks, taking into account accurate conduction velocity measurements derived from collision tests and from spike-triggered averaging. Discrimination was made against peaks resulting from presynaptic synchronization. 3. Monosynaptic connections to motoneurones were identified for twenty-three out of twenty-seven neurones. The connections to nerves on the side ipsilateral to the cell somata were, on average, about 36% of the strength of those on the contralateral side. The overall strength of the connections was about twice as strong as previous estimates for similar connections from inspiratory bulbospinal neurones to phrenic motoneurones. The monosynaptic pathway was calculated to be able to provide most of the depolarization for the motoneurones concerned and therefore was likely to be the main determinant of their firing patterns under the conditions of these experiments. 4. However, taking into account previous measurements it is considered possible that these connections may only involve a minority of motoneurones, perhaps only 10% of the expiratory population. Thus, in general, the control of the whole pool of expiratory motoneurones, despite the strong monosynaptic connections measured here, is suggested to be mainly dependent on spinal interneurones, as has been concluded previously for inspiratory motoneurones. 5. Spike-triggered averaging revealed that nearly all neurones gave signs of collaterals in each of the segments investigated (T7, T8 or T9), as shown by the presence of terminal potentials or focal synaptic potentials, but the projection within a given thoracic segment was non-uniform, in that large-amplitude potentials were more common in the rostral than the caudal part of the segment. This non-uniformity could be a factor involved in the apparently non-heterogeneous connections to the motoneurones.

Action Potentials↗
PubMed1992

Involvement of GABA and glycine in recurrent inhibition of spinal motoneurons.

1. Recurrent inhibitory postsynaptic potentials (IPSPs) were recorded intracellularly from chloride-loaded motoneurons in the isolated lumbar spinal cord of neonatal rats (day 5-day 12). This in vitro preparation exhibited an intact and functional recurrent inhibitory pathway that displayed characteristics previously described for this pathway in other species. 2. Although strychnine (1-5 microM) depressed the chloride-dependent recurrent synaptic potentials evoked by ventral root stimulation by 48.2 +/- 2.7% (mean +/- SE, n = 13), confirming that part of the recurrent IPSP is mediated by a glycinergic mechanism, in every case a residual strychnine-resistant synaptic potential was observed. 3. The gamma-aminobutyric acid (GABA) antagonist bicuculline, in low concentrations (2-10 microM), depressed the recurrent synaptic potentials in a dose-dependent manner by 27.0 +/- 4.3% (range 0-49%, n = 19). Application of bicuculline almost eliminated the strychnine-resistant component of the IPSP. However, in some motoneurons, a small synaptic potential remained after combined application of strychnine and bicuculline. 4. The selective antagonists of GABA uptake, (+/-)-nipecotic acid (1 mM) and guvacine (1 mM), increased the amplitude of recurrent synaptic potentials in 12 of 16 motoneurons by 37.2 +/- 7.2% (range 12.6-84.2%). 5. The excitatory amino acid antagonists kynurenic acid (1 mM), 6-cyano-7-nitroquinoxaline-2,3-dione [CNQX (10 microM)] and 6,7-dinitroquinoxaline-2,3-dione (10 microM) potentiated recurrent synaptic potentials in 5 of 7 motoneurons. However, CNQX (10-15 microM) in the presence of strychnine and bicuculline virtually abolished the synaptic potential remaining after application of the inhibitory amino acid antagonists. It is concluded that ventral root stimulation evokes a small excitatory amino acid-mediated synaptic potential in neonatal rat motoneurons. 6. An antidromic synaptic potential due to electrotonic coupling between motoneurons was unaffected by changes in membrane potential, chloride loading, or antagonists of glycine, GABA, excitatory amino acid, and acetylcholine receptors. 7. The results suggest that a major portion of the strychnine-resistant component of the IPSP is mediated by a GABAergic mechanism. It is concluded that both glycinergic and GABAergic mechanisms play a role in recurrent inhibition of motoneurons in the mammalian spinal cord. It is unknown whether these inhibitory amino acids are released by a single pool of Renshaw cells or by neurochemically distinct populations.

Animals↗
PubMed1992

Electrophysiological consequences of exposure of hippocampal slices to dihydroxyfumarate, a generator of superoxide radicals.

In an effort to understand the damaging actions of free radicals to neuronal electrophysiology, the superoxide generator, dihydroxyfumarate (DHF), was evaluated in slices of guinea pig hippocampus. Using field potential recording techniques, population spikes and population synaptic potentials were recorded in field CA1. Slices were exposed to 3 mM DHF either alone or in the presence of a protectant. DHF did not alter the ability of the afferent volley to generate a synaptic potential, but it did impair the ability of the synaptic potential to elicit a population spike. In addition, DHF induced lipid peroxidation as measured by the thiobarbituric acid assay. Superoxide dismutase (SOD) provided no protection. Instead, SOD treatment promoted DHF damage to synaptic potentials. Catalase alone mitigated the actions of DHF, but only in SOD plus catalase was the DHF-induced electrophysiological deficit and lipid peroxidation completely antagonized. The iron chelator, Desferal, did not protect but promoted synaptic damage. Desferal may be ineffective because of the nitroxide radical formed upon its reaction with DHF. The hydroxyl radical scavenger, dimethylsulfoxide, prevented lipid peroxidation and reduced the DHF-induced deficit but did not completely prevent the impairment of spike generation. These data suggest that DHF exerts its actions through generation of hydrogen peroxide which would further react with tissue iron to produce hydroxyl radicals.

Animals↗
PubMed1974

The effects of physostigmine on synaptic transmission in the inferior mesenteric ganglion of guinea-pigs.

1. Synaptic potentials were recorded with intracellular electrodes from cells in the inferior mesenteric ganglion of the guinea-pig.2. Half-widths of the synaptic potentials recorded fell into two groups: type L cells had long synaptic potentials (11.6-15.2 msec) and low thresholds (14.6 mV mean), type S cells had short synaptic potentials (6.1-9.3 msec) and high thresholds (29.9 mV mean).3. Physostigmine (1.2 x 10(-6)M) caused a significant increase in the half-width of both types of synaptic potential.4. Physostigmine caused a significant increase in the half-width of spontaneous synaptic potentials and an increase in their amplitude.5. Repetitive preganglionic stimulation, in the presence of physostigmine, led to a marked and prolonged depolarization in all cells. In most cells repetitive spontaneous firing of action potentials was then observed. This effect was blocked by atropine (1.4 x 10(-7)M).6. The effect of atropine on the half-width in a physostigmine-treated cell was inconsistent: although synaptic potentials in some cells were slightly shortened their half-widths were always greater than the control.7. It is concluded that cholinesterase plays a role in limiting the time course of the synaptic potential, by limiting the duration of action of acetylcholine.

Acetylcholine↗
PubMed1982

The action of piracetam on the electrical activity of the hippocampal slice preparation: a field potential analysis.

The action of various doses of piracetam on the electrical responses of in vitro hippocampal slices from the rat was investigated. Piracetam increased dose dependently the amplitude of the population spike response of pyramidal neurons evoked by stimulation of the stratum radiatum. Piracetam began to affect the population spike at a dose of 100 microM and consistently increased it at a dose of 1 mM. The drug had a rapid onset of action and recovery was seen within a few minutes following its removal. The response of the pyramidal neurons to antidromic stimulation was not affected by piracetam at concentrations up to 50 mM. Also, neither the amplitude nor the slope of the dendritic response was changed by the drug.l Piracetam also did not affect either posttetanic or long-term potentiation of synaptic potentials. These findings suggest that the drug does not act through depolarization of the pyramidal cells or potentiation of the synaptic processes located on their dendrites. The action of piracetam on the feedforward- and feedback-mediated inhibition of pyramidal cells by basket cells was investigated in several series of experiments. At concentrations of 1 and 10 mM, piracetam did not change either of the two types of inhibitory mechanisms. Several hypothetical sites of action of piracetam are discussed.

Animals↗
PubMed1992

Cholinergic suppression specific to intrinsic not afferent fiber synapses in rat piriform (olfactory) cortex.

1. Differences in the cholinergic suppression of afferent and intrinsic fiber synaptic transmission were studied in the rat piriform cortex. Extracellular and intracellular recording techniques were applied in an in vitro transverse slice preparation. Afferent and intrinsic fiber systems were differentially stimulated with electrodes placed in layer Ia or layer Ib, respectively. Synaptic responses were monitored in the presence of cholinergic agonists and antagonists. 2. Afferent and intrinsic fiber synaptic potentials measured extracellularly showed large differences in sensitivity to micromolar concentrations of the cholinergic agonists carbachol or (+/-)-muscarine, or to acetylcholine combined with neostigmine. Intrinsic fiber synaptic responses in layer Ib were strongly reduced in the presence of cholinergic agonists, whereas afferent fiber synaptic responses in layer Ia were largely unaffected. At a concentration of 100 microM, all three agonists caused a greater than 60% decrease in the height of the intrinsic fiber synaptic potential but less than 15% reduction in the afferent fiber synaptic potential. 3. Intracellular recordings confirmed that the cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials recorded from the same pyramidal cell. 4. Dose-response curves to carbachol were obtained for both fiber systems using extracellular recording of evoked field potentials. Carbachol suppressed intrinsic fiber synaptic potentials with a coefficient of dissociation (KD) estimated at 2.9 microM and an inhibitory concentration for 50% response estimated at 6.6 microM. 5. Carbachol produced a proportionately greater suppression of the first pulse than the second pulse of a pulse pair. This increase in the level of facilitation accompanying suppression suggests a presynaptic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1999

Presynaptic muscarinic (M3) receptors reduce excitatory transmission in dopamine neurons of the rat mesencephalon.

The effects of carbachol (0.01-30 microM) and muscarine (10-30 microM) on the excitatory synaptic potentials were studied using conventional intracellular recordings from dopaminergic neurons in rat mesencephalic slices. Both muscarinic agonists reversibly reduced the excitatory synaptic potentials, evoked by local electrical stimulation. The EC50 for carbachol was determined to be 4.5 microM. The maximal degree of the excitatory synaptic potentials suppression caused by carbachol and muscarine was around 40% of control. This suppression was completely blocked by the non-specific muscarinic antagonist atropine (1 microM) and the selective M3 antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (1 microM). Other antagonists, preferentially acting at M1, M2 and M4 receptors, were not effective. Furthermore, the acetylcholinesterase inhibitor, physostigmine (50 microM), decreased the amplitude of the excitatory synaptic potentials, indicating that ambient acetylcholine can depress this potential. Direct depolarizing responses to glutamate were not changed by muscarine. In addition, muscarine facilitated the second excitatory synaptic potentials during a paired-pulse protocol. Thus, the effect of the muscarinic agonists is attributable to a presynaptic locus of action. The action of muscarine was not mediated by an N-ethylmaleimide-sensitive G-protein since it was not modified by a treatment of the slices with this agent. The calcium channels blockers, omega-conotoxin GIVA, omega-agatoxin IVA and omega-conotoxin MVIIC did not affect the action of muscarine on the excitatory synaptic potentials. When the potassium currents were reduced by extracellular barium and 4-aminopyridine, the muscarinic agonists still depressed the excitatory synaptic potentials. Our data indicate that presynaptically located M3 receptors modulate the excitatory transmission to midbrain dopaminergic neurons via a N-ethylmaleimide-insensitive G-protein which activates mechanisms neither linked to N-, P-, Q-type calcium channels nor to barium- and 4-aminopyridine-sensitive potassium channels.

4-Aminopyridine↗