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PubMed1998

Intravenously administered cell-permeant calcium buffer decreases evoked synaptic potentials in rat dentate gyrus in vivo.

We examined the effects of the neuroprotective cell-permeant Ca2+ buffer, 2-aminophenol-N,N,O-triacetic acid acetoxymethyl ester (APTRA-AM, 20-40 mg/kg), on synaptically evoked potentials in the dentate gyrus of awake rats. Intravenous APTRA-AM (20 mg/kg) decreased the evoked potentials with peak effects approximately 6 h after infusion, and recovery to control levels by 24 h. Peak decrease in the population spike (PS) amplitude was by 72+/-17% of control, and the excitatory postsynaptic potential (EPSP) slope was decreased by 31+/-12%. APTRA-AM (40 mg/kg), decreased the PS amplitude and EPSP slope by 58+/-7% and 31+/-6% of pre-drug levels, respectively. These effects were qualitatively similar to the presynaptically mediated decreases in synaptic potentials previously demonstrated in vitro with APTRA-AM. These results indicate that the cell-permeant Ca2+ buffer, APTRA-AM, attenuates hippocampal excitability in vivo, most likely by decreasing synaptic neurotransmission.

Animals↗
PubMed1987

Long-term blockade by toxin F of nicotinic synaptic potentials in cultured sympathetic neurons.

The effects of a recently identified blocker of neuronal nicotinic transmission, toxin F, were studied in cultured sympathetic neurons. Single principal neurons, dissociated from superior cervical ganglia of newborn rats, were grown on cardiac myocytes in microculture. The toxin blocked nicotinic synaptic potentials in these cultures but had no effect on muscarinic interactions. When toxin F was applied by addition to the perfusion medium, the concentration required for blocking most of the nicotinic potential was 40 nM, and the recovery from blockade was slow (t1/2 = 95 +/- 64 min). When the toxin was briefly applied by pressure ejection from a pipette, the concentration in the pipette necessary for blockade was 21 microM, and 30-60% of the response recovered within a few minutes while the remainder recovered slowly (t1/2 of the remainder = 105 +/- 82 min). One possible explanation for the difference in recovery time is that toxin F binds initially with low affinity to the nicotinic receptor but with time the toxin receptor complex converts to a high affinity state. The presence of dihydro-beta-erythroidine during perfusion of toxin F prevented the long-lasting blockade by the toxin, suggesting that toxin F and dihydro-beta-erythroidine act through a common binding site. The specificity, potency, and slow reversibility of the effects of toxin F make it useful as a probe for studying neuronal nicotinic receptors of cultured sympathetic neurons.

Adrenergic Fibers↗
PubMed1987

Distribution of single-axon recurrent inhibitory post-synaptic potentials in a single spinal motor nucleus in the cat.

1. The distribution of recurrent Renshaw inhibition was examined in the medial gastrocnemius motor nucleus of the cat by measurement of single-axon recurrent inhibitory post-synaptic potentials (recurrent i.p.s.p.s) in motoneurones supplying medial gastrocnemius produced by single impulses of antidromically stimulated single motor axons supplying the same muscle. 2. Stimulated motor-axon-recorded-motoneurone pairs were classified as 'close' if both contributed their axons to the same portion of the ventral roots (L7 rostral, L7 caudal or S1). Alternatively, they were classified as 'distant' if their axons were in different portions of these ventral roots. 3. Both the incidence and amplitude of 'close-pair' recurrent i.p.s.p.s were shown to be significantly larger than the corresponding values for 'distant-pair' recurrent i.p.s.p.s. 4. The results provided evidence of a strong topographic effect on the distribution of recurrent Renshaw inhibition within a single spinal motor nucleus. This finding is discussed in relation to the roles of topographic and species specificity in determining the organization of recurrent inhibition and to the partitioned distribution of monosynaptic Ia excitation in single motor nuclei.

Action Potentials↗
PubMed1981

Effects of opioid peptides on synaptic potentials in explants of rat hippocampus.

Bath application of 10(-8) M FK 33-824 (an enkephalin analogue) and 10(-7) M beta-endorphin reversibly induced stimulus-evoked bursting activity with depolarization shifts in cultured hippocampal pyramidal cells. Statistical analysis of the data revealed that in the majority of cells, inhibitory postsynaptic potentials were markedly decreased and excitatory postsynaptic potentials increased prior to the development of bursting activity, although some inhibition persisted in cells exposed to opioid peptides. In a minority of cells, no alteration in synaptic potentials were observed to precede the stimulus-evoked bursts induced by the opioid peptides.

Action Potentials↗
PubMed2001

Changes of oligosaccharides and fatty acids in monkey hippocampus by synaptic potentiation.

We measured the release of free fatty acids and structural changes of glycoprotein glycans induced by tetraethylammonium (TEA) salt in hippocampal slices of cynomolgus monkey brain. The release of free fatty acids in the hippocampal slices occurred after synaptic potentiation by TEA in a different manner from rat hippocampus. Arachidonic acid release in monkey hippocampus occurred much faster than that in rat. Several types of glycans of monkey hippocampal glycoproteins were determined depending on the duration time after TEA treatment. 5-Mannose was increased within 2 min, while polysialoglycans were increased after 5 min or later. Comparative study of glycans of monkey and rat hippocampal slices revealed the presence of relatively larger amount of sialo- and multi-anntenary glycans in rat than in monkey. These results indicate that the depolarizing stimulation of monkey hippocampal slices induced the change of glycoprotein glycan structures and release of free fatty acids in a different manner from rat hippocampus.

Animals↗
PubMed1997

Role of ATP in fast excitatory synaptic potentials in locus coeruleus neurones of the rat.

1. Intracellular recordings were made in a pontine slice preparation of the rat brain containing the nucleus locus coeruleus (LC). The pressure application of alpha,beta-methylene ATP (alpha,beta-meATP) caused reproducible depolarizations which were depressed by suramin (30 microM) and abolished by suramin (100 microM). Pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 10, 30 microM) also concentration-dependently inhibited the alpha,beta-meATP-induced depolarization, although with a much slower time-course than suramin. Almost complete inhibition developed with 30 microM PPADS. Reactive blue 2 (30 microM) did not alter the effect of alpha,beta-meATP, while reactive blue 2 (100 microM) slightly depressed it. 2. Pressure-applied (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) also depolarized LC neurones. Kynurenic acid (500 microM) depressed and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 50 microM) abolished the response to AMPA. Suramin (100 microM) potentiated the AMPA effect. 3. Pressure-applied noradrenaline hyperpolarized LC neurones. Suramin (100 microM) did not alter the effect of noradrenaline. 4. Focal electrical stimulation evoked biphasic synaptic potentials consisting of a fast depolarization (p.s.p.) followed by a slow hyperpolarization (i.p.s.p.). A mixture of D(-)-2-amino-5-phosphonopentanoic acid (AP-5; 50 microM), CNQX (50 microM) and picrotoxin (100 microM) depressed both the p.s.p. and the i.p.s.p. Under these conditions suramin (100 microM) markedly inhibited the p.s.p., but did not alter the i.p.s.p. In the combined presence of AP-5 (50 microM), CNQX (50 microM), picrotoxin (100 microM), strychnine (0.1 microM), tropisetron (0.5 microM) and hexamethonium (100 microM), a high concentration of suramin (300 microM) almost abolished the p.s.p. without changing the i.p.s.p. 5. In the presence of kynurenic acid (500 microM) and picrotoxin (100 microM), PPADS (30 microM) depressed the p.s.p. Moreover, the application of suramin (100 microM) to the PPADS (30 microM)-containing medium failed to cause any further inhibition. Neither PPADS (30 microM) nor suramin (100 microM) altered the i.p.s.p. 6. It was concluded that the cell somata of LC neurones are endowed with excitatory P2-purinoceptors. ATP may be released either as the sole transmitter from purinergic neurones terminating at the LC or as a co-transmitter of noradrenaline from recurrent axon collaterals or dendrites of the LC neurones themselves.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2004

Melatonin-induced inhibition of spinal cord synaptic potentiation in rats is MT2 receptor-dependent.

Systemically administered melatonin has been reported to produce antinociception and to inhibit spinal nociceptive transmission in rats. The present study was designed to investigate in anesthetized rats (i) whether intrathecally administered melatonin can depress synaptic potentiation (wind-up) in the spinal cord, and (ii) whether this effect is prevented by intrathecal (i.t.) administration of the MT2 receptor antagonist luzindole. Results showed that melatonin i.t. (10, 30 and 90 microg) induced dose-dependent inhibition of wind-up activity (ED50=52.06 microg i.t.), an effect that was prevented by 100 microg i.t. of luzindole. Since wind-up is dependent on NMDA receptor activation, the results suggest that melatonin can interfere with the NMDA-mediated glutamatergic component of pain transmission in rat spinal cord by acting on MT2 receptors.

Animals↗
PubMed1978

Quantal analysis of the size of excitatory post-synaptic potentials at synapses between hair cells and afferent nerve fibres in goldfish.

1. A statistical analysis has been made of the transmitter release at the hair cell afferent fibre synapse in the sacculus of the goldfish, using the amplitude of the excitatory post-synaptic potentials (e.p.s.p.s) in response to stimulus tone as a measure of the transmitter release under application of tetrodotoxin. 2. Application of binomial statistics allowed a direct calculation of the mean probability of release (p) and the readily available store (n), and the X2-test showed that the binomial predictions fitted fairly well with the observed distribution of the responses. 3. Adaptive rundown of e.p.s.p.s during sound stimulation, i.e. the successive rundown in the size of the mean quantal content (m), was found to be associated with a reduction in the size of parameter n, but not of p. 4. A marked negative correlation was demonstrated between the amplitude of two consecutive e.p.s.p.s, supporting the depletion hypothesis of the adaptive rundown of e.p.s.p.s. 5. The increase in the e.p.s.p. amplitude and the increase in the mean quantal content, m, brought about by an increase in the tone intensity were found mostly explicable in terms of an increase in the statistical parameter n. The probability parameter p was found largely in invariable, although in certain instances the increase in m was also accompanied by a slight increase in the parameter p.

Animals↗
PubMed1997

Differential impact of miniature synaptic potentials on the soma and dendrites of pyramidal neurons in vivo.

We studied the impact of transmitter release resistant to tetrodotoxin (TTX) in morphologically identified neocortical pyramidal neurons recorded intracellularly in barbiturate-anesthetized cats. It was observed that TTX-resistant release occurs in pyramidal neurons in vivo and at much higher frequencies than was previously reported in vitro. Further, in agreement with previous findings indicating that GABAergic and glutamatergic synapses are differentially distributed in the somata and dendrites of pyramidal cells, we found that most miniature synaptic potentials were sensitive to gamma-aminobutyric acid-A (GABA(A)) or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) antagonists in presumed somatic and dendritic impalements, respectively. Pharmacological blockage of spontaneous synaptic events produced large increases in input resistance that were more important in dendritic (approximately 50%) than somatic (approximately 10%) impalements. These findings imply that in the intact brain, pyramidal neurons are submitted to an intense spike-independent synaptic bombardment that decreases the space constant of the cells. These results should be taken into account when extrapolating in vitro findings to intact brains.

Anesthesia↗
PubMed2002

Impaired spatial cognition and synaptic potentiation in a murine model of human immunodeficiency virus type 1 encephalitis.

Injection of human immunodeficiency virus type 1 (HIV-1)-infected human monocyte-derived macrophages (MDMs) into the basal ganglia of severe combined immunodeficient mice recapitulates histopathologic features of HIV-1 encephalitis (HIVE). Here, we show that the neural damage in HIVE mice extends beyond the basal ganglia and is associated with cognitive impairment. Morris water maze tests showed impaired spatial learning 8 d after MDM injection. Moreover, impaired synaptic potentiation in the hippocampal CA1 subregion was demonstrated at 8 and 15 d. By day 15, post-tetanic, short-term, and long-term potentiation were reduced by 14.1, 29.5, and 45.3% in HIVE mice compared with sham-injected or control animals. Neurofilament (NF) and synaptophysin (SP) antigens were decreased significantly in the CA2 hippocampal subregion of HIVE mice with limited neuronal apoptosis. By day 15, the CA2 region of HIVE mice expressed 3.8- and 2.6-fold less NF and SP than shams. These findings support the notion that HIV-1-infected and immune-competent brain macrophages can cause neuronal damage at distant anatomic sites. Importantly, the findings demonstrate the value of the model in exploring the physiological basis and therapeutic potential for HIV-1-associated dementia.

AIDS Dementia Complex↗
PubMed1985

Characterization of miniature inhibitory post-synaptic potentials in rat spinal motoneurones.

Intracellular recordings were made from motoneurones in the isolated spinal cord of neonatal rats. After action potentials had been abolished by tetrodotoxin (TTX, 10(-6) g/ml), small (approximately 0.4 mV) depolarizing potentials occurred spontaneously in motoneurones at low frequencies (approximately 1.5 Hz). These potentials were detectable only after the intracellular Cl- concentration of motoneurones was raised by using KCl electrodes and most of them were blocked by strychnine, suggesting that they are inhibitory post-synaptic potentials (i.p.s.p.s). These spontaneous i.p.s.p.s under TTX are designated as 'miniature i.p.s.p.s' in order to distinguish them from i.p.s.p.s arising from spontaneous impulse activities of interneurones or afferent fibres. The miniature i.p.s.p.s were still observed after Ca2+ in saline was substituted by Mg2+ or Mn2+. In low Ca2+ and high Mg2+ saline, the amplitude distribution of miniature i.p.s.p.s was essentially the same as in normal saline. The frequency of miniature i.p.s.p.s increased when external Ca2+ concentration was raised. The frequency decreased to about 60% of the control when external Ca2+ was substituted by Mg2+ (2-4 mM), whereas it increased to more than 20-fold when substituted by Mn2+ (3-5 mM). When the external K+ concentration was raised, the frequency of miniature i.p.s.p.s under TTX increased non-linearly with the K+ concentration. The maximum slope in the relation between the log frequency and log K+ concentration was about 3.6. When the osmotic pressure was increased by adding sucrose, miniature i.p.s.p.s increased in frequency. The effect of osmotic pressure was relatively mild compared with that reported for the miniature end-plate potentials (e.p.p.s) in the frog. When the temperature was raised, the frequency of miniature i.p.s.p.s increased. The relation between frequency and temperature fitted approximately to a straight line in Arrhenius plot with a Q10 of about 2.6. These characteristics of the miniature i.p.s.p.s closely resemble those of the miniature e.p.p.s. It is concluded that the miniature i.p.s.p.s recorded in motoneurones are equivalent in nature to the miniature e.p.p.s in neuromuscular junctions, thus reflecting the spontaneous release of quantal packages of the inhibitory transmitter.

Action Potentials↗
PubMed1982

Muscarinic synaptic potentials in guinea-pig myenteric plexus neurones.

1. Intracellular recordings were made from neurones in the myenteric plexus of the guinea-pig ileum in vitro. 2. A single pulse stimulus to the presynaptic fibres entering a myenteric ganglion elicited a fast excitatory post-synaptic potential (e.p.s.p.) in type 1 (S) cells: in about one-quarter of cells this was followed by a slow e.p.s.p. 3. The slow e.p.s.p. had a latency of 122 ms and a total duration of 3-15 s. It was reversibly abolished by hyoscine (1 microM). 4. Both the fast e.p.s.p. and the slow e.p.s.p. could be mimicked by ionophoretic application of a single brief pulse of acetylcholine (ACh) to the neurone soma. The depolarization which mimicked the fast e.p.s.p. was reversibly blocked by hexamethonium. The depolarization which mimicked the slow e.p.s.p. was reversibly blocked by hyoscine. 5. Type 2 (AH) neurones did not show fast or slow e.p.s.p.s in response to a single pulse stimulus. Stimuli comprising many pulses (typically 10 Hz for 3 s) evoked a slow e.p.s.p. in which the initial portion was partly blocked by hyoscine, but which was predominantly non-cholinergic.

Acetylcholine↗
PubMed1984

Miniature synaptic potentials recorded intracellularly from Purkinje cell dendrites in guinea pig cerebellar slices.

Intracellular recordings from Purkinje cell dendrites in guinea pig cerebellar slices revealed the existence of miniature spikes with various amplitudes, which were firing apparently without any externally applied stimulations. These spikes were in a hyperpolarizing direction at a resting membrane potential, and their apparent reversal potential was at about -60 mV, indicating their inhibitory nature. Based on the blocking actions of high-Mg2+, tetrodotoxin and amino acid antagonists such as bicuculline etc., these spikes were suggested to be inhibitory synaptic potentials generated by cerebellar interneurons.

Amino Acids↗
PubMed1981

Slow synaptic potentials in AH-type myenteric plexus neurons.

Two types of slow depolarization were recorded in AH-type guinea pig myenteric plexus neurons when the myenteric plexus-longitudinal muscle preparation was stimulated transmurally with external electrodes. One depolarization was associated with a fall and the other with a rise in membrane resistance, the latter type (slow EPSP) being encountered about six times more commonly than the former. In some instances both types of potential were recorded in the same AH neuron. When this occurred the amplitude and duration of the slow EPSP was attenuated if it was timed to occur at about the same time as the other slow synaptic potential.

Animals↗
PubMed1984

Inhibitory miniature synaptic potentials in rat motoneurons.

In the newborn rat spinal cord, spontaneous potentials were recorded, with KCl electrodes, from motoneurons in the presence of tetrodotoxin (10(-6) g ml-1) to abolish nerve impulses. These potentials occurred at low frequencies (less than 2 Hz), and their mean amplitude was a fraction of 1 mV. An increase of osmolarity with sucrose or an increase of extracellular K+, increased the frequency of miniature synaptic potentials. The amplitude of the spontaneous potentials was increased by intracellular injection of Cl-. Strychnine (2-25 microM) completely abolished the spontaneous potentials. It is suggested that these potentials are produced by the spontaneous release of packages of inhibitory transmitter at synapses on motoneurons.

Action Potentials↗
PubMed1999

Fast excitatory post synaptic potentials and their response to catecholaminergic antagonists in rat sympathetic preganglionic neurones in vitro.

In an in vitro slice preparation from neonatal rats intracellular recordings were made from electrophysiologically identified sympathetic preganglionic neurones. Electrical stimulation in the lateral funiculus (>500 microm) from the recording site elicited a mono- or polysynaptic excitatory post synaptic potential. The latter potential was blocked with the dopamine D2 antagonist haloperidol but not with the dopamine D1 antagonist SCH 23390. We therefore report the first showing of a functional descending pathway in an in vitro slice preparation describing both the transmitter and the receptor subtype involved and physiologically show that dopamine may exert an indirect excitatory influence on sympathetic preganglionic neurones possibly via interneurones present in the spinal cord.

Autonomic Fibers, Preganglionic↗
PubMed1980

Slow synaptic potentials in neurones of the myenteric plexus.

1. Intracellular recordings were made in vitro from neurones in the myenteric plexus of the guinea-pig ileum. Potential changes were recorded in response to focal stimulation of the surface of the myenteric ganglion at a distance of 30-100 microM from the impaled cell. 2. Stimuli comprising single pulses evoked cholinergic excitatory post-synaptic potentials ('fast' e.p.s.p.s) in S cells. In a small proportion (20%) of both S and AH cells such stimuli also evoked depolarizing potentials with a time course about 1000 times slower than that of the fast e.p.s.p. 3. Stimuli comprising repeated pulses (up to 20 Hz for 2 sec) evoked the slow depolarizing potentials in a higher proporton of neurones (42%). These stimuli caused a hyperpolarizing potential change in 9% of cells, and in a very few cells biphasic changes i membrane potential were observed. 4. Both the slow depolarizing and the slow hyperpolarizing responses persisted in atropine (up to 5 microM) and hexamethonium (up to 200 microM), but were reversibly abolished by changing to calcium-free solutions. 5. Evidence is presented which suggests that the slow depolarizing response is caused by inactivation of the membrane potassium conductance, and the slow hyperpolarizing response is due to activaton of the potassium conductance.

Animals↗
PubMed1993

Synaptic potentials in the central terminals of locust proprioceptive afferents generated by other afferents from the same sense organ.

Afferent neurons from a proprioceptor [the femoral chordotonal organ (FCO)] at the femoro-tibial joint of a locust hindleg carry patterns of spikes to the CNS in which information is coded about the positions and movements of the tibia. Intracellular recordings from the afferents of this organ as they enter the CNS reveal spikes and depolarizing post-synaptic potentials (PSPs) during voluntary or imposed movements of the joint. Some of these PSPs are generated as a result of spikes in other FCO afferents, and can be evoked experimentally by electrical stimulation of the nerve from the organ. One afferent does not appear to synapse directly on another, but instead activates reliable pathways involving other central neurons. Current clamping of individual afferents in isolated ganglia shows that the PSPs are increased in amplitude by hyperpolarizing currents injected into an afferent, and decreased by depolarizing ones. They reverse at about -68 mV (n = 5). At the normal resting potential of the afferents, -72 mV (+/- 0.42 SE, n = 57), the PSPs are therefore depolarizing, and are associated with an increased conductance of the membrane. The changes in membrane potential and conductances associated with the PSPs can be mimicked by pressure injection of GABA into the regions of neuropil that contain the terminals of the afferents. The potential evoked by GABA is associated with an increased conductance of the membrane and reverses at the same potential as the PSPs. GABA also reduces the PSPs evoked in the terminals, either by movements of the FCO or by electrical stimulation of its nerve. The PSPs and the effects of the GABA-evoked potentials are mimicked by the GABA agonist muscimol. The PSPs are blocked reversibly by picrotoxin. The PSPs and the GABA-evoked potentials both alter the excitability of an afferent terminal by reducing the ability of the membrane to support an action potential. It is suggested that the PSPs are depolarizing, inhibitory potentials generated in the terminals of the afferents by central neurons that release GABA, and that their role is to change the efficacy of the afferent spikes at their first output synapses in the CNS. These interactions could form a graded, gain control mechanism for synaptic transmission at the afferent output synapses that is directly dependent on the features of the mechanical movements of the joint.

Action Potentials↗