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At least 217 records · Page 12Linked to original sources
PubMed1985

Inhibitory synaptic potentials resulting from alpha 2-adrenoceptor activation in guinea-pig submucous plexus neurones.

Intracellular recordings were obtained from neurones of the guinea-pig submucous plexus. Inhibitory synaptic potentials (i.p.s.p.s) were compared with hyperpolarizations evoked by brief, local applications of noradrenaline and by superfusion with adrenoceptor agonists. Hyperpolarizing potentials elicited by brief applications of noradrenaline were similar to the i.p.s.p. in latency of onset, amplitude, time course, conductance increase, reversal potential and ionic dependence. Both responses were blocked by low concentrations of Ba2+ and quinine. 6-hydroxydopamine selectively and irreversibly abolished the i.p.s.p. and resulted in a complete loss of catecholamine fluorescent nerve fibres in the submucous plexus. The alpha 2-adrenoceptor antagonists, phentolamine, yohimbine and RX781094, reversibly blocked the i.p.s.p. and the noradrenaline hyperpolarization. Prazosin, propranolol, atropine and naloxone had no effect on these responses. Superfusion with noradrenaline and clonidine produced dose-dependent membrane hyperpolarizations. Noradrenaline and clonidine dose-hyperpolarization curves were shifted to the right in a parallel fashion by alpha 2-adrenoceptor antagonists. Determination of the dissociation equilibrium constants for phentolamine, yohimbine and RX781094 showed that the hyperpolarization produced by noradrenaline perfusion is due to alpha 2-adrenoceptor activation. It is concluded that the release of noradrenaline from sympathetic nerves activates post-synaptic alpha 2-adrenoceptors, resulting in the K+ conductance increase which underlies the i.p.s.p. in submucous plexus neurones.

Action Potentials↗
PubMed1998

Expression of a dominant negative TrkB receptor, T1, reveals a requirement for presynaptic signaling in BDNF-induced synaptic potentiation in cultured hippocampal neurons.

We have developed a method to analyze the relative contributions of pre- and postsynaptic actions of a particular gene product in neurons in culture and potentially in slices using adenovirus-mediated gene transfer. A recombinant virus directed the expression of both a GFP reporter protein and TrkB.T1, a C-terminal truncated dominant negative TrkB neurotrophin receptor. When expressed in the presynaptic cell at synapses between embryonic hippocampal neurons in culture, the dominant negative TrkB.T1 inhibited two forms of synaptic potentiation induced by the neurotrophin brain-derived neurotrophic factor (BDNF): (i) greater evoked synaptic transmission and (ii) higher frequency of spontaneous miniature synaptic currents. These inhibition effects are not seen if the transgene is expressed only in the postsynaptic cell. We conclude that BDNF-TrkB signal transduction in the presynaptic terminal leads to both types of potentiation and is therefore the primary cause of synaptic enhancement by BDNF in these neurons.

Animals↗
PubMed2006

Age-related effects of the neuromodulator D-serine on neurotransmission and synaptic potentiation in the CA1 hippocampal area of the rat.

The effects of the co-agonist of the N-methyl-D-aspartate receptor (NMDAr) D-serine on glutamatergic neurotransmission and synaptic potentiation were studied in the CA1 hippocampal field of young (3-5 months old) and aged (25-27 months old) Sprague-Dawley rats using ex vivo extracellular electrophysiological recording techniques. Exogenous d-serine depressed fast neurotransmission mediated by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate subtype of glutamate receptors in young but not in aged rats by acting on inhibitory glycinergic interneurons. In contrast, D-serine dose-dependently enhanced NMDAr-mediated synaptic responses in both groups of animals, but with a larger magnitude in aged rats, thus preventing the age-related decrease in NMDAr activation. D-serine also increased the magnitude of long-term potentiation in aged but not in young rats. Finally, D-serine levels were dramatically reduced in hippocampal tissues of aged rats. Taken together, these results indicate a weaker activation of the NMDAr glycine modulatory site by endogenous D-serine in aged animals, which accounts for a reduced NMDAr contribution to synaptic plasticity in ageing.

Aging↗
PubMed1987

Postganglionic stimulation activates synaptic potentials in cat bladder parasympathetic neurons.

Responses elicited by stimulating the pre-versus postganglionic nerves were compared in cat bladder parasympathetic neurons. We observed that synaptic potentials recorded on stimulating the postganglionic nerve trunk were different from those elicited with preganglionic nerve stimulation. These findings suggest that local neuronal interactions occur within bladder parasympathetic ganglia and may play a physiological role in the neuronal integration in bladder ganglia.

Animals↗
PubMed1983

Localization of monosynaptic Ia excitatory post-synaptic potentials in the motor nucleus of the cat biceps femoris muscle.

Evidence is presented for the existence of a localization of monosynaptic Ia excitatory post-synaptic potentials (e.p.s.p.s) in the motor nucleus of a cat hind limb muscle. Intracellular recordings from biceps femoris motoneurones were made in anaesthetized low spinal cats of the effects of stimuli to the nerve branches supplying the anterior, middle, and posterior portions of the biceps femoris muscle. Recordings were also made during stimulation of nerves to semimembranosus and semitendinosus in order to provide a means of categorizing middle biceps cells as 'extensors' (middle biceps-extensor; i.e. like anterior biceps cells) or as 'flexors' (middle biceps-flexor; like posterior biceps). Homonymous nerve-branch (i.e. from anterior, middle or posterior biceps) monosynaptic Ia e.p.s.p.s were compared within unifunctional (flexor or extensor) groups of motoneurones. In three of four comparisons (anterior biceps nerve branch onto anterior and middle biceps-extensor cells, middle biceps onto middle biceps-flexor and posterior biceps, posterior biceps onto middle biceps-flexor and posterior biceps) the anterior, middle and posterior biceps nerve branches contributed larger e.p.s.p.s to their 'own' motoneurones than to motoneurones supplying other 'compartments' of the muscle. In the fourth case, middle biceps's input appeared to have similar effects onto anterior biceps and middle biceps-extensor cells. A normalization was performed to eliminate the possibility that the differences in e.p.s.p. sizes were due to differences in cell type within the four cell groupings (i.e. differences in the number of cells supplying FF, F(int.), FR and S muscle units). This normalization confirmed that the localization in the first three comparisons was not a consequence of differences in motoneurone type and, in addition, suggested that middle biceps may indeed have greater effects on middle biceps-extensor than anterior biceps cells. In addition to the asymmetrical effects of anterior and middle biceps nerve branches onto anterior biceps and middle biceps-extensor motoneurones, it was shown that while semitendinosus and posterior biceps contributed larger e.p.s.p.s to middle biceps-flexor than to middle biceps-extensor cells, the anterior biceps nerve branch and semimembranosus nerve contributed equally to the two middle biceps groups. Analysis of cell location in the spinal cord and rostro-caudal differences in group I volley sizes gave evidence of a topographic organization of the biceps femoris motor nucleus which could contribute to the observed localization. However, localization was also evident when comparing e.p.s.p. amplitudes in pairs of neighbouring cells of different category, indicating a role for neuronal recognition factors.

Action Potentials↗
PubMed1985

Partitioning of monosynaptic Ia excitatory post-synaptic potentials in the motor nucleus of the cat semimembranosus muscle.

In anaesthetized low-spinal cats, intracellular recordings were made of the Ia excitatory post-synaptic potential (e.p.s.p.) responses of semimembranosus motoneurones to electrical stimulation (Group I range) of nerve branches supplying the anterior and posterior heads of semimembranosus, the anterior and posterior parts of biceps femoris, and the distal part of semitendinosus. Recordings were also made during stimulation of nerves to the gracilis muscle and to the vasti muscle group. Stimulation of the semimembranosus-anterior nerve branch produced Ia e.p.s.p.s. of greater amplitude in semimembranosus-anterior motoneurones than in semimembranosus-posterior cells; likewise, stimulation of the semimembranosus-posterior nerve branch produced larger e.p.s.p.s. in cells which supplied the posterior head than in those which supplied the anterior head. Stimulation of the nerve branches to components of two 'flexor' muscles (Sherrington, 1910), biceps-posterior and semitendinosus-distal, produced larger e.p.s.p.s in semimembranosus-posterior cells than in the anterior motoneurones. A tendency was found for stimulation of the nerve to biceps femoris-anterior (an 'extensor') to produce larger e.p.s.p.s in semimembranosus-anterior than in-posterior motoneurones. However, this effect was of borderline (0.06 greater than P greater than 0.05) significance. The limited monosynaptic input produced by stimulation of the nerves to the gracilis and vasti muscles showed that their Ia axons do not distinguish between the two semimembranosus cell groups. A slight topographic organization of motoneurones within the semimembranosus motor nucleus was found, with anterior cells encountered, on average, at a more rostral level of the spinal cord than posterior cells. A similar topographic arrangement was observed in the rostrocaudal distribution of Group I afferent fibres in the dorsal roots and motor axons from the two sets of motoneurones in the ventral roots. These findings are consistent with 'location specificity' (Scott & Mendell, 1976) being a factor which contributes to the observed pattern of homonymous Ia connexions. A role for 'species specificity' (Scott & Mendell, 1976) in determining the observed pattern of homonymous Ia connexions was indicated by species-dependent differences in e.p.s.p. amplitude in pairs of semimembranosus-anterior and -posterior motoneurones at similar rostrocaudal locations in the spinal cord. The pattern of heteronymous connexions to the semimembranosus motor nucleus also showed evidence for species specificity. However, no clear topographic pattern was evident in these connexions.

Action Potentials↗
PubMed1981

Effects of stimulation on the multiquantal spontaneous synaptic potentials in guinea pig hypogastric ganglia.

Loss frequency (0.5-2 Hz) stimulation of the preganglionic nerve produced calcium ion (Ca2+)-dependent increases in the frequency of spontaneous synaptic potentials recorded from guinea-pig hypogastric ganglion cells. The increased frequency was accompanied by a marked increase in the proportion of multiquantal spontaneous potentials and this was also dependent on extracellular Ca2+. The latter effect was interpreted as an increase in the degree of bursting within the spontaneous release process, supporting the hypothesis that the bursting is related to the cytoplasmic Ca2+ concentration.

Animals↗
PubMed2000

Electrical properties and synaptic potentials of rabbit pancreatic neurons.

Pancreatic ganglia receive innervation from a wide variety of extrinsic nerves and supply the predominant innervation to pancreatic acini, islets, and ducts. This study used intracellular recordings to investigate the electrical properties and synaptic potentials of rabbit pancreatic neurons. Neurons had a mean resting membrane potential of -54+/-0.4 mV and generated action potentials with a mean overshoot of 10+/-0.4 mV and a mean after-spike hyperpolarization (ASH) of 11+/-0.5 mV with duration of 210+/-19 ms. Action potentials exhibited a high threshold (-15+/-1 mV) for intracellular stimulation and a phasic firing pattern was observed in response to prolonged depolarizing currents. Stimulation of attached nerve bundles evoked multiple fast excitatory postsynaptic potentials (fEPSPs) which were abolished by hexamethonium in 75% of neurons, while a non-cholinergic fEPSP was observed in 25% of the neurons. Repetitive stimulation (3-30 Hz) evoked muscarinic slow EPSPs with a mean amplitude of 8+/-2 mV and duration of 5+/-1 s in a small subset (21%) of neurons. Exogenous muscarine evoked a mean slow depolarization of 10+/-1 mV amplitude in 22% of neurons tested. Following repetitive nerve stimulation non-cholinergic late, slow EPSPs with a mean amplitude of 4.3+/-0.4 mV were recorded in 32% of neurons. Nicotinic transmission was subject to inhibition mediated by presynaptic muscarinic receptors at low (0.5 Hz) stimulus frequencies in 80% of neurons. At higher frequencies (> or =1 Hz), either facilitation or depression of nicotinic transmission was observed depending on the ganglion studied. A population (9%) of neurons exhibited spontaneous, low-amplitude pacemaker-like potentials. Spontaneous fEPSPs and action potentials were also observed and these occasionally occurred in rhythmically timed bursts. Thus, distinct subpopulations of pancreatic neurons could be identified on the basis of both their intrinsic electrical properties and the receptors mediating and/or modulating synaptic transmission. These neurons function as critical sites of integration for synaptic input from extrinsic pancreatic nerves and thereby determine the postganglionic firing patterns presented to the pancreatic exocrine and endocrine secretory cells.

Animals↗
PubMed2006

Timing is essential for rapid effects of corticosterone on synaptic potentiation in the mouse hippocampus.

Stress facilitates memory formation, but only when the stressor is closely linked to the learning context. These effects are, at least in part, mediated by corticosteroid hormones. Here we demonstrate that corticosterone rapidly facilitates synaptic potentiation in the mouse hippocampal CA1 area when high levels of the hormone and high-frequency stimulation coincide in time, but not when corticosterone is given either before or after repetitive stimulation. This effect could not be blocked by antagonists of the mineralocorticoid receptor and glucocorticoid receptor (spironolactone and RU 38486, respectively). These data provide a biological substrate for the important behavioral observation that stress and corticosteroid hormones can facilitate learning and memory processes.

Analysis of Variance↗
PubMed1993

Enhancement of NMDA receptor-mediated synaptic potential by isoproterenol is blocked by Rp-adenosine 3',5'-cyclic monophosphothioate.

The intracellular mechanisms underlying the facilitatory action of isoproterenol (Iso) on the NMDA receptor-mediated synaptic potential (EPSPNMDA) was investigated in an in vitro slice preparation of rat amygdala. Intracellular recordings were made from basolateral amygdala neurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and picrotoxin (50 microM) which block non-NMDA and GABAA receptors, respectively. Superfusion of Iso (15 microM) produced a sustained increase in EPSPNMDA. Rp-adenosine-3',5'-cyclic monophosphotioate (Rp-cAMPS), a potent inhibitor of protein kinase A (PKA) alone decreased the amplitude of EPSPNMDA below baseline values and prevented the subsequent potentiation by Iso. Forskolin, a direct activator of adenylate cyclase, mimics the effect of Iso, and Rp-cAMPS also reversed forskolin-induced enhancement of EPSNMDA. These results suggest that cAMP-dependent protein kinase mediates the enhancement of EPSPNMDA by Iso in the amygdala.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1987

Spontaneous synaptic potentials in dopamine-denervated neostriatal neurons.

Intracellular spontaneous activity was recorded in neostriatal slices from rats with 6-hydroxydopamine-induced lesion of the left nigrostriatal dopaminergic system. Recordings were made at different times after denervation. Dopaminergic denervation caused the appearance of spontaneous synaptic potentials, which were present even after 8 months. The results suggest a tonic inhibitory influence of the dopaminergic innervation on the synaptic input of neostriatal neurons.

Action Potentials↗
PubMed1985

Gamma-aminobutyric acid uptake and the termination of inhibitory synaptic potentials in the rat hippocampal slice.

Intracellular recordings were made from CA1 pyramidal cells in the rat hippocampal slice to study the processes that influence the time course of inhibitory post-synaptic potentials (i.p.s.p.s) mediated by gamma-aminobutyric acid (GABA), and conductance changes evoked by ionophoretically applied GABA. The GABA-uptake inhibitors, nipecotic acid and cis-4-OH-nipecotic acid (1 mM), greatly prolonged conductance increases associated with both hyperpolarizing and depolarizing responses to ionophoretically applied GABA. In contrast to their effects on GABA-evoked conductances, uptake inhibitors only slightly prolonged antidromically evoked i.p.s.p.s. Their primary effect occurred after the i.p.s.p. had decayed to 5-30% of its peak. 4-OH-isonipecotic acid, a nipecotic acid analogue that does not inhibit GABA uptake, did not prolong i.p.s.p.s or ionophoretically evoked conductance changes. Sodium pentobarbitone (100 microM), a drug that prolongs the open time of GABA-activated chloride channels, potentiated both i.p.s.p.s and responses to ionophoretically applied GABA. Whereas pentobarbitone also prolonged i.p.s.p.s, it did not prolong responses to ionophoretically applied GABA. The prolongation of i.p.s.p.s by pentobarbitone occurred equally in both the early and late phases of the i.p.s.p., in contrast to the effects of GABA-uptake inhibitors. I.p.s.p.s did not usually decay exponentially. The observation that uptake inhibitors prolonged the late but not the early decay phase of the i.p.s.p., together with the previous finding that the conductance change persists for the duration of the i.p.s.p., indicate that GABA is present in the synapse throughout much of the i.p.s.p. These data suggest that diffusion of GABA out of the synapse, a non-exponential process, is an important determinant of the i.p.s.p. decay time course. Increasing the extracellular potassium concentration from 3.5 to 8.5 mM resulted in spontaneously occurring, synchronous burst firing of pyramidal cells. Cis-4-OH-nipecotic acid significantly reduced the number and amplitude of extracellularly recorded population spikes within each burst. We conclude that diffusion, channel open time and GABA uptake all influence the time course of GABA-mediated i.p.s.p.s. The time course of a single, brief i.p.s.p. is determined predominantly by post-synaptic channel kinetics and diffusion of GABA out of the synapse, whereas the inhibition produced by prolonged synaptic bursts or relatively long application of exogenous GABA can be markedly influenced by GABA uptake.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2004

Neuroprotective effects of melatonin against anoxia/aglycemia stress, as assessed by synaptic potentials and superoxide production in rat hippocampal slices.

Melatonin, which plays an important role in circadian rhythm regulation, is highly potent endogenous free radical scavenger and antioxidant. To clarify the neuroprotective effects of melatonin as a free radical scavenger, we recorded changes in synaptic potentials and monitored the generation of superoxide (O)(2)(-) (using hydroethidine) in the CA1 pyramidal layers of rat hippocampal slices exposed to anoxia/aglycemia ('ischemic') stress. Synaptic responses evoked by stimulation of Schaffer collateral/commissural afferents were suppressed by ischemic stress. When the duration of the stress was 8 min, the suppression was reversible, irrespective of the presence or absence of melatonin treatment, while the amount of O(2)(-) generated was reduced by the presence of melatonin. When stress duration was 12 min, the suppression of synaptic responses lasted more than 90 min, but melatonin significantly improved the recovery. The amount of O(2)(-) generated in the 'recirculation' phase after a 12 min ischemic stress was less in the ischemic alone group than in the melatonin-treated group. This probably reflects that the number of viable cells with the ability to generate O(2)(-) had been reduced by the more severe ischemic stress. Other radical scavengers (ascorbic acid and alpha-tocopherol) had similar effects. These results show that melatonin has the potential to protect the functions of neurons against an ischemic insult by reducing O(2)(-) generation.

Animals↗
PubMed1989

Serotonin agonists inhibit synaptic potentials in the rat locus ceruleus in vitro via 5-hydroxytryptamine1A and 5-hydroxytryptamine1B receptors.

Intracellular recordings were made from rat locus ceruleus neurons in the slice preparation in vitro. Depolarizing synaptic potentials (DSP)2 elicited by electrical stimulation were typically 10 to 15 mV in amplitude and 200 msec in duration. Superfusion with 5-hydroxytryptamine (5-HT, serotonin) or the 5-HT1 receptor agonist 5-carboxamidotryptamine (5-CT), produced an inhibition of the DSP. The maximal inhibition was 55 +/- 2% (mean +/- S.E.M.). The EC50 for 5-CT was 60 nM, whereas for 5-HT it was 12 microM. Cocaine (10 microM) shifted the 5-HT concentration-response curve to the left and the EC50 to 320 nM. 8-Hydroxy-2-(di-n-propylamino)tetralin, a selective 5-HT1A receptor ligand, also inhibited the DSP, but only produced about 65% of the maximal 5-CT or 5-HT response (EC50 = 50 nM). A relatively selective 5-HT1B ligand (65-fold 5-HT1B greater than 5-HT1A), 1-(m-trifluoromethyl-phenyl)-piperazine, acted as a full agonist (EC50 = 110 nM). None of these compounds had any effects on the membrane properties of the cell at the doses tested. The response to 8-hydroxy-2-(di-n-propylamino) tetralin was antagonized by pretreatment with the 5-HT1A antagonist spiperone (1 microM). The estimated KD for spiperone was 16 nM. At this same concentration, however, there was no effect on the 5-CT-induced inhibition. The antagonist 4-(3-ter-butyl-amino-2-hydroxy-propoxyl)-indol-2-carbonic acid isopropyl ester (LM 21-009, 100 nM) was found to be a partial agonist producing a 26 +/- 4% inhibition of the DSP.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Paired-pulse depression of the N-methyl-D-aspartate receptor-mediated synaptic potentials in the amygdala.

1. An in vitro slice preparation of rat amygdala was used to study the paired-pulse depression of the N-methyl-D-aspartate (NMDA) receptor-mediated synaptic potential e.p.s.p.NMDA. 2. The e.p.s.p.NMDA was isolated pharmacologically by applying a solution containing the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the gamma-aminobutyric acidA (GABAA) blocker picrotoxin and increasing the stimulus intensity. 3. When two stimuli of identical strength were applied in close succession, the second e.p.s.p.NMDA was depressed. This paired-pulse depression was seen with interstimulus intervals of between 100 ms and 2000 ms; the maximal depression was observed at interval of 200 ms. 4. Superfusion of phaclofen or 2-hydroxy-saclofen inhibited the paired-pulse depression indicating the involvement of GABAB receptors. 5. Bath applications of Ba2+ or intracellular injection of Cs+ to block post- but not presynaptic GABAB receptors failed to inhibit the paired-pulse depression (PPD). 6. Incubation of slices with pertussis toxin prevented the postsynaptic hyperpolarization induced by baclofen. The PPD of e.p.s.p.NMDA, however, was not affected by pertussis toxin treatment. 7. These results suggest that GABA released by the first stimulus acts on GABAB receptors to suppress the second e.p.s.p.NMDA via mechanisms other than activation of a postsynaptic GABAB receptor-coupled K+ conductance.

Amygdala↗
PubMed1998

Duration of NMDA-dependent synaptic potentiation in piriform cortex in vivo is increased after epileptiform bursting.

Stimulation of afferent fibers with current pulse trains has been reported to induce long-term potentiation (LTP) in piriform cortex in vitro but not in vivo. LTP has been observed in vivo only when trains are paired with behavioral reinforcement and as a consequence of kindled epileptogenesis. This study was undertaken in the urethan-anesthetized rat to determine if the reported failures to observe pulse-train evoked LTP in vivo may be related to a lesser persistence rather than lack of occurrence, if disinhibition might facilitate induction, and to examine the nature of the relationship between seizure activity and LTP. Stimulation of afferent fibers in the lateral olfactory tract with theta-burst trains under control conditions potentiated the monosynaptic field excitatory postsynaptic potential (EPSP) by approximately the same extent (20.3 +/- 2%; n = 12) as reported for the slice. However, in contrast to the slice, potentiation in vivo decayed to a low level within 1-2 h after induction (70% loss in 1.5 h, on average). The N-methyl--aspartate (NMDA)-receptor antagonists -APV and MK-801 blocked the induction of this decremental potentiation. Pharmacological reduction of gamma-aminobutyric acid-mediated inhibition at the recording site did not increase the duration of potentiation. In contrast, theta-burst stimulation applied after recovery from a period of epileptiform bursting induced stable NMDA-dependent potentiation. Mean increase in the population EPSP was approximately the same as under control conditions (21 +/- 2%; n = 6), but in five of six experiments there was little or no decay in potentiation for the duration of the monitoring period (</=6 h). It is concluded that seizure activity has an enabling action on the induction of persistent synaptic potentiation by stimulus trains that bypasses the need for behavioral reinforcement.

2-Amino-5-phosphonovalerate↗