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PubMed1983

Effects of excitatory amino acids and their antagonists on membrane and action potentials of cat caudate neurones.

The electrical activity of caudate neurones was recorded with intracellular electrodes in halothane anaesthetized cats. Agonists and antagonists of excitatory amino acid receptors were applied by micro-ionophoresis and their effects on membrane- and action potentials and on cortically evoked synaptic potentials evaluated. The agonists, L-aspartate (asp), L-glutamate (glu), N-methyl-DL-aspartate (NMA), quinolinate and quisqualate all depolarized the membrane, caused repetitive firing, reduced the apparent amplitude of the cortically evoked excitatory post-synaptic potentials (e.p.s.p.s) and increased the amplitude of the associated inhibitory post-synaptic potential. Two of the agonists, NMA and quinolinate, additionally caused the appearance of up to 500 ms long depolarizations (plateaus) on the falling phase of action potentials. These plateaus were seen in about two-thirds of the cells in this sample while in the other third the excitatory effects of NMA and quinolinate were indistinguishable from those of glu and quisqualate. The N-methyl-D-aspartate (NMDA) receptor antagonist D-alpha-aminoadipate (DAA) reversibly inhibited the effects of NMA and quinolinate but only on those cells where these two agents evoked action potential plateaus while on the same cells the effects of asp, glu and quisqualate were either only weakly antagonized or not affected. On cells not displaying plateaus to NMA or quinolinate none of the effects of the agonists could be antagonized by DAA. DAA applications that completely antagonized the effects of NMA never reduced the amplitudes of cortically evoked e.p.s.p.s. Cis-2,3-piperidine dicarboxylate also blocked the effects of NMA and asp at low application currents while at higher currents it enhanced the effects of glu or asp although still retaining its NMA antagonistic activity. High-frequency stimulation of the cortico-caudate pathway resulted in long-lasting depolarizations and repetitive firing, but plateaus of the type caused by NMA or quinolinate were not seen.

2-Aminoadipic Acid↗
PubMed1960

Integrative synaptic mechanisms in the caudal ganglion of the crayfish.

A study of activity recorded with intracellular micropipettes was undertaken in the caudal abdominal ganglion of the crayfish in order to gain information about central fiber to fiber synaptic mechanisms. This synaptic system has well developed integrative properties. Excitatory post-synaptic potentials can be graded, and synaptic potentials from different inputs can sum to initiate spike discharge. In most impaled units, the spike discharge fails to destroy the synaptic potential, thereby allowing sustained depolarization and multiple spike discharge following single pulse stimulation to an afferent input. Some units had characteristics which suggest a graded threshold for spike generation along the post-synaptic fiber membrane. Other impaled units responded to afferent stimulation with spike discharges of two distinct amplitudes. The smaller or "abortive" spikes in such units may represent non-invading activity in branches of the post-synaptic axon. On a few occasions one afferent input was shown to inhibit the spike discharge initiated by another presynaptic input.

Animals↗
PubMed1986

Synaptic inputs to immunohistochemically identified neurones in the submucous plexus of the guinea-pig small intestine.

1. Electrophysiological recordings were made from neurones in the submucous plexus of the guinea-pig small intestine, and these neurones were classified according to their synaptic inputs. 2. The neurones from which recording were made were filled during the recording period with the fluorescent dye, Lucifer Yellow, so they could be re-identified after processing for immunohistochemical localization of vasoactive intestinal peptide (VIP). 3. The presence or absence of VIP-like immunoreactivity was determined for a total of 130 neurones whose synaptic inputs had been fully characterized and eighty-two were found to be VIP reactive. After the VIP reactivity had been assessed, the preparations were reprocessed to reveal immunoreactivity for neuropeptide Y (NPY) and a further twenty-three neurones (none of which were reactive for VIP) were found to be reactive for this peptide. Of the remaining twenty-five neurones, nineteen were not reactive for either VIP or NPY and six could not be re-identified after reprocessing. 4. Electrical stimulation of internodal strands evoked excitatory synaptic potentials lasting 20-30 ms (fast responses) in all but one of the 130 neurones studied. 5. Almost all the VIP-reactive neurones (seventy-eight of eighty-two cells) exhibited inhibitory synaptic potentials, ranging in amplitude from 2 to 30 mV and lasting 150-1500 ms, but few of the VIP-negative neurones had such responses (six of forty-eight cells). No inhibitory synaptic potentials could be evoked in any of the NPY-reactive neurones. 6. Most VIP-reactive neurones (sixty-nine) had a slow excitatory synaptic potential which could be evoked by a single stimulus, lasted 5-20 s and was associated with an increase in input resistance. Only one NPY-reactive neurone had a slow excitatory potential, but such potentials were seen in nine of the nineteen VIP-negative, NPY-negative neurones. 7. In nine of the twenty-three NPY-reactive neurones a single stimulus evoked an excitatory synaptic potential (intermediate excitatory synaptic potential) lasting 500-1500 ms and associated with a fall in the input resistance. None of the VIP-negative, NPY-negative neurones exhibited the intermediate excitatory potentials but it was not possible to determine whether such potentials could be evoked in VIP-reactive neurones because the inhibitory synaptic potentials would obscure such events. 8. It is concluded that neurochemically distinct populations of submucous neurones can be distinguished physiologically on the basis of the differing combinations of types of synaptic input they receive.

Action Potentials↗
PubMed2001

Brain-derived neurotrophic factor induces long-lasting potentiation of synaptic transmission in visual cortex in vivo in young rats, but not in the adult.

Brain-derived neurotrophic factor (BDNF) rapidly enhances excitatory synaptic transmission in cortical slices. To date, however, a question of how long such an action persists remains unanswered as it is hard to record synaptic responses longer than several hours in slice preparations. To address this question and to investigate possible age-dependency of the action, we analysed effects of a brief application of BDNF and nerve growth factor (NGF) on field potentials of visual cortex in rats of postnatal days 13-17 and 19-24 and in the adulthood for 10-24 h. Evoked potentials to stimulation of the lateral geniculate nucleus were recorded simultaneously from two cortical sites into which the neurotrophin and control solution were injected. An application of BDNF induced a slowly developing increase in the field potential amplitude in young rats. The amplitude attained a plateau level 3-4 h after the infusion; 139 +/- 26% (mean +/- SD) and 132 +/- 21% of the baseline in the rats at P13-17 and P19-24, respectively. This potentiation remained stable from 4 to 8 h, then gradually decreased to the baseline 15-16 h after the infusion. NGF applied in the same way did not induce potentiation. An inhibitor of BDNF receptors blocked the potentiation when it was applied immediately after the BDNF application, but was not effective about 2 h later. In the adults, BDNF did not potentiate field potentials. These results indicate that BDNF induces synaptic potentiation lasting for several hours only in the developing cortex through processes downstream of receptor activation.

Aging↗
PubMed1994

Inhibition by opioids acting on mu-receptors of GABAergic and glutamatergic postsynaptic potentials in single rat periaqueductal gray neurones in vitro.

1. Membrane properties of rat periaqueductal gray neurones were investigated by use of intracellular recordings from single neurones in brain slices. Morphological properties and anatomical location of each impaled neurone were characterized by intracellular staining with biocytin. The present paper considers the properties of electrically-evoked and spontaneous postsynaptic potentials impinging on periaqueductal gray neurones, and the actions of opioids on postsynaptic potentials in neurones which were not directly hyperpolarized by opioids. The preceding paper considers neurones which were hyperpolarized by opioids. 2. Electrical stimulation in the vicinity of impaled neurones evoked postsynaptic potentials having fast (duration at half-maximal amplitude 37 +/- 2 ms, n = 65) and in some cases slow (duration at half-maximal amplitude 817 +/- 187 ms, n = 3) components. Amplitudes of evoked potentials were dependent on stimulus voltage, membrane potential, and were abolished during superfusion with solutions containing tetrodoxotoxin (100 nM to 1 microM, n = 5) or Co2+ (4 mM, n = 2). 3. Fast postsynaptic potentials were mediated predominantly by activation of glutamate and GABAA receptors. The GABAA-receptor antagonist, bicucuilline (30 microM), inhibited postsynaptic potentials by 44 +/- 8% (n = 14). The non-NMDA-receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM), inhibited postsynaptic potentials by 48 +/- 6% (n = 16). Combined superfusion of bicuculline (30 microM) and 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM) inhibited postsynaptic potentials by 93 +/- 1% (n = 8). Additional superfusion of the NMDA-receptor antagonist, (+/-)-2-amino-5- phosphonovaleric acid (50 microM) inhibited synaptic potentials by 94 +/- 1% (n = 3). 5. Selective micro-receptor agonists inhibited fast postsynaptic potentials in all neurones tested which were not directly hyperpolarized by opioids. Met-enkephalin (30 micro M) and Tyr-D-Ala-Gly-MePhe-Glyol (3 microM)inhibited postsynaptic potentials by 53 +/- 3% and 49 +/- 3%, respectively. This effect was completely antagonised by naloxone (1 micro M, n = 3). A small inhibition produced by the selective delta-receptor agonist,Tyr-D-Pen-Gly-Phe-D-Pen-enkephalin (3 micro M, 26 +/- 4%, n = 14), was antagonized by naloxone (1 micro M), but not by the selective delta-receptor antagonist, naltrindole (10 nM), suggesting non-specific micro-receptor activation by this agonist. The selective K-receptor agonist, U50488H (3 micro M), also consistently inhibited postsynaptic potentials by 45 +/- 15% (n = 4). However, this effect was not fully reversed by naloxone(1 micro M) suggesting a non-specific action.6. Both glutamatergic and GABAergic components of fast postsynaptic potentials were inhibited by Met-enkephalin (10 or 30 micro M). Met-enkephalin inhibited postsynaptic potentials by 55 +/- 5% (n = 12) in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM, predominantly GABAergic component).Met-enkephalin did not affect the response to GABA applied directly by pressure ejection, indicating that opioids exclusively inhibited presynaptic release of GABA. Met-enkephalin (10-30 micro M) inhibited postsynaptic potentials by 48 +/- 6% (n = 11) in the presence of bicuculline (30 micro M, predominantly glutamatergic component). In the presence of both bicuculline and 6-cyano-7-nitroquinoxaline-2,3-dione,Met-enkephalin inhibited the small residual component of the synaptic potential by 42 +/- 15% (n = 2).7. Frequent spontaneous synaptic potentials were also observed in 11% (10/94) of the neurones which were not directly hyperpolarized by opioids. These were reversibly abolished by bicuculline (30 micro M,n = 5) and substantially inhibited by Met-enkephalin (30 micro M, n = 6), but were unaffected by 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM, n = 2).8. In conclusion, fast glutamatergic and GABAergic synaptic potentials were evoked by electrical stimulation throughout the lateral and ventrolateral periaqueductal gray. Slow inhibitory synaptic potentials were also evoked in some neurones. Opioids acting on micro-receptors inhibited both GABAergic and glutamatergic components of synaptic potentials throughout this brain region.

Amino Acid Sequence↗
PubMed1984

The electrical properties of neurones of the rat suprachiasmatic nucleus recorded intracellularly in vitro.

Stable intracellular recordings were obtained from 22 suprachiasmatic neurones in isolated brain slices. These cells were characterized by resting potentials of about -60 mV, high input resistances, relatively short time constants and action potentials of short duration. The action potentials were preceded by a slow depolarization and followed by a relatively brief afterhyperpolarization and long-lasting increase in membrane conductance. Current-voltage relations were usually linear between 0 and 80 mV negative to the resting potential. Postsynaptic potentials were evoked in these cells by electrical stimulation of the optic chiasm or contralateral suprachiasmatic nucleus. Both excitatory postsynaptic potentials, which evoked action potentials, and inhibitory postsynaptic potentials were recorded. Synaptic potentials were associated with an increase in membrane conductance. Action potentials evoked by synaptic activation were sometimes followed by up to three small, fast potentials. Small fast potentials were not seen to occur spontaneously, or to follow spontaneous, or current-evoked spikes, nor were they evoked by synaptic potentials that failed to evoke action potentials. The suprachiasmatic nucleus is essential for the generation of normal biological rhythms in mammals. The input it receives from the optic nerve is thought to be important in this role. It is hoped that these preliminary intracellular studies will form a basis for further work on the inherent properties of suprachiasmatic neurones and their responses to visual input.

Animals↗
PubMed1990

Opioid actions on single nucleus raphe magnus neurons from rat and guinea-pig in vitro.

1. Intracellular recordings were made from neurons of the nucleus raphe magnus (NRM) from rat (n = 128) and guinea-pig (n = 115). Two types of cells were found in each, primary (103 in rat, 27 in guinea-pig) and secondary cells (25 in rat, 88 in guinea-pig). 2. Primary cells had input resistances of 186 +/- 9 M omega (n = 9) in rat and 255 +/- 50 M omega (n = 11) in guinea-pig. The action potential in each was about 1.5 ms in duration. Synaptic potentials were evoked by focal electrical stimulation and consisted of both gamma-aminobutyric acid (GABA) and excitatory amino acid components. 3. Morphine, [Met5]enkephalin (ME) and [D-Ala2,N-Me-Phe4, Gly5-ol]enkephalin (DAMGO) depressed the amplitude of the GABA-mediated synaptic potential by a maximum of 50-65% and had little effect on the excitatory amino acid-mediated synaptic potential. There was no effect of these opioids on the resting membrane potential or input resistance of primary cells in rat or guinea-pig. 4. Secondary cells had short duration action potentials (less than 1 ms) and an input resistance of 354 +/- 47 M omega in rat (n = 6) and 290 +/- 40 M omega in guinea-pig (n = 15). The synaptic potential observed in the cells of this group was mediated by activation of only excitatory amino acid receptors. 5. ME hyperpolarized and/or abolished the spontaneous firing in sixteen out of twenty-four neurons in the secondary group from rat and eight out of eighty-four neurons from guinea-pig. ME induced an outward current at -60 mV that reversed polarity at potentials more negative than -92 +/- 3 mV in rat (n = 6) and -98 +/- 2 mV in guinea-pig (n = 18). The reversal potential of the opioid current was shifted to less negative potentials when the external potassium concentration was increased, as predicted by the Nernst equation. 6. The morphology of the two types of cells were distinguishable in that primary cells were oval (29 x 18 microns in rat; 36 x 19 microns in guinea-pig) with two to four thick tapering dendrites that branched within 50 microns of the cell body. Secondary cells were generally round or oval (about 24 x 13 microns in rat; 27 x 17 microns in guinea-pig) with two to five thin non-tapering dendrites.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1999

Potentiation of synaptic transmission by (S)-3,5-dihydroxy phenylglycine in the rat dentate gyrus in vitro: a role for voltage dependent calcium channels and protein kinase C.

1. The authors have previously shown that direct activation of metabotropic glutamate receptors (mGluRs) by (S)-3,5-dihydroxyphenylglycine ((S)-DHPG) can induce a long-lasting potentiation of synaptic transmission in the rat dentate gyrus in vitro. Here the authors provide further characterisation of this agonist-induced potentiation. 2. Field excitatory post-synaptic potentials were recorded from the denate gyrus of rat hippocampal slices prepared by standard methods. 3. (S)-DHPG (40 microM) induced a significant potentiation of the field EPSP slope (148.6 +/- 4.3% compared to controls, n = 5), which occluded tetanically-induced LTP. 4. This potentiation was inhibited by the PKC inhibitors staurosporine (0.1 microM) and H-7 (100 microM) and by the voltage dependent Ca2+ channel (VDCC) blockers NiCl2 (50 microM) and nifedipine (20 microM). 5. The mGluR5 specific agonist (RS)-2-Chloro-5-Hydroxyphenylglycine (CHPG) did not induce a potentiation when applied to slices at concentrations from 20 microM to 1 mM indicating that the (S)-DHPG potentiation may be mediated through group I subtype 1 mGluRs. 6. In conclusion the (S)-DHPG-induced potentiation observed in our studies may be PKC dependent and is likely to be mediated through both T/L subtype VDCC and mGluR1 subtype receptors.

Animals↗
PubMed1975

An electrophysiological analysis of the effect of Ca ions on neuromuscular transmission in the mouse vas deferens.

1 A study has been made of the effects of changing the external calcium concentration [Ca]0 and the external magnesium concentration [Mg]0 on the synaptic potential due to noradrenaline release. 2 When [Ca]0 was varied in the range 0.7 to 1.8 mM, the synaptic potential increased as about the second power of [Ca]0. 3 Increasing [Mg]0 depressed the synaptic potential; however, variation of [Ca]0 in the presence of high [Mg]0 did not significantly change the power relationship between the synaptic potential and [Ca]0. 4 The facilitated increase in the synaptic potential during short trains of impulses at different frequencies was quantitatively predicted on the assumption that each impulse leaves residual Ca ions bound to release receptors in the nerve terminal.

Action Potentials↗
PubMed1999

Electrophysiological changes in hippocampal slices isolated from rats embedded with depleted uranium fragments.

Although nephrotoxicity is considered to be the most serious consequence of uranium exposure, several studies have previously suggested the potential for neurotoxicity. In Operation Desert Storm, U.S. military personnel were wounded by fragments of depleted uranium (DU). This study was initiated to test the potential for DU fragments to cause electrophysiological changes in the central nervous system. Rats were surgically implanted with pellets of DU or tantalum (Ta) as a control metal. After 6, 12 and 18 months rats were euthanized, hippocampi removed and electrophysiological potentials analyzed by extracellular field potential recordings. Six months after implantation, synaptic potentials in DU-exposed tissue were less capable of eliciting spikes (E/S coupling). At 12 months, amplitudes of synaptic potentials were significantly increased in tissue from DU treated rats compared to Ta controls. E/S coupling was reduced. The differences between the electrophysiological measurements in DU-treated and control tissue were no longer evident at the 18 month time point. An analysis of the changes in the synaptic potentials and E/S coupling over the three time points suggests that by 18 months, the effects of aging and DU exposure converge, thereby obscuring the effects of the metal. Since kidney toxicity was not evident in these animals, effects secondary to nephrotoxicity are unlikely. This study raises the possibility that physiological changes occur in the brain with chronic exposure to DU fragments, which could contribute to neurological deficits.

Aging↗
PubMed1998

Synaptic activation of efferent neuromodulatory neurones in the locust Schistocerca gregaria.

The segmental ganglia of the locust contain efferent neuromodulatory neurones with cell bodies at the dorsal midline and axons that supply muscles and other tissue on both sides of the body. These are the dorsal unpaired median (DUM) neurones. Intracellular recordings were made from pairs of known metathoracic efferent DUM neurones in locusts in which all nerves were intact and in isolated metathoracic ganglia. The 19 metathoracic, efferent DUM neurones were identified according to the nerve roots through which their axons emerge from the ganglion. The synaptic potentials in these DUM neurones have been analysed to investigate how these neurones are activated and how their spikes are controlled. The degree of correlation between the synaptic potentials in particular pairs of neurones was quantified using a correlation analysis. This allowed the population of DUM neurones to be divided into three subsets that also map onto an anatomical grouping based on the distribution of their axons in the lateral nerves: (i) DUM1 neurones (DUMDL and DUM1b); (ii) DUM3 and DUM3,4 neurones; and (iii) DUM3,4,5, DUM5b neurones and DUMETi. Individual neurones within each subset showed strong correlations between their synaptic potentials, in both intact locusts and isolated ganglia, and tended to spike at the same time. Neurones in different subsets had few synaptic potentials in common and tended to spike independently. The persistence of common synaptic potentials in neurones of the three subsets in isolated ganglia indicates that they are derived from neurones within the metathoracic ganglion. The DUM neurones that had many common synaptic potentials in a quiescent locust responded in similar ways to mechanosensory stimulation of different parts of the body. DUM3,4, 5 and DUM5 neurones gave the clearest and most consistent responses to stimulation of mechanoreceptors on either hind leg. DUM3 and DUM3, 4 neurones responded variably, but usually with a hyperpolarisation. DUM1 neurones were rarely excited by mechanosensory stimuli but, like the preceding group, their responses were dependent upon whether the locust was moving its legs. These results lend further support to the idea that there is a subdivision of action amongst this population of DUM neurones, with those supplying the same targets being driven by the same presynaptic local neurones.

Animals↗
PubMed1988

Intracellular recordings from cells in the myenteric plexus of the rat duodenum.

Intracellular recordings were made in vitro from neurons in the myenteric plexus of freshly dissected preparations of the duodenum of the rat. Nearly one-quarter of neurons (18 out of 77) had long after-hyperpolarizations following their action potentials. Over 60% of neurons (20 out of 32) which were tested exhaustively by focal stimulation at seven points around the recording site were seen to receive fast excitatory synaptic inputs. These were of very short duration (10-30 ms) and were reversibly blocked by the nicotinic antagonist hexamethonium. Only four out of 18 after-hyperpolarization cells (22%) had visible fast synaptic inputs. Seven out of 32 neurons tested received slow excitatory synaptic inputs lasting up to 60 s that were associated with a decrease in conductance and an increase in excitability. No evidence for muscarinic synaptic potentials was seen; only four cells out of 30 with fast excitatory postsynaptic potentials had slow excitatory synaptic potentials visible after a single-shot stimulus; in none of these were the slow excitatory postsynaptic potentials blocked by atropine (up to 1 x 10(-5) M). No inhibitory postsynaptic potentials were recorded in any of the 77 neurons recorded in this study. The effects of five neurotransmitter candidates (acetylcholine, GABA noradrenaline, 5-hydroxytryptamine and substance P) applied by pressure microejection were studied. It is concluded that most of the neurophysiological features reported in the extensively studied guinea-pig small bowel myenteric plexus are present in the rat duodenum. However, the apparent lack of muscarinic synaptic potentials and inhibitory synaptic potentials suggests that there may be some differences between the two species. Our recordings also differ slightly from recently reported studies of rat myenteric neurons grown in cell culture.

Acetylcholine↗
PubMed1991

Long-term potentiation of synaptic responses in the rat dentate gyrus is due to increased quantal content.

Long-term potentiation (LTP) of synaptic responses in the dentate gyrus neurons of the rat hippocampus was studied in in vitro slices with the use of intracellular recordings. The goal of the study was to determine if the expression of LTP is pre- or postsynaptic. LTP was induced by tetanic stimulation of the perforant pathway in the presence of bicuculline. The expression of potentiation was measured during low-intensity stimulation at 1-5 Hz. It was found that a 104% (S.E.M. +/- 35, n = 5) increase in the amplitude of evoked synaptic potentials was associated with a reduction in the number of transmission failures to 38% (S.E.M. +/- 15, n = 5) of the control values. The size of quantal responses was determined on the basis of asynchronous release from stimulated synapses. The average size of the quanta remained unchanged during LTP. The evident increase of quantal content suggests a presynaptic locus for expression of LTP.

Animals↗
PubMed1973

Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path.

1. The after-effects of repetitive stimulation of the perforant path fibres to the dentate area of the hippocampal formation have been examined with extracellular micro-electrodes in rabbits anaesthetized with urethane.2. In fifteen out of eighteen rabbits the population response recorded from granule cells in the dentate area to single perforant path volleys was potentiated for periods ranging from 30 min to 10 hr after one or more conditioning trains at 10-20/sec for 10-15 sec, or 100/sec for 3-4 sec.3. The population response was analysed in terms of three parameters: the amplitude of the population excitatory post-synaptic potential (e.p.s.p.), signalling the depolarization of the granule cells, and the amplitude and latency of the population spike, signalling the discharge of the granule cells.4. All three parameters were potentiated in 29% of the experiments; in other experiments in which long term changes occurred, potentiation was confined to one or two of the three parameters. A reduction in the latency of the population spike was the commonest sign of potentiation, occurring in 57% of all experiments. The amplitude of the population e.p.s.p. was increased in 43%, and of the population spike in 40%, of all experiments.5. During conditioning at 10-20/sec there was massive potentiation of the population spike (;frequency potentiation'). The spike was suppressed during stimulation at 100/sec. Both frequencies produced long-term potentiation.6. The results suggest that two independent mechanisms are responsible for long-lasting potentiation: (a) an increase in the efficiency of synaptic transmission at the perforant path synapses; (b) an increase in the excitability of the granule cell population.

Action Potentials↗
PubMed1982

Cholinergic transmission in cat parasympathetic ganglia.

1. Intracellular electrical recording techniques were used to study the ionic mechanisms of cholinergic synaptic transmission in cat vesical pelvic ganglia (v.p.g.). 2. Orthodromic nerve stimulation as well as ionophoretic application of acetylcholine (ACh) resulted in, first, a fast excitatory post-synaptic potential (f.e.p.s.p.) and secondly, a slow inhibitory post-synaptic potential (s.i.p.s.p). These distinct post-synaptic responses were direct actions of ACh and not mediated through an interneurone. In addition, a slow excitatory post-synaptic potential (s.e.p.s.p.) was observed in 44% of the cells. 3. The f.e.p.s.p., mediated via nicotinic receptors, had a reversal potential of -10 mV and resembled the conventional rapid depolarization in other ganglia. The s.i.p.s.p., mediated by muscarinic receptors, had a reversal potential of about -100 mV and resulted from an increase in potassium conductance. 4. The slow muscarinic hyperpolarization could be observed in the absence of antagonists and it was elicited at stimulus frequencies in the physiological range (2-10 Hz). the s.i.p.s.p. induced orthodromically or ionophoretically inhibited firing in spontaneously active neurones. These observations suggest that the muscarinic hyperpolarization may occur under physiological conditions and has sufficient magnitude to be inhibitory to neuronal activity.

Acetylcholine↗
PubMed1987

Intracellular recording from hippocampal CA1 interneurons before and after development of long-term potentiation.

Synaptic efficacy is modified following a brief train of high frequency stimulation (HFS) to a cell's afferent fibers (long-term potentiation, LTP). Modulation of synaptic efficacy could be achieved through changes in excitability of interneurons. To test this hypothesis, we used the in vitro hippocampal slice to record intracellularly from CA1 basket cell interneurons before and following a period of HFS to fibers in stratum radiatum. Stimulation of stratum radiatum consistently produced action potential discharge in the basket cell interneuron prior to the discharge of a population spike in stratum pyramidale. This result is consistent with findings that basket cells may receive direct excitatory afferent input from neurons extrinsic to the CA1 region, and mediate a powerful feed-forward inhibition. Interneuron responses were recorded under 3 experimental conditions, in which stimulus intensity was varied. The level of basket cell excitability, as assessed by responses to orthodromic input, was not decreased following a train of HFS. Rather, the evoked EPSP in basket cells was often enhanced following high frequency stimulation to the cell's afferent fibers. These findings support the notion that decrement in basket cell activity is not responsible for LTP in CA1 hippocampus.

Action Potentials↗
PubMed1994

ATP regulates synaptic transmission by pre- and postsynaptic mechanisms in guinea-pig myenteric neurons.

Intracellular recordings were made from myenteric neurons of the guinea-pig ileum in vitro; they were classified into S and AH neurons according to electrophysiological criteria. ATP (10 nM-100 microM) inhibited excitatory synaptic potentials in the myenteric plexus; fast excitatory postsynaptic potentials and slow excitatory postsynaptic potentials of S neurons and slow excitatory postsynaptic potentials in AH neurons. This inhibitory action was reversible and dose-dependent, and was usually followed by a transient augmentation of the synaptic potentials after washing of ATP. The actions of ATP on the synaptic potentials were prevented by pretreatment with theophylline, caffeine, quinidine and 8-phenyl theophylline. The ATP analogues, ATP-gamma-s (100 nM-100 microM) and alpha-beta-methylene ATP (100 nM-100 microM) also depressed the synaptic potentials recorded from both types of neurons. The inhibitory effect of adenosine on the synaptic potentials was 10 times weaker than that of ATP. Thus, it seems clear that the presynaptic inhibition is not occurring through adenosine A1 or A2 receptors. Furthermore, ATP at high concentrations ( > or = 1 microM) augmented nicotinic fast depolarizations of S neurons produced by extracellular acetylcholine. However, ATP at the same concentrations inhibited the slow depolarizations of S and AH neurons caused by exogenous acetylcholine (muscarinic) and substance P. It is concluded that ATP regulates synaptic transmission in the myenteric plexus of the guinea-pig ileum and the sites of ATP actions are pre- and postsynaptic.

Adenosine↗
PubMed1998

Passive electrical properties of ventral horn neurons in rat spinal cord slices.

Recordings were made from large neurons located in the ventral horn of transverse spinal cord slices from young rats (7-15 days). Whole cell recordings were made simultaneously with two electrodes from the soma of these neurons, visualized using infra-red differential interference contrast optics. Positive identification of motoneurons could not always be achieved. The response of a neuron to a brief pulse of current delivered by one electrode, and recorded by the other electrode, were matched optimally to responses of a compartmental model of the same neuron with an identical current pulse as input. The compartmental model was based on a reconstruction of the neuron, using Biocytin staining. The compartmental model had three free parameters: specific membrane capacitance (Cm), membrane resistivity (Rm), and cytoplasmatic resistivity (Ri), all assumed to be uniform throughout the neuron. The experimental and model responses could be matched unequivocally for four neurons, giving Cm = 2.4 +/- 0.5 microF/cm2, Rm = 5.3 +/- 0. 9 kOmega/cm2, and Ri = 87 +/- 22 Omega/cm. No somatic shunt was required. For the remaining six neurons, a less perfect fit (but still within 95% confidence limits) was indicative of nonhomogeneous membrane properties. The electrotonic length of uncut dendrites was 0.85 +/- 0.14 lambda. The results resolve the issue of a somatic shunt conductance for motoneurons, relegating it to a microelectrode impalement artifact. They are consistent with previous reports on the electrical compactness of motoneurons to steady state currents and voltages. However, the much higher value of Cm (than the previously assumed 1 microF/cm2) implies much greater dendritic attenuation of fast synaptic potentials, and a much enhanced integrative response of motoneurons to synaptic potentials.

Action Potentials↗