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PubMed1998

Electrophysical properties, synaptic transmission and neuromodulation in serotonergic caudal raphe neurons.

1. We studied electrophysiological properties, synaptic transmission and modulation by 5-hydroxytryptamine (5-HT) of caudal raphe neurons using whole-cell recording in a neonatal rat brain slice preparation; recorded neurons were identified as serotonergic by post-hoc immunohistochemical detection of tryptophan hydroxylase, the 5-HT-synthesizing enzyme. 2. Serotonergic neurons fired spontaneously (approximately 1 Hz), with maximal steady state firing rates of < 4 Hz. 5-Hydroxytryptamine caused hyperpolarization and cessation of spike activity in these neurons by activating inwardly rectifying K+ conductance via somatodendritic 5-HT1A receptors. 3. Unitary glutamatergic excitatory post-synaptic potentials (EPSP) and currents (EPSC) were evoked in serotonergic neurons by local electrical stimulation. Evoked EPSC were potently inhibited by 5-HT, an effect mediated by presynaptic 5-HT1B receptors. 4. In conclusion, serotonergic caudal raphe neurons are spontaneously active in vitro; they receive prominent glutamatergic synaptic inputs. 5-Hydroxytryptamine regulates serotonergic neuronal activity of the caudal raphe by decreasing spontaneous activity via somatodendritic 5-HT1A receptors and by inhibiting excitatory synaptic transmission onto these neurons via presynaptic 5-HT1B receptors. These local modulatory mechanisms provide multiple levels of feedback autoregulation of serotonergic raphe neurons by 5-HT.

Animals↗
PubMed1993

Nicotinic and muscarinic modulations of excitatory synaptic transmission in the rat prefrontal cortex in vitro.

The importance of the cholinergic innervation of the neocortex in cognitive functions has been shown in a number of clinical and animal studies. Until recently, attempts to study the mode of action of acetylcholine in the neocortex have concentrated on muscarinic effects, whereas cholinergic actions mediated by nicotinic receptors have been difficult to demonstrate. The present work was undertaken to study the mechanism of action of nicotinic agents on cortical neurons and compare it to muscarinic effects by means of intracellular recordings in a slice preparation. The study was performed in the prelimbic area of the rat prefrontal cortex, a cortical region particularly involved in cognitive processes. Recordings were made from pyramidal cells located in layers II/III and synaptic potentials were evoked by stimulation of superficial cortical layers. Iontophoretic applications of nicotinic agonists (nicotine, dimethylphenylpiperazinium, cytisine) increased the amplitude of the monosynaptic excitatory postsynaptic potential mediated by non-N-methyl-D-aspartate glutamate receptors in 14% (22/159) of cells. This effect was abolished by the selective nicotinic blocker, neuronal bungarotoxin (IC50 = 0.6-0.7 microM) and by dihydro-beta-erythroidine (IC50 = 20-30 microM), whereas hexamethonium, mecamylamine, curare and alpha-bungarotoxin were ineffective. The nicotinic agonists did not change resting membrane potential, input resistance or current-voltage relationship. They also did not affect the depolarizations produced by glutamate applied by iontophoresis in the somatic or dendritic area. In contrast, the muscarinic agonists (muscarine, acetyl-beta-methylcholine) decreased the amplitude of the excitatory postsynaptic potential in 100% of the neurons tested. Atropine was more effective (IC50 = 0.08 microM) than pirenzepine (IC50 = 2 microM) to antagonize the muscarinic action. These effects were observed in the absence of any direct postsynaptic change in membrane potential or input resistance, provided that the site of the iontophoretic application was more than 100 microM distant from the soma. The muscarinic agonists did not influence the actions of iontophoretically applied glutamate. These results suggest that nicotinic and muscarinic agonists modulate excitatory synaptic transmission mediated at dendritic sites by non-N-methyl-D-aspartate glutamate receptors, possibly through a presynaptic action. Thus ascending cholinergic systems may take part in information processing in the prefrontal cortex through the control of ongoing excitation to pyramidal cells.

2-Amino-5-phosphonovalerate↗
PubMed2003

Polysynaptic slow depolarization and spiking activity elicited after induction of long-term potentiation in rat auditory cortex.

Polysynaptic activity was recorded in supragranular pyramidal neurons before and after the induction of long-term potentiation (LTP) in slices obtained from rat auditory cortex. LTP was induced by tetanic stimulation of layer IV. In the pyramidal neurons exhibiting LTP, repetitive stimulation at 50 Hz with 15 pulses triggered a slow 15-35 mV depolarization lasting 0.5-2 s with two to five spike discharges. There was no such response before the induction of LTP or in the neurons that did not exhibit LTP. Slow depolarization with spike discharges was blocked by an NMDA receptor antagonist but not by a metabotropic glutamate receptor antagonist. The reversal potential of the slow depolarization was approximately -7 mV and the membrane resistance decreased during slow depolarization, suggesting that the slow depolarization was produced by polysynaptic excitatory post-synaptic potentials. LTP was also induced by low frequency stimulation paired with a depolarizing current injection. In the pyramidal neurons exhibiting LTP after the paired stimulation, the slow depolarization amplitude was small and repetitive stimulation did not trigger spike discharges. Tetanic stimulation is expected to induce LTP in the polysynaptic neural circuits connecting many pyramidal neurons. The present findings suggest that polysynaptic activity can be generated in the potentiated neural circuits. Such activity might serve to read out the memory stored in polysynaptic neural circuits in the cerebral cortex.

Action Potentials↗
PubMed1989

Re-development of synaptic connections after implanted single 5-HT containing neuron in isolated leech ganglia.

Single mature Retzius cells which contain 5-HT have been implanted in isolated ganglia of Whitmania pigra. The properties of the implanted Retzius cell and its connections with the original identified nerve cells of the ganglia have been measured by intracellular microelectrodes. At 3 days in culture an implanted Retzius cell maintains its normal electrical membrane properties. It also forms the non-rectifying electronic coupling with the original Retzius cell and rectifying junctions with the L motor neuron of the host ganglion. In addition it receives chemical inputs of the impulse from T and N sensory neurons of ganglion. Impulses in the implanted Retzius cell evoke synaptic potentials in the L motor neuron. In this paper the appearance of novel synapses, which are formed by implanting an extra mature neuron as a pre- or post-synaptic element, is described. It might represent functional development of central nervous system at an earlier stage.

Animals↗
PubMed1987

Effects of alpha 2-adrenergic agonists and antagonists on photoreceptor membrane currents.

Type B photoreceptors of the nudibranch mollusc Hermissenda crassicornis receive excitatory synaptic potentials (EPSPs) whose frequency is controlled by potential changes of a neighboring cell known as the S optic ganglion cell which is thought to be electrically coupled to the presynaptic source of these EPSPs, the E optic ganglion cell. The frequency of the EPSPs increases when a conditioned stimulus (light) is paired with an unconditioned stimulus (rotation) during acquisition of a Pavlovian conditioned response. The results of the present study are consistent with an adrenergic origin for these EPSPs. Noradrenergic agonists (greater than 100 microM), norepinephrine and clonidine, only slightly depolarize the type B cell but clearly prolong its depolarizing response to light. Serotonin, by contrast, causes hyperpolarization of the type B cell's resting potential as well as after a light step. Clonidine reduces voltage-dependent outward K+ currents (IA, an early current, ICa2+-K+, a late Ca2+-dependent current) that control the type B cell's excitability (and thus its light response and membrane potential). These effects of clonidine are reduced or blocked by the alpha 2-receptor antagonist, yohimbine (0.5 microM), but not the alpha 1-blocker, prazosin. The same yohimbine concentration also blocked depolarizing synaptic excitation of the type B cell in response to depolarization of a simultaneously impaled S optic ganglion cell. Histochemical techniques (both the glyoxylic acid method of de la Torre and Surgeon and the formaldehyde-induced fluorescence or Falck-Hillarp method) demonstrated the presence of a biogenic amine(s) within a single neuron in each optic ganglion as well as three or four cells within the vicinity of previously identified visual interneurons. No serotonergic neurons were found within the optic ganglion or in proximity to visual interneurons. A clonidine-like synaptic effect on type B cells, therefore, could amplify conditioning-specific changes of membrane currents by increasing type B depolarization and possibly, as well, by elevating intracellular second messengers.

Adrenergic alpha-Agonists↗
PubMed1982

Visualization of the spread of electrical activity in rat hippocampal slices by voltage-sensitive optical probes.

1. Voltage-sensitive membrane-bound dyes and a matrix of 100 photodetectors were used to detect the spread of evoked electrical activity at the CA1 region of rat hippocampus slices. A display processor was designed in order to visualize the spread of electrical activity in slow motion.2. The stimulation of the Schaffer collateral-commissural path in the stratum radiatum evoked short latency (2-4 msec) fast optical signals, followed by longer latency (4-15 msec) slow signals which decayed within 20-50 msec. Multiple fast signals were frequently detected at the stratum pyramidale; they propagated toward the stratum oriens with an approximate conduction velocity of 0.1 m/sec.3. The fast signals were unaltered in a low Ca(2+) high Mg(2+) medium but were blocked by tetrodotoxin. These signals probably represent action potentials in the Schaffer collateral axons. Their conduction velocity was about 0.2 m/sec and their refractory period about 3-4 msec.4. The slow signals were absent in a low Ca(2+) medium and probably represent excitatory post-synaptic potentials (e.p.s.p.s) generated in the apical dendrites of the pyramidal cells. They were generated in the stratum radiatum, where the presynaptic signals were seen, and spread into somata and basal dendrites (the stratum pyramidale and oriens, respectively).5. The timing of the signals with fast rise-time, which were detected at the statum pyramidale, approximately coincided with the timing of the extracellularly recorded field potentials. These multiple discharges probably represent action potentials of the pyramidal cells. They spread back into the apical dendrites but with significant attenuation of the amplitudes of the high frequency components of the pyramidal action potentials.6. Hyperpolarizing potentials could be detected when strong stimuli were applied to the stratum radiatum or alveus. The net hyperpolarizations were detected only in the stratum pyramidale and the border region between the stratum pyramidale and radiatum. Frequently the inhibition was masked by the large e.p.s.p.s. However, its existence could be demonstrated by treatment of the slice with picrotoxin or a low Cl(-) medium. Under these conditions a long-lasting depolarization of the apical dedrites was evoked by the stimulation. This was associated with an increase of the multiple discharges in the stratum pyramidale and oriens.7. These studies illustrate the usefulness of voltage-sensitive dyes in the analysis of passive and active electrical properties, pharmacological properties and synaptic connexions in mammalian brain slices, at the level both of small neuronal elements (dendrites, axons) and of synchronously active neuronal populations.

Action Potentials↗
PubMed1992

K-dependent inhibition in the dentate-CA3 network of guinea pig hippocampal slices.

1. The occurrence of potassium-dependent inhibitory postsynaptic potentials (K-IPSPs) in relation to burst discharges induced by 4-aminopyridine (4-AP; 30 microM) was studied in CA3, granule and hilar neurons in guinea pig hippocampal slices with the use of paired extra- and/or intracellular recording. 2. Slow small (2-5 mV) and large (up to 30 mV) K-IPSPs were observed in CA3, granule and in some hilar neurons during 4-AP applications in the presence of blockers for fast synaptic transmission, picrotoxin (50 microM), and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 5-10 microM). Amplitudes of K-IPSPs were linearly related to voltage, and they reversed in sign close to -100 mV, as expected for synaptic potentials generated by an increase in K-conductance. 3. In CA3 neurons, 4-AP applied in the presence of picrotoxin elicited burst discharges and K-IPSPs. CNQX blocked the burst discharge activity and increased the amplitude of K-IPSPs. 4. In granule cells, 4-AP applied in the presence of picrotoxin elicited K-IPSPs and only inconsistently small excitatory postsynaptic potentials (EPSPs). The EPSPs were blocked by CNQX, but CNQX application did not affect the K-IPSPs. However, in granule cells it could be observed that blockade of Cl-inhibition by picrotoxin in the presence of CNQX increased the amplitude of K-IPSPs. 5. In hilar neurons, 4-AP applied in the presence of picrotoxin elicited mainly burst discharges. CNQX blocked the burst discharges only in a few cells. In most hilar neurons K-IPSPs were observed at the beginning of the 4-AP effect, but subsequently K-IPSPs were replaced by burst discharges. 6. To determine the type of cells that burst in picrotoxin and 4-AP, neurons were stained intracellularly with horseradish peroxidase. Neurons stained in the granule cell layer did not burst and were morphologically identified as granule cells. Neurons stained in the hilar region burst and were nonpyramidal, nongranule cells. Bursting cells stained in the CA3 area were all pyramidal cells. 7. The hilar neurons varied considerably in size and dendritic organization. They could be classified as aspiny and spiny cells, the latter including mossy cells. 8. We conclude that K-dependent inhibition may explain the long-lasting IPSPs observed in in vivo recordings from hippocampal cells. In a hippocampal lamella, burst discharge activity of hilar neurons including presumed excitatory mossy cells is associated with inhibition of granule cells.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗
PubMed2001

Changes in hippocampal adenosine efflux, ATP levels, and synaptic transmission induced by increased temperature.

Previous studies have demonstrated that when the temperature of hippocampal brain slices is increased, there is a corresponding depression of synaptic potentials mediated by an increased activation of presynaptic adenosine A(1) receptors. The present experiments demonstrate that when the temperature of hippocampal slices is raised from 32.5 degrees C to either 38.5 degrees C or 40.0 degrees C there is a marked, temperature-dependent increase in the efflux of endogenous adenosine and a corresponding decrease in excitatory synaptic responses. The increase in efflux is rapidly reversible on lowering the slice temperature and the temperature-induced efflux is repeatable. Control experiments suggest that this increased efflux of adenosine is not the result of hypoxia or ischemia secondary to a temperature-induced increase in the metabolic rate of the slice. The increase in adenosine efflux was not accompanied by any significant change in the ATP levels in the brain slice, whereas a hypoxic stimulus sufficient to produce a comparable depression of excitatory transmission produced an approximately 75% decrease in ATP levels. These experiments indicate that changes in brain slice temperature can alter purine metabolism in such a way as to increase the adenosine concentration in the extracellular space, as well as adenosine efflux from hippocampal slices, in the absence of significant changes in ATP levels.

Adenosine↗
PubMed1998

Gamma frequency oscillation in the hippocampus of the rat: intracellular analysis in vivo.

Gamma frequency field oscillations reflect synchronized synaptic potentials in neuronal populations within the approximately 10-40 ms range. The generation of gamma activity in the hippocampus was investigated by intracellular recording from principal cells and basket cells in urethane anaesthetized rats. The recorded neurones were verified by intracellular injection of biocytin. Gamma frequency field oscillations were nested within the slower theta waves. The phase and amplitude of intracellular gamma were voltage dependent with an almost complete phase reversal at Cl- equilibrium potential in pyramidal cells. Basket cells fired at gamma frequency and were phase-locked to the same phase of the gamma oscillation as pyramidal cells. Current-induced depolarization coupled with synaptically induced inhibition resulted in gamma frequency discharge (30-80 Hz) of pyramidal cells without accommodation. These observations suggest that at least part of the gamma frequency field oscillation reflects rhythmic hyperpolarization of principal cells, brought about by the rhythmically discharging basket neurones. Resonant properties of pyramidal cells might facilitate network synchrony in the gamma frequency range.

Action Potentials↗
PubMed1996

Neuroprotection by propofol in acute mechanical injury: role of GABAergic inhibition.

1. Whole cell patch-clamp and extracellular field recordings were obtained from granule cells of the dentate gyrus in 400-microns-thick brain slices of the adult rat to determine the actions of the intravenous general anesthetic 2,6-diisopropylphenol (propofol) on acute neuronal survival and preservation of synaptic integrity after amputation of dendrites (dendrotomy), and to determine the role of gamma-aminobutyric acid-A (GABAA)-receptor-mediated inhibition in the neuroprotective effects of propofol. The actions of propofol were compared with those exerted by another widely used intravenous general anesthetic, 5-ethyl-5-[1-methylbutyl]-2-thiobarbituric acid (thiopental). 2. Propofol (10 microM) increased the frequency (control: 5.9 +/- 0.9 Hz, mean +/- SE; propofol: 10.5 +/- 1.3 Hz) and the single-exponential decay time constant (tau D) (control: 4.5 +/- 0.2 ms; propofol: 15.3 +/- 1.5 ms) of miniature inhibitory postsynaptic currents (mIPSCs) recorded in control neurons. Thiopental (25 microM) also increased the tau D (14.3 +/- 0.9 ms) of mISPCs, but had no effect on mIPSC frequency. Both anesthetics potentiated mIPSCs at low concentrations (propofol: 5 microM; thiopental: 1 microM). Propofol and thiopental did not change the peak amplitude and rise times of mIPSCs. 3. Propofol (10 microM) was able to depress the excitability of control granule cells, as determined by the reduction in the amplitude of the orthodromic population spikes. This depression could be prevented by the GABAA receptor antagonist bicuculline (50 microM), indicating that propofol reduces excitability via GABAA receptor functions. 4. Propofol and thiopental were neuroprotectant (assessed by antidromic population responses 2-5 h after injury) if present before and during the amputation of the granule cell dendrites. The protective actions were dose dependent, and at high doses (propofol: 200 microM; thiopental: 400 microM) the anesthetics were as neuroprotective against dendrotomy-induced cell death as 2-amino 5-phosphovaleric acid (APV) and 6-cyano-7-nitroquinoxaline-2,3 dione (CNQX). The protective effects of the anesthetics were completely blocked with the GABAA receptor antagonists picrotoxin or bicuculline, and were mimicked by the GABAA receptor agonist muscimol (100 microM). 5. Propofol, in contrast to APV and CNQX, could not prevent the dendrotomy-induced Ca(2+)-dependent and long-lasting changes in mIPSC decay kinetics (appearance of a double-exponential, prolonged decay). 6. The protective effects of the anesthetics and those of APV and CNQX on neuronal survival were not significant when the drugs were applied after dendrotomy, indicating that dendrotomy carried out 150-200 microns from the soma without neuroprotective agents rapidly induces irreversible acute degeneration in most injured neurons. The failure to rescue cells from dendrotomy-induced injury did not result from a decreased sensitivity of the GABAA receptors to the anesthetics, because the potentiating effects of the anesthetics on mIPSCs from control and dendrotomized neurons were not different. 7. These data indicate that propofol potentiates synaptic inhibition pre- and postsynaptically, and, when present during dendrotomy, it can protect neurons from acute mechanical-injury induced cell death via potentiation of GABAA receptor functions. However, propofol fails to provide neuroprotection against dendrotomy-induced changes in synaptic physiology.

Acute Disease↗
PubMed1989

Laser microbeam axotomy and conduction block show that electrical transmission at a central synapse is distributed at multiple contacts.

Touch (T) sensory neurons in the leech innervate defined regions of skin and synapse on other neurons, including other T cells, within the ganglionic neuropil. The cells' receptive fields in the periphery are comprised of a central region, innervated by thick axons, and adjoining regions (minor fields) innervated by thinner axons. Secondary branches, known to be sites of synapses, emerge from the thinner and thicker axons. Pairs of T cells appear to make up to 200 separate contacts distributed within the neuropil. When the T cell is hyperpolarized, as occurs during natural stimulation of the cell, action potentials generated in the minor field and travelling into the ganglion along the thin axons may fail to conduct at central branch points. Evidence is presented, using axon conduction block and laser axotomy of cells filled with 6-carboxy-fluorescein, that synapses between separate groups of branches can function independently. Thus, selective activation of branches of the thin anterior axon produced a synaptic potential 36 +/- 6% of control amplitude, which was consistent with counts of 39 +/- 6% of contacts made by these branches. Laser axotomy of postsynaptic neurons showed that the anterior contacts indeed made the principal or only contacts activated during anterior conduction block. The results show that conduction block can modulate transmission within the ganglion, and it operates by silencing particular contacts between cells.

Animals↗
PubMed1998

Impaired expression of long-term potentiation in hippocampal slices 4 and 48 h following mild fluid-percussion brain injury in vivo.

The effect of fluid percussion brain injury on hippocampal long-term potentiation (LTP) was investigated in hippocampal slices in vitro. Mild to moderate (1.7-2.1 atm) lateral fluid percussion head injury or sham operation was produced in rats 4 or 48 h prior to harvesting brain slices from the ipsilateral hippocampus. Field excitatory post-synaptic potentials (fEPSPs) were recorded in stratum radiatum of hippocampal subfield CA1 in response to electrical stimulation of the Schaffer collaterals. The initial slope of fEPSPs was used to investigate changes in synaptic strength prior to and following 100 or 200 Hz (1 s) tetanic stimulation. TBI significantly inhibited expression of LTP in hippocampal slices in vitro. Post-tetanus fEPSP slopes increased more than 100% in hippocampal slices from sham-operated animals but less than 50% in slices from rats following TBI. The data suggest that changes in functional synaptic plasticity in the hippocampus may contribute to cognitive disorders associated with TBI (traumatic brain injury). The data also indicate that TBI-induced effects on hippocampal LTP are robust and may be investigated in the hippocampal slice preparation in vitro.

Animals↗
PubMed1987

Kappa opioid receptor activation depresses excitatory synaptic input to rat locus coeruleus neurons in vitro.

Intracellular recordings were made from neurons of the rat locus coeruleus contained within a brain slice maintained in vitro. When applied to the slice in known concentrations the selective kappa opioid receptor agonist trans-(+)-3,4-dichloro-N-methyl-[2-(1-pyrrolidinyl)cyclohexyl] benzeneacetamide methane sulphonate (U50488) (0.01-1 microM) produced a concentration-dependent depression of the excitatory post-synaptic potential evoked by electrical stimulation of afferent inputs to the locus coeruleus. This effect was antagonized by naloxone with an apparent dissociation equilibrium constant (Kd) of 28 nM. U50488 did not completely abolish the EPSP. Over the same concentration range U50488 had no effect on the resting membrane potential, input resistance or action potential waveform of locus coeruleus neurons, nor did U50488 depress the depolarization produced by local application of L-glutamic acid. The mu opioid receptor agonists [D-Ala2, NMe Phe4, Gly-ol5] enkephalin (0.003-1 microM) and [D-Ala2, NMe Phe4, Met(O)5] enkephalinol (0.003-1 microM) caused a membrane hyperpolarization concomitant with a fall in neuronal input resistance. These effects were concentration-dependent and antagonized by naloxone with an apparent Kd of 1.5 nM. Mu agonists also caused a depression of the tetrodotoxin resistant action potential. An in vitro autoradiographic study of [3H]bremazocine binding within the locus coeruleus revealed that, although the majority of binding appears to be to mu sites, a significant proportion was displaceable by unlabelled U50488 and thus represented kappa binding sites. The possibility that kappa opioid receptors may be located pre-synaptically within the locus coeruleus, and that activation of these receptors depresses excitatory synaptic input, is discussed.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1984

Quantal release of neurotransmitter: an iterative method for the automatic computation of binomial distribution parameters.

A computational method is presented by which, when the amplitude-frequency histogram of the excitatory post-synaptic potentials shows a binomial distribution, an accurate evaluation of the statistical parameters p and n may be obtained. The entire procedure is a combination of 3 basic methods: steepest descent, parabolic interpolation and Montecarlo technique. The two statistical parameters are evaluated independently with respect to each other, which makes an effective control of the accuracy of the calculation possible by comparing the p by n product with the average number of quanta released in response to each nerve impulse, conventionally computed. Applications to quantal release studies in both rat and guinea-pig superior cervical ganglia are also presented.

Animals↗
PubMed2000

The serotonin 5-HT2 receptor-phospholipase C system inhibits the induction of long-term potentiation in the rat visual cortex.

The effect of serotonin 5-HT2 receptor stimulation on long-term potentiation (LTP) in the primary visual cortex was investigated by using rat brain slices in vitro. Field potentials evoked by stimulation of layer IV were recorded in layer II/III. The 5-HT2 receptor agonist 1-(2,5-dimethyl-4-iodophenyl)-2-aminopropane (DOI) did not affect baseline synaptic potentials evoked by single-pulse test stimulation, but significantly inhibited the induction of LTP in a concentration-dependent manner (0.1-10 microM). The LTP-inhibiting effect of DOI (10 microM) was blocked by the 5-HT2,7 receptor antagonist ritanserin (10 microM), but not by the 5-HT1A receptor antagonist NAN-190 (10 microM) nor by the 5-HT3,4 receptor antagonist MDL72222 (10 microM). The inhibitory effect of DOI was also blocked by the phospholipase C inhibitor U73122, but not by its inactive analogue U73343. These results suggest that visual cortex LTP is inhibited by activation of the 5-HT2 receptor-phospholipase C system. In addition, the LTP-inhibiting effect of DOI was abolished by the presence of the GABAA receptor antagonist bicuculline (10 microM), suggesting that 5-HT2 receptor-mediated inhibition of visual cortex LTP is dependent on GABAergic inhibition.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1972

Cyclic adenosine monophosphate in the nervous system of Aplysia californica. II. Effect of serotonin and dopamine.

Serotonin and dopamine, both likely transmitter substances in Aplysia, stimulated formation of adenosine-3',5' monophosphate (cAMP) in ganglia, connectives, and identified nerve cell bodies. This widespread distribution suggests that receptors for the response are localized throughout the nervous system, as is adenyl cyclase. Both synthesis of cAMP-(3)H from precursor previously labeled in incubations with adenine-(3)H and total content of cAMP were stimulated up to 15-fold. The acetylcholine analogue carbachol, glutamate, norepinephrine, and histamine were inactive. Full stimulation occurred within 2-4 min of applying serotonin; the extent of the effect was half maximal at 6micro serotonin. Even in the continued presence of serotonin, the increased cAMP diminished with time. When serotonin was removed, tissue remained refractory for 15-20 min; sensitivity returned after 25 min. Serotonin stimulated cAMP after removal of extracellular Na, K, or Cl and in isotonic sucrose, with all extracellular ions removed. Elevating Mg, which blocked the stimulation of cAMP caused by synaptic activity, did not affect the response to serotonin. Thus the response appeared to be independent of transmitter release and of changes in synaptic potentials and current flow. The role of cAMP in neuronal functioning remains to be determined. Conditions which markedly increased cAMP in neurons, however, did not affect the rate of RNA synthesis, nor did they alter the distribution of phosphorylated adenine or uridine nucleotides.

Action Potentials↗
PubMed1986

Muscarinic slow excitation and muscarinic inhibition of synaptic transmission in the rat neostriatum.

Intracellular recording from neurones in rat neostriatal slices was used to compare the muscarinic effects of endogenous acetylcholine (ACh) released from cholinergic neostriatal synapses with the action of exogenously applied muscarinic agonists. Repetitive electrical stimulation in the neostriatum evoked a series of fast excitatory post-synaptic potentials (e.p.s.p.s) followed by a short, variable period of input resistance decrease. In the presence of the acetylcholinesterase (AChE) inhibitor, physostigmine, these potentials were followed by a slow e.p.s.p. which lasted about 60 s. Higher stimulus intensities were needed to elicit the slow e.p.s.p. than the fast e.p.s.p. The slow e.p.s.p. could not be observed after a single stimulus. Its amplitude was graded and increased with stimulus strength. The slow e.p.s.p. was blocked by the muscarinic antagonist atropine (10 microM) and by Ba2+ (100 microM). Input resistance increased during the slow e.p.s.p. Depolarization of the cell increased the size of the slow e.p.s.p. and hyperpolarization decreased it. Simultaneously, resting input resistance increased with membrane depolarization and decreased with membrane hyperpolarization. Repetitive intrastriatal stimulation was followed by a hyperpolarization instead of the depolarization at membrane potentials negative to -75 mV. Input resistance increased during this hyperpolarization as it did during the slow e.p.s.p. The slow e.p.s.p. persisted at membrane potentials of -70 to -80 mV if K+ concentration in the saline was reduced from 5 to 2 mM. In 10 mM-K+, the repetitive stimulation was followed by a hyperpolarization even at membrane potentials as low as -60 to -50 mV. Bath perfusion of high concentrations (100 microM) of muscarine or carbachol induced a sustained increase in the input resistance. The muscarinic agonists also reduced the amplitude of intrastriatally evoked fast e.p.s.p.s; however, this effect was transient and compensated by the increase in input resistance. The effects of the muscarinic agonists on input resistance and e.p.s.p. amplitude were antagonized by atropine (10 microM). Sustained decreases of e.p.s.p. amplitude were induced by the bath application of low doses (0.5-10 microM) of muscarine or carbachol. Input resistance was not altered. Atropine (1-10 microM) antagonized this effect. A sustained reduction of fast e.p.s.p. amplitude resulted also from inhibition of AChE by application of physostigmine (1-100 microM). Input resistance and neuronal excitability were not affected by AChE blockade.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1981

Presynaptic inhibition of transmission from identified interneurons in locust central nervous system.

1. Intracellular recordings near the output terminals of an identified interneuron (the descending contralateral movement detector, DCMD) in the locust revealed the occurrence of depolarizing synaptic potentials. These presynaptic depolarizing potentials were evoked by spikes in both DCMDs, by auditory stimuli, and by electrical stimulation of the pro- to mesothoracic connectives. The occurrence of the depolarizing potentials decreased the amplitude of the action potentials close to the output terminals. 2. The stimuli that produced depolarizing potentials in the presynaptic terminals reduced the amplitude of the monosynaptic excitatory postsynaptic potentials evoked by the DCMDs in identified follower interneurons. We conclude that at least part of this reduction in transmission from the DCMDs results from presynaptic inhibition and that the presynaptic inhibition is related to a reduction in the amplitude of the presynaptic action potentials. 3. We propose that the function of the presynaptic inhibition of the DCMDs is to ensure that the interneurons triggering a jump are never activated by the DCMDs in the absence of proprioceptive signals from the legs indicating the animal's readiness to jump.

Action Potentials↗