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PubMed1989

Anaesthetic depression of excitatory synaptic transmission in neocortex.

A decrease in synaptic excitation as well as an enhancement of neuronal inhibition in the central nervous system have been suggested as possible mechanisms of anaesthesia which we have investigated with intraneuronal recording techniques in neocortex. The effects of a volatile agent--isoflurane and a steroid preparation--Althesin, on excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) evoked by epicortical electrical stimulation were investigated in in vitro slice preparations of anterior cingulate and sensorimotor cortices of guinea pig. Applications of isoflurane (0.5-2.5 minimum alveolar concentration or MAC) and Althesin (10-200 microM) induced a dose-dependent, reversible depression of EPSPs with EC50's of 1 MAC and approximately 50 microM respectively. In order to eliminate the possibilities of a shunting effect on EPSPs by the conductances involved in the concomitant IPSPs, a GABAA-antagonist (bicuculline) was applied together with the anaesthetics. With this IPSP blockade, both anaesthetics depressed the EPSPs and were effective in reducing the epileptiform activities evoked by bicuculline during the subpial stimulation. The IPSPs also were evoked during the blockade of K-conductances by internal Cs-applications in order that the effects of anaesthetics could be studied exclusively on the Cl-mediated GABAergic IPSPs. Both isoflurane (0.5-2.5 MAC) and Althesin (10-100 microM) depressed the IPSPs in a dose dependent manner. These investigations demonstrate that applications of isoflurane and Althesin depressed the excitabilities of neocortical neurons by interfering with synaptic excitation, possibly at pre- and postsynaptic sites, rather than by potentiating neuronal inhibition.

Action Potentials↗

PubMed1991

Afterpotentials following penicillin-induced paroxysmal depolarizations in rat hippocampal CA1 pyramidal cells in vitro.

Epileptic discharges were induced by superfusion of rat hippocampal slices with penicillin. Under these conditions the neurons generated paroxysmal depolarization shifts (PDS) after electrical stimulation of Schaffer collaterals. The PDS were followed by large afterhyperpolarizations lasting about 2 s. The mechanisms causing these afterhyperpolarizations were studied in CA1 pyramidal cells. A late component of the afterhyperpolarizations, which determined their overall duration, was blocked by intracellular application of EGTA and reduced by superfusion with 8-Br-cAMP. In the same neurons these drugs had a comparable effect on afterhyperpolarizations following depolarizing current injections; it was therefore concluded that the late component of the PDS afterhyperpolarizations was caused by a slow Ca2(+)-activated K+ current. An initial fast component of PDS afterhyperpolarizations, which peaked about 60 ms after PDS onset, was reduced by EGTA but not affected by 8-Br-cAMP suggesting that the fast Ca2(+)-activated K+ current also contributed to the PDS afterhyperpolarizations. Superfusion of the slice with the gamma-aminobutyric acid B receptor (GABAB) antagonists phaclofen or 5-aminovalerate reduced the amplitude of the afterhyperpolarizations during the first 1000 ms but did not affect the late Ca2(+)-dependent component, indicating that a GABAB-mediated K+ inhibitory postsynaptic potential (IPSP) contributed to the PDS afterhyperpolarization. Intracellular injection of Cl- revealed that an early part of the afterhyperpolarizations lasting about 500 ms was Cl(-)-dependent. This component was blocked by superfusion of the slices with bicuculline, suggesting that a GABAA-mediated Cl- IPSP contributed to the PDS afterhyperpolarization.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

4-Aminopyridine-induced synaptic GABAB currents in granule cells of the guinea-pig hippocampus.

Sharp-electrode and tight-seal perforated-patch and whole-cell recording techniques were used to evaluate K(+)-dependent inhibitory postsynaptic potentials (K-IPSPs) and currents (K-IPSCs) induced by the convulsant 4-aminopyridine (50 mumol l-1) in granule cells of guinea-pig hippocampal slices. The responses were recorded in the presence of blockers for glutamatergic and GABAA-receptor-mediated synaptic transmission, 6-cyano-7-nitroquinoxaline-2,3-dione, picrotoxin and bicuculline. The input resistance was much larger (approximately 300 M omega) in tight-seal recording than in sharp-electrode recording (approximately 100 M omega), but the amplitudes of K-IPSPs recorded at -65 mV holding potential were similar in all three recording configurations. The 4-aminopyridine-induced currents reversed near the K+ equilibrium potential, and the reversal potentials shifted with changes in [K+]out or [K+]in as expected for a K+ current. Slope conductance measurements indicated a conductance increase during the peak of the K-IPSP up to 5 nS (mean 2.4 nS). The peak conductance was underestimated in whole-cell recordings unless the pipette contained Cs+. Considering the high membrane resistance of granule cells, K-IPSCs induced by 4-aminopyridine hyperpolarize the cells considerably and thereby are likely to contribute to the failure of 4-aminopyridine to induce burst discharges in granule cells.

4-Aminopyridine↗

PubMed1984

Interaction of penicillin and pentobarbital with inhibitory synaptic mechanisms in neocortex.

In this study we characterized the responses of neocortical neurons to iontophoretically applied gamma-aminobutyric acid (GABA) and examined how these GABA responses as well as the inhibitory postsynaptic potentials (IPSPs) were affected by the presence of penicillin or pentobarbital. Intracellular recordings were obtained from slices of rat neocortex maintained in vitro; injection of the dye Lucifer yellow indicated that recordings were primarily from pyramidal neurons. Orthodromically evoked responses were always depolarizing at the cell's resting membrane potential. Such depolarizing responses could easily be reversed in polarity by depolarizing the cell 10-15 mV, suggesting that the response consisted partly of an IPSP. In some cases, depolarization unmasked a small, short-latency excitatory postsynaptic potential (EPSP). Responses to iontophoretically applied GABA were also depolarizing at rest. Biphasic hyperpolarizing-depolarizing responses were occasionally observed upon depolarization of the neuron. Bath application of penicillin (1.7-3.4 mM) decreased the amplitude of the IPSPs and increased their time to peak, an effect associated with the development of epileptiform activity. Penicillin also reduced the maximum response to iontophoretically applied GABA without affecting the dose required to obtain a half-maximal response, suggesting a noncompetitive antagonism. Pentobarbital (100-200 microM) prolonged the time course and increased the amplitude of the IPSPs while producing a leftward shift in the GABA charge-response relation. These results suggest that the convulsant penicillin and the anticonvulsant pentobarbital have opposing actions on GABAergic inhibition in the neocortex.

Animals↗

PubMedDate not supplied

Endomorphins: localization, release and action on rat dorsal horn neurons.

Endomorphin (Endo) 1 and 2, two tetrapeptides isolated from the bovine and human brain, have been proposed to be the endogenous ligand for the mu-opiate receptor. A multi-disciplinary study was undertaken to address the issues of localization, release and biological action of Endo with respect to the rat dorsal horn. First, immunohistochemical studies showed that Endo-1- or Endo-2-like immunoreactivity (Endo-1- or Endo-2-LI) is selectively expressed in fiber-like elements occupying the superficial layers of the rat dorsal horn, which also exhibit a high level of mu-opiate receptor immunoreactivity. Second, release of immunoreactive Endo-2-like substances (irEndo) from the in vitro rat spinal cords upon electrical stimulation of dorsal root afferent fibers was detected by the immobilized antibody microprobe technique. The site of release corresponded to laminae I and II where the highest density of Endo-2-LI fibers was localized. Lastly, whole-cell patch clamp recordings from substantia gelatinosa (SG) neurons of rat lumbar spinal cord slices revealed two distinct actions of exogenous Endo-1 and Endo-2: (1) depression of excitatory and/or inhibitory postsynaptic potentials evoked by stimulation of dorsal root entry zone, and (2) hyperpolarization of SG neurons. These two effects were prevented by the selective mu-opiate receptor antagonist beta-funaltrexamine. The localization of endomorphin-positive fibers in superficial layers of the dorsal horn and the release of irEndo upon stimulation of dorsal root afferents together with the observation that Endo inhibits the activity of SG neurons by interacting with mu-opiate receptors provide additional support of a role of Endo as the endogenous ligand for the mu-opiate receptor in the rat dorsal horn.

Afferent Pathways↗

PubMed1990

Extensive monosynaptic inhibition of ventral respiratory group neurons by augmenting neurons in the Bötzinger complex in the cat.

Axonal projections and synaptic connectivity of expiratory Bötzinger neurons with an augmenting firing pattern (Bot-Aug neurons) to neurons in the ipsilateral ventral respiratory group (VRG) were studied in anaesthetized cats. Antidromic mapping revealed extensive axonal arborizations of Bot-Aug neurons (24 of 45) to the rostral or caudal VRG, with some having arbors in both regions. Of 234 pairs of neurons studied with intracellular recording and spike-triggered averaging, monosynaptic inhibitory postsynaptic potentials (IPSPs) were evoked in 49/221 VRG neurons by 38/98 Bot-Aug neurons. The highest incidence of monosynaptic inhibition was found in inspiratory bulbospinal neurons (10 of 23 tested). Evidence was also found for monosynaptic inhibition, by a separate group of Bot-Aug neurons, of expiratory bulbospinal neurons (12/58), while excitatory postsynaptic potentials (EPSPs) were identified in another two of these neurons. In addition, monosynaptic IPSPs were recorded from 13 of 53 identified laryngeal motoneurons, and from 14 of 100 respiratory propriobulbar neurons. Presumptive disynaptic IPSPs were recorded from 11 of the 221 VRG neurons. We conclude that Bot-Aug neurons exert widespread inhibition on all major neuron categories in the ipsilateral VRG, and should be regarded as an important element in shaping the spatiotemporal output pattern of both respiratory motoneurons and premotor neurons.

Animals↗

PubMed1998

Blockade of GABA(B) receptors facilitates muscarinic agonist-induced epileptiform activity in immature rat piriform cortex in vitro.

The effects of the selective GABA(B) receptor antagonist [3-[[(3,4-dichlorophenyl)methyl]aminolpropyl] (diethoxymethyl) phosphinic acid (CGP 52432) on muscarinic (mAChR) and metabotropic glutamate (mGluR) responsiveness were studied in slices of piriform cortex from both immature (P16-P22) and adult (> or =P40) rats, using a conventional intracellular recording technique. In both adult and immature slices, CGP 52432 (1 microM) had no effect on neuronal membrane properties, whereas it selectively abolished the late inhibitory postsynaptic potential (IPSP) evoked by local electrical stimulation of association fibre terminals. Age-related changes in mAChR (but not mGluR) responsiveness were also detected. In adult neurones, bath-application of the mAChR agonist oxotremorine-M (OXO-M; 10 microM), or the selective mGluR agonist 1S,3R-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD; 10 microM) evoked similar membrane depolarization and inhibition of evoked excitatory postsynaptic potentials (EPSPs). However, while 1S,3R-ACPD and OXO-M produced indistinguishable slow excitatory effects in immature slices, during superfusion with OXO-M, neurones exhibited spontaneous paroxysmal depolarizing shifts (PDSs) that were suppressed in the presence of atropine (1 microM) or the selective GABA(B) receptor agonist beta-parachlorophenyl-gamma-aminobutyric acid [(-)baclofen; 10 microM]. Also, application of OXO-M resulted in a pronounced prolongation (rather than a decrease) of electrically evoked postsynaptic potentials (PSPs) which now exhibited recurrent superimposed spike discharges. In adult slices, in the continuous presence of CGP 52432 (1 microM; 20 min pre-incubation), a subsequent exposure to 10 microM OXO-M or 1S,3R-ACPD failed to induce any spontaneous epileptiform activity, and evoked PSPs were consistently suppressed. In contrast, in immature slices, after incubation in CGP 52432 (1 microM; 20 min), a subsequent application of a low dose of OXO-M (2.5 microM), which was inactive per se, was able to produce spontaneous PDSs and a prolongation of evoked PSPs. We conclude that a reduction in GABA(B)-mediated synaptic inhibition in immature slices (in co-operation with other factors) may contribute to the facilitation of excitatory neurotransmission and therefore play a role in the generation of mAChR-induced epileptiform activity.

Animals↗

PubMed2005

Synaptic influences of pontine nuclei on cochlear nucleus cells.

Using the in vitro isolated whole brain preparation of the guinea pig, we tested the synaptic effects induced by the stimulation of pontine nuclei (PN) in intracellularly recorded and stained principal cells of the cochlear nucleus (CN). Twenty percent of the recorded cells in all CN subdivisions responded to stimulation of either ipsilateral or contralateral PN, and 12% of the cells exhibited convergence of inputs from both sides. The responses were recorded only in stellate cells of the ventral CN and in the pyramidal cells of the dorsal CN, whereas no responses were observed in bushy, octopus, and giant cells. PN stimulation produced excitatory and inhibitory postsynaptic potentials as well as mixed responses. The heterogeneous nature and the wide latency range (3.2-18 ms) of observed responses suggest significant variability in the underlying synaptic mechanisms and the implicated pathways. We propose that PN projections to the CN, terminating mainly in the granule cell domain (GCD), together with other non-auditory and auditory inputs contribute to multimodal convergence in the GCD leading ultimately to modulatory actions on the output activity of CN principal cells.

Animals↗

PubMed2005

Activation of group I metabotropic glutamate receptors depresses recurrent inhibition of motoneurons in the neonatal rat spinal cord in vitro.

This study examined whether activation of group I metabotropic glutamate receptors (mGluRs) could modulate synaptic inhibition of spinal motoneurons in the neonatal rat isolated spinal cord. Recurrent inhibitory postsynaptic potentials (IPSPs) generated by Renshaw cells were evoked via antidromic stimulation of motor axon collaterals and recorded intracellularly from lumbar motoneurons. The selective agonist of group I mGluRs DHPG (5 micromol L-1) depressed the recurrent IPSP, an effect prevented by the selective antagonist AIDA (500 micromol L-1). The depression by DHPG was use-independent and could be partly counteracted by increasing stimulus strength. Paired pulse depression observed at <or=50-ms intervals was blocked by DHPG in an AIDA-sensitive manner. These results suggest that, in the presence of DHPG, smaller recurrent IPSPs can contribute to the excitatory action of mGluR activation on spinal networks, including the generation of synchronous oscillations recorded from motoneurons.

Analysis of Variance↗

PubMed2000

Convergence pattern of uncrossed excitatory and inhibitory semicircular canal-specific inputs onto second-order vestibular neurons of frogs. Organization of vestibular side loops.

Second-order vestibular neurons of frogs receive converging monosynaptic excitatory and disynaptic excitatory and inhibitory inputs following electrical pulse stimulation of an individual semicircular canal nerve on the ipsilateral side. Here we revealed, in the in vitro frog brain, disynaptic inhibitory postsynaptic potentials (IPSPs) by bath application of antagonists specific for glycine or gamma-aminobutyric acid-A (GABA(A)) receptors. Differences in the response parameters between disynaptic IPSPs and excitatory postsynaptic potentials (EPSPs) suggested that disynaptic IPSPs originated from a more homogeneous subpopulation of thicker vestibular nerve afferent fibers than mono- or disynaptic EPSPs. To investigate a possible size-related organization of these canal-specific, parallel pathways, we combined long-lasting anodal currents of variable intensities with strong cathodal test pulses, to block pulse-evoked responses reversibly in a graded manner according to the size-related sensitivity of vestibular nerve afferent fibers. The anodal current intensity required to block a particular response component was about 15 times lower than the strength of the cathodal test pulse that activated this response component. These large threshold differences were exploited for a selective anodal suppression of the responses from thick vestibular nerve afferent fibers. In fact, response components known to originate exclusively from thick-caliber afferent fibers such as the electrically transmitted monosynaptic EPSP component exhibited the lowest thresholds for cathodal test pulses and were the first to disappear in the presence of small anodal polarization steps. Thresholds for the activation/inactivation of responses and current intensities required for response saturation/blockade were used to assess the fiber spectrum that evoked the different response components. Mono- and disynaptic EPSPs appeared to originate from a broad spectrum of thick and thin vestibular nerve afferent fibers. The spectrum of afferent fibers that activated disynaptic IPSPs on the other hand was more homogeneous and consisted of thick and intermediate fibers. Such a canal-specific and fiber type-related organization of converging inputs of second-order vestibular neurons via feedforward projections was shown for the first time by this study in frogs, but might also prevail in mammals. Similar differences in these feedforward pathways have been proposed earlier in a vestibular side-loop model. Our results are consistent with the basic assumptions of this model and relate to the processing and tuning of dynamic vestibular signals.

Animals↗

PubMed2006

Differential phosphoinositide binding to components of the G protein-gated K+ channel.

The regulation of ion channels and transporters by anionic phospholipids is currently very topical. G protein-gated K(+) channels from the Kir3.0 family are involved in slowing the heart rate, generating late inhibitory postsynaptic potentials and controlling hormone release from neuroendocrine cells. There is considerable functional precedent for the control of these channels by phosphatidylinositol 4,5-bisphosphate. In this study, we used a biochemical assay to investigate the lipid binding properties of Kir3.0 channel domains. We reveal a differential binding affinity to a range of phosphoinositides between the C termini of the Kir3.0 isoforms. Furthermore, the N terminus in addition to the C terminus of Kir3.4 is necessary to observe binding and is decreased by the mutations R72A, K195A and R196A but not K194A. Protein kinase C phosphorylation of the Kir3.1 C-terminal fusion protein decreases anionic phospholipid binding. The differential binding affinity has functional consequences as the inhibition of homomeric Kir3.1, occurring after M3 receptor activation, recovers over minutes while homomeric Kir3.2 does not.

Amino Acid Sequence↗

PubMed2004

Continuum limit of discrete neuronal structures: is cortical tissue an "excitable" medium?

As a simple model of cortical tissue, we study a locally connected network of spiking neurons in the continuum limit of space and time. This is to be contrasted with the usual numerical simulations that discretize both of them. Refractoriness, noise, axonal delays, and the time course of excitatory and inhibitory postsynaptic potentials have been taken into account explicitly. We pose, and answer, the question of whether the continuum limit presents a full description of scenarios found numerically (the answer is no, not quite). In other words, can the numerics be reduced to a continuum description of a well-known type? As a corollary, we derive some classical results such as those of Wilson and Cowan (1973), thus indicating under what conditions they are valid. Furthermore, we show that spatially discrete objects may be fragile due to noise arising from the stochasticity of the individual neurons, whereas they are not once the continuum limit has been taken. This, then, resolves the above question. Finally, we indicate how one can directly incorporate orientation preference of the neurons.

Action Potentials↗

PubMed2002

Parvalbumin 3 is an abundant Ca2+ buffer in hair cells.

Ca2+ signaling serves distinct purposes in different parts of a hair cell. The Ca2+ concentration in stereocilia regulates adaptation and, through rapid transduction-channel reclosure, underlies amplification of mechanical signals. In presynaptic active zones, Ca2+ mediates the exocytotic release of afferent neurotransmitter. At efferent synapses, Ca2+ activates the K+ channels that dominate the inhibitory postsynaptic potential. A copious supply of diffusible protein buffer isolates the three signals by restricting the spread of free Ca2+ and limiting the duration of its action. Using cDNA subtraction and a gene expression assay based on in situ hybridization, we detected abundant expression of mRNAs encoding the Ca2+ buffer parvalbumin 3 in bullfrog saccular and chicken cochlear hair cells. We cloned cDNAs encoding this protein from the corresponding inner-ear libraries and raised antisera against recombinant bullfrog parvalbumin 3. Immunohistochemical labeling indicated that parvalbumin 3 is a prominent Ca2+-binding protein in the compact, cylindrical hair cells of the bullfrog's sacculus, and occurs as well in the narrow, peanut-shaped hair cells of that organ. Using quantitative Western blot analysis, we ascertained that the concentration of parvalbumin 3 in saccular hair cells is approximately 3 mM. Parvalbumin 3 is therefore a significant mobile Ca2+ buffer, and perhaps the dominant buffer, in many types of hair cell. Moreover, parvalbumin 3 provides an early marker for developing hair cells in the frog, chicken, and zebrafish.

Amino Acid Sequence↗

PubMed1993

Inhibitory commissural connections of neurones in the trigeminal motor nucleus of the rat.

Physiological evidence is presented for the existence of commissural fibres that cross the midsagittal plane in the medulla of the rat at the level of the trigeminal motor nucleus (Mo5). These fibres, which have their origin in the Mo5, terminated in the contralateral Mo5. Small inhibitory postsynaptic potentials were recorded in jaw-closing motoneurones by electrical activation of the commissural fibres; jaw-opening and fusimotor neurones as well as the jaw-closing and jaw-opening reflex were not affected. Electromyographic recordings from jaw-closing and jaw-opening muscles in the unrestrained rat showed that masseter activity was inhibited by the commissural fibres. These trigeminal commissural connections might play a part in the co-ordination of bilateral activity of the jaw-closing musculature during unilateral chewing.

Animals↗

PubMed1995

Interneurones of the supratrigeminal area mediating reflex inhibition of trigeminal and facial motorneurones in the rat.

Whether sensory information from the inferior alveolar nerve is mediated by different types of interneurones in the supratrigeminal area (Su5) and whether different types of these interneurones have different inhibitory actions on jaw-closing motor neurones of the trigeminal motor nucleus was investigated. The intracellular responses of periodontal afferents in the mesencephalic trigeminal nucleus, Su5 interneurones and jaw-closing motor neurones were studied in response to graded, single-shock stimulation of the ipsilateral inferior alveolar nerve. It was found that the inhibitory action of afferent inflow from the inferior alveolar nerve to jaw-closing motor neurones is possibly mediated by two types of Su5 interneurones (T-I and T-II). These Su5 neurones were discriminated on the basis of their firing characteristics. The findings also indicated that: (1) T-I neurones are responsible for short-latency, low-threshold inhibitory postsynaptic potentials (IPSPs) observed in the trigeminal motor nucleus neurones; (2) T-II interneurones mainly contribute to the amplitude of these IPSPs at higher stimulus strengths; (3) the late part of plateau IPSPs in the jaw-closing motor neurones is induced by a characteristic firing of T-II neurones. It was also shown that afferent inflow from the inferior alveolar nerve, probably mediated by collaterals of T-I and T-II interneurones, also evokes IPSPs in neurones of the intermediate subnucleus of the facial motor nucleus. The characteristics of these IPSPs resemble those of the IPSPs recorded in the jaw-closing motor neurones.

Action Potentials↗

PubMed1990

Acute effects of lithium on synaptic transmission in rat hippocampus studied in vitro.

Acute effects of lithium on synaptic transmissions in the CA1 neurones of rat hippocampus were examined. Perfusion of 2-10 mM lithium chloride (LiCl) produced a dose-dependent increase in the amplitude of field EPSPs, whereas change in the population spikes was variable. The increasing ratio of second field EPSP, which was examined by paired-pulse stimulation, was reduced about 10% by 5 mM LiCl. Intracellularly recorded EPSPs and IPSPs were facilitated by 10 mM LiCl, and the soma membrane was depolarized about 3.2 mV. Intracellular calcium concentration was measured in single hippocampal neurones using fura-2. Although calcium concentration at rest was approximately 30 nM and was increased to an average of 220 nM by 10(-5) M glutamate, 10 mM LiCl had no influence on it. The effects of Li on calcium-dependent processes were not manifested in this study. Variable changes of population spikes may be dependent on the balance between the excitatory and inhibitory postsynaptic potentials during lithium application.

Action Potentials↗

PubMed1976

Studies on the neuropharmacological activity of bicuculline and related compounds.

Bicuculline and 3 chemical derivatives were assayed on a variety of biological systems. Consistent with reports of studies on other animals, some of these compounds caused convulsions in insects and blocked inhibitory postsynaptic potentials in insect muscle. They all potently inhibited mouse brain acetylcholinesterase. Bicuculline and its analogs inhibited the binding of GABA in vitro to sites in crayfish muscle membranes which have properties of receptor sites; this site of action could explain the activity of bicuculline at arthropod neuromuscular junctions. These compounds, at high concentrations (over 100 muM), also inhibited GABA uptake by mouse brain homogenates at 0 degrees C apparently non-competitively. Bicucine methyl ester inhibited GABA transport by brain at 37 degrees C, consistent with non-specific membrane effects at high concentrations of drug. These and other observations cast doubt upon the specificity of bicuculline-like compounds for action on GABA synapses, especially for in vitro studies at high drug concentrations (over 10 muM). The neuroactivity of low doses of bicuculline is apparently not explained by these in vitro effects, and could very well be due to inhibition of GABA synapses at either receptor or ionophore sites. At physiological conditions of pH and temperature, bicuculline is hydrolyzed at its lactone moiety to the less active compound bicucine; this could lead to underestimates of the biological activity of bicuculline. More stable analogs studied so far are not more potent, however.

Acetylcholinesterase↗

PubMed1978

Strychinine binding associated with synaptic glycine receptors in rat spinal cord membranes: ionic influences.

Ammonium salts of some anions decrease the potency of glycine in inhibiting (3H)strychnine binding associated with synaptic glycine receptors. A correspondence exists between the ability of the ammonium salts of anions to increase the IC50 of glycine in inhibiting the (3H) strychnine binding, their capacity to reduce the (3H) strychnine binding itself, and their capacity to reverse inhibitory postsynaptic potentials. The decrease of (3H)strychnine binding in the presence of chloride is abolished by sodium, while the decrease of the potency of glycine in inhibiting (3H)strychnine is not. Binding of (3H)strychnine is influenced by monovalent cations in a biphasic fashion. Concentrations of Li+, K+, and Na+ up to 150mM decrease (3H)strychnine binding, while higher concentrations of the cations increase (3H)strychnine binding. Inhibition by glycine of (3H)strychnine binding is enhanced by low concentrations of these cations.

Action Potentials↗