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Biomedical subjects

R Anwyl

Publications and source records attributed to R Anwyl.

At least 91 records · Page 5Linked to original sources
PubMed1988

Changes in auditory evoked responses and in the inhibitory action of 5-hydroxytryptophan following chronic treatment with imipramine in the rat.

The neurophysiological effects of acute and chronic treatment with the tricyclic antidepressant drug imipramine were investigated. Brainstem (BAER) and middle latency (MLR) auditory evoked responses were monitored in the alert and immobile rat. Daily injection of imipramine (10 mg/kg, IP) for 2 weeks produced a 13% increase in the latency and a 35% reduction in the amplitude of the N17 component of the MLR. Acute imipramine treatment had no effect. There was no observable change in the BAER after either acute or chronic drug administration. Serotonergic function was assessed by studying the inhibitory effects of 5-hydroxytryptophan on the BAER and MLR. Chronic application of imipramine caused an apparent reduction of the effects of 5-hydroxytryptophan (75 mg/kg, IP) on the N17 component of the MLR. This may, however, be due to the shift in baseline latency and amplitude. Inhibition of the BAER by 5-hydroxytryptophan was unaltered by long term exposure to imipramine. Acute treatment with imipramine was without effect on the modulation of the BAER and the MLR by 5-hydroxytryptophan. These results provide evidence that chronic, as opposed to acute, administration of imipramine had an inhibitory effect on auditory processing at the level of the MLR and that this may be associated with a change in the net output of the serotonergic system.

5-Hydroxytryptophan↗
PubMed1987

Electroconvulsive treatment reduces long-term potentiation in rat hippocampus.

The effect of repeated electroconvulsive treatment (ECT) was investigated on long-term potentiation (LTP) in the rat hippocampal slice. Extracellular, recordings of population spikes and excitatory postsynaptic potentials (EPSP) were made from the pyramidal cell layer of CA1 in response to stimulation of the stratum radiatum. LTP was induced by 5 high-frequency trains of stimuli. ECT (10 treatments, 1 treatment every day for 20 days) markedly inhibited LTP of the population spike and EPSP. Thus LTP of the 25% maximum population spike was 104% in control, and 20% in rats 24 h after ECT. LTP of the EPSP was 35% in control and 12% after ECT.

Animals↗
PubMed1987

Caffeine inhibits post-tetanic potentiation but does not alter long-term potentiation in the rat hippocampal slice.

The effects of caffeine were investigated on the extracellular excitatory postsynaptic potentials (EPSPs) recorded in the stratum radiatum of CA1 of the rat hippocampal slice in response to stimulation of the Schaffer collaterals. Caffeine in concentrations from 500 microM to 10 mM caused an increase in the amplitude of the EPSP, which reached a peak after 5-10 min perfusion. This increase was antagonized by pretreatment with 20 microM trifluoperazine. Paired-pulse facilitation, augmentation and potentiation were strongly inhibited by caffeine. Augmentation was most sensitive to caffeine, being abolished by 500 microM caffeine. Long-term potentiation (LTP) induced by high-frequency stimulation was not significantly inhibited by caffeine either by 5-10 min or by 60 min perfusion with 10 mM caffeine. Moreover, the caffeine-induced increase in the low-frequency EPSP could be reversed by 30 min washout, demonstrating that it was not an LTP type increase.

Afferent Pathways↗
PubMed1987

Enhancement of long-term potentiation by the calcium channel agonist Bayer K8644 in CA1 of the rat hippocampus in vitro.

The effect of the Ca agonist BAY K8644 was studied on long-term potentiation (LTP) of extracellular excitatory postsynaptic potentials in the stratum radiatum of CA1 of the hippocampus in vitro. LTP was evoked by brief trains of high-frequency stimulation applied to the stratum radiatum of CA1. 0.5% Ethanol, the vehicle used to dissolve BAY K8644, reduced LTP from 43% to 15%. An amount of 15 microM BAY K8644, in 0.5% ethanol, enhanced LTP from 13% in the ethanol control to 57%. The Ca channel antagonist verapamil did not alter control LTP, but did inhibit the potentiating action of BAY K8644 on LTP. It is postulated that the enhancement of LTP by BAY K8644 may occur through enhancement of Ca influx through voltage-dependent Ca channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Neurophysiological effects of buspirone and isapirone in the hippocampus: comparison with 5-hydroxytryptamine.

The neurophysiological effects of two novel anxiolytic compounds, buspirone and isapirone (TVX Q 7821), were compared with those of 5-hydroxytryptamine (5-HT) on the population spike in the CA1 region of the rat hippocampal slice. Micromolar concentrations of the two drugs mimicked the inhibitory effect of 5-HT but unlike 5-HT they did not produce any significant excitation. In slices in which 5-HT was purely excitatory, there was a marked reduction in the inhibitory response to these agents. The effect of isapirone was antagonised by spiperone. These results suggest that buspirone and isapirone are agonists for 5-HT1A receptors in the hippocampus.

Animals↗
PubMed1986

4-Aminopyridine-mediated increase in long-term potentiation in CA1 of the rat hippocampus.

The effect of 4-aminopyridine (4-AP) on long-term potentiation (LTP) was studied in the hippocampal slice preparation of the rat. Field excitatory postsynaptic potentials (EPSPs) were recorded and evoked in the stratum radiatum of the CA1. Both the low frequency EPSP and LTP of the EPSP were significantly increased by treatment with 4-AP. These effects were inhibited by increasing the magnesium concentration from 1 to 4 mM. Pretreatment with 20 microM DL-2-amino-5-phosphonovalerate antagonized only the increase in LTP produced by 4-AP. It is suggested that 4-AP enhances Ca influx either pre- or postsynaptically and thereby increases LTP.

4-Aminopyridine↗
PubMed1986

Action of halothane on rat soleus muscle: temperature dependent induction of contractures and modification of caffeine and potassium contractures.

Halothane induced calcium-dependent contractures in rat soleus muscle at temperatures between 4 degrees C and 13 degrees C, but not at higher temperatures. The peak tension of the contractures increased as temperature was decreased below 13 degrees C. The magnitudes of the contractures were reduced by the addition of cobalt or lanthanum ions to the medium in the water bath. The anaesthetic also potentiated caffeine-induced contractures in muscle at 22 degrees C and 37 degrees C in a calcium-dependent manner. The contractures at 37 degrees C were more sensitive to the concentration of this ion than were contractures at 22 degrees C. Halothane increased peak tension and prolonged the time course of potassium-induced contractures, but did not alter their threshold values at either 22 degrees C or 37 degrees C. It was concluded that, in rat muscle, halothane may act at a site on the plasmalemma, retard the onset of inactivation and move the inactivation curve further from the resting membrane potential.

Animals↗
PubMed1985

The effect of prolonged treatment with tricyclic antidepressants on the actions of 5-hydroxytryptamine in the hippocampal slice of the rat.

The effect of long-term treatment with the tricyclic antidepressants imipramine (IMI) and desmethylimipramine (DMI) on neuronal responsiveness to 5-hydroxytryptamine (5-HT) was examined in the hippocampal slice preparation from the rat. Population spikes, evoked by electrical stimulation of the stratum radiatum, were recorded in the pyramidal cell layer of the CA1 region of the isolated hippocampus. When 5-HT (10(-7) to 2 X 10(-5) M) was applied there was an initial increase followed by a decrease in the amplitude of the population spike. On washout of 5-HT the amplitude increased transiently above control levels. Daily injection of 10 mg/kg of imipramine or desmethylimipramine, intraperitoneally, into rats for 4-5 weeks was found to produce a significant decrease in the inhibitory effect of 10(-5) M 5-HT, whereas there was no apparent change in the excitatory effects. The acute application of 10(-5) M imipramine or desmethylimipramine antagonized the inhibitory effect of 10(-5) M 5-HT without affecting the excitatory effects. Acute application of the 5-HT receptor antagonists cyproheptadine (10(-5) M) and ketanserin (7.5 X 10(-6) M) completely prevented the appearance of the inhibitory effect of 10(-5) M 5-HT without affecting the excitatory effects. It was concluded that the decreased inhibitory effect of 5-HT which was produced by chronic treatment with imipramine or desmethylimipramine was probably due to a reduction in the number of 5-HT receptors or a reduction in the post-receptor effector mechanisms for 5-HT.

Animals↗
PubMed1985

Frequency-dependent block of field potentials in the rat hippocampal slice caused by tricyclic antidepressants.

The effect of the tricyclic antidepressants imipramine and desipramine were studied on field potentials in the rat hippocampal slice. The electrically evoked stratum radiatum nerve volley, excitatory postsynaptic potential (e.p.s.p.) and pyramidal cell layer population spike (PS) were recorded in the CA1 region. At concentrations of 10(-6)M to 10(-5)M, impramine did not affect the amplitude of the nerve volley, e.p.s.p. or PS at low frequencies of stimulation (0.01 Hz). At higher frequencies of stimulation (1-100 Hz), imipramine caused a frequency-dependent block of the nerve volley, e.p.s.p. and PS. The time course of onset of the frequency-dependent block in the presence of imipramine was very slow. Maximum inhibition was reached after 3-4 h treatment with imipramine. Desipramine (10(-6)-10(-5)M) also caused a frequency-dependent block of the hippocampal field potentials. Only slight frequency-dependent block was observed in slices from rats injected in vivo with desipramine (10 mg kg-1) for 14 days.

Action Potentials↗
PubMed1984

Neurophysiological evidence for tricyclic antidepressant-induced decreased beta-adrenergic responsiveness in the rat hippocampus.

A study was made in rats of the effects of chronic treatment with the tricyclic antidepressant agent imipramine on the increase in the population spike amplitude produced by the beta-adrenergic receptor agonist isoproterenol in the 'in vitro' slice preparation of the hippocampus. A significant reduction of 39% and 44% of the population spike increase was observed at 5 X 10(-7) M and 1 X 10(-6) M isoproterenol respectively in rats treated for 28 days with 10 mg/kg i.p. imipramine.

Action Potentials↗
PubMed1984

The effects of external potassium, multivalent cations and temperature on caffeine contractures in rat skeletal muscle.

The effects of multivalent cations, membrane potential and temperature on caffeine contractures of rat soleus and extensor digitorus longus (e.d.l.) muscles were investigated. The amplitude of the caffeine contracture was depressed by the removal of calcium and by the addition of a high concentration (1 mM) of lanthanum. Low concentrations of lanthanum (0.1-0.5 mM) augmented the caffeine contracture. Low levels of depolarization by potassium (10-40 mM) augmented the amplitude of the caffeine contracture, while higher concentrations of potassium depressed the contracture. Maximum augmentation of the caffeine contracture occurred with a higher concentration of potassium (20 mM vs 10 mM) in the e.d.l. than in the soleus muscle. The amplitude of contractures was directly related to temperature between 22 and 37 degrees C and inversely related to temperature below 22 degrees C. The effects of caffeine in rat skeletal muscle are suggested to be exerted on the sarcolemma and the mechanisms of action are by modification of the processes of activation and inactivation.

Animals↗
PubMed1984

Potassium contractures and mechanical activation in rat skeletal muscle: effects of multivalent cations, temperature and tetracaine.

The effects of cations, temperature and tetracaine on potassium-induced contractures of rat soleus and extensor digitorus longus (e.d.l.) muscles were investigated. In the soleus, the threshold for the potassium contracture was lower (10-20 vs 20-40 mM), the peak amplitude was up to fourteen times larger, and the time course was about one half that in the e.d.l. muscle. The extent of inactivation of a test potassium contracture was directly related to the concentration of potassium in the conditioning solution and the period of exposure. Removal of calcium reduced the amplitude and time course of potassium contractures in both preparations. Addition of cobalt (10 mM) reduced the amplitude but prolonged the time course of contractures. Exposure of muscles to tetracaine (10(-5)-10(-6) M for 30 min) increased, but higher concentrations reduced, the amplitude of potassium contractures. When present for one minute, tetracaine (1 mM) moved the potassium activation curve to higher, and the potassium inactivation curve to lower, potassium concentrations.

Animals↗
PubMed1983

Acetylcholine-induced electrical responses in neuroblastoma cells.

The response to iontophoretic application of acetylcholine in the mouse neuroblastoma cell line N1E-115 was composed of three phases. The initial fast depolarizing phase was blocked by 10 microM d-tubocurarine, but not by 0.1 microM atropine. This phase was followed by a transient hyperpolarization which in turn was followed by a secondary slow depolarization. Both the hyperpolarization and slow depolarization were blocked by atropine (0.1 microM), but not by d-tubocurarine (10 microM). The hyperpolarization and slow depolarization were also evoked by iontophoretic application of the muscarinic agonist methacholine. Under voltage-clamp conditions, an initial fast inward current, a transient outward current, and a secondary slow inward current were recorded in response to acetylcholine application. These three phases of current correspond to the three phases of the membrane potential response. The initial fast inward current increased in amplitude by hyperpolarization of the membrane, and decreased by depolarization. The mean reversal potential was estimated to be -1 mV. The outward current increased in amplitude by depolarization, decreased by hyperpolarization, and reversed its polarity at -67 mV. Alteration of external K+ concentration shifted the reversal potential in the manner expected for an increase in potassium permeability. The slow inward current increased in amplitude by hyperpolarization, decreased by depolarization, and reversed its polarity at +20 mV. It is concluded that the initial fast inward current is mediated by a nicotinic receptor similar to that in muscle end-plate membranes and in postsynaptic membranes of the sympathetic ganglia. Both the outward current and the slow inward current are mediated by muscarinic receptors. The outward current results from an increase in the membrane permeability to K+, and the slow current appears to be carried, at least in part, by Na+.

Acetylcholine↗
PubMed1982

Alterations of spontaneous quantal transmitter release at the mammalian neuromuscular junction induced by divalent and trivalent ions.

The present studies have demonstrated that Ca and Sr have a similar ability to support the release of spontaneous quanta of transmitter at the rat neuromuscular junction. The foreign ions Co, Pb, Zn and La have also been shown to support spontaneous release, although the time course of the increase in miniature end-plate potentials (m.e.p.p.s) caused by these ions is much slower than that caused by Ca and Sr. However, Sr, Co, Pb and Zn were unable to sustain m.e.p.p.s for prolonged periods. High extracellular K (10--15 mM) inhibited the steady state m.e.p.p. frequency in Ca and Sr concentrations above 1 mM, and also delayed the m.e.p.p. frequency increase induced by 1 mM Pb. It is suggested that K ions directly inhibit divalent ion entry into the nerve terminal.

Animals↗
PubMed1980

Inhibition of the acetylcholine receptor by histrionicotoxin.

1 The action of C5-decahydrohistrionicotoxin (C5-HTX) has been investigated on the extrajunctional acetylcholine (ACh) receptors of denervated rat muscle. 2 C5-HTX causes both a rapid and slow reduction in amplitude of iontophoretic ACh potentials evoked at all frequencies from the extrajunctional receptors. 3 C5-HTX also causes a time-dependent inhibition of the iontophoretic potentials evoked at frequencies greater than 0.02 Hz. This inhibition was observed either alone or superimposed upon desensitization, and may be caused by a similar mechanism to desensitization.

Acetylcholine↗
PubMed1980

Desensitization of the acetylcholine receptor of denervated rat soleus muscle and the effect of calcium.

1 Desensitization of the extrajunctional acetylcholine receptors of denervated rat soleus muscle has been studied by evoking iontophoretic acetylcholine potentials at a high frequency (10 Hz). 2 Desensitization occurred with a slow and at least one fast component. 3 Increasing the dose of acetylcholine decreased the half time of onset of desensitization, but did not alter recovery half time. 4 Alteration of external calcium between 0 and 50 mM, or perfusion with agents which increase intracellular calcium such as 2,4-dinitrophenol and the calcium ionophores, X537A and A23187, did not alter desensitization half time. 5 The cholinoceptor agonists acetylcholine, acetylthiocholine, tetramethylammonium and phenyltrimethylammonium all caused desensitization at the same rate.

Acetylcholine↗
PubMed1980

Comparison of desensitization and time-dependent block of the acetylcholine receptor responses by chlorpromazine, cytochalasin B, triton X-100 and other agents.

1 Chlorpromazine, cytochalasin B, Triton X-100, lidocaine, QX-314, pentobarbitone, heptanol and ethanol, but not benzocaine or methylguanidine, caused a time-dependent inhibition of acetylcholine (ACh) potentials. Increasing the concentration of the agents increased the rate of inhibition. 2 The recovery rate from the time-dependent inhibition was the same as from desensitization except in Triton X-100 which slowed the recovery. 3 Hyperpolarizing the membrane potential caused an increase in the rate of the time-dependent inhibition. 4 It is suggested that the time-dependent inhibition and desensitization are very similar phenomena, with either ACh (in desensitization) or an agent (in time-dependent inhibition) causing a block of the activated ACh receptor, and with dissociation from the binding site being very slow. 5 Many of the agents also cause a steady state inhibition of the ACh receptor which appears to be caused by a separate blocking action of the agents.

Acetylcholine↗