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Biomedical subjects

A Constanti

Publications and source records attributed to A Constanti.

At least 73 records · Page 4Linked to original sources
PubMed1981

Who do barium ions imitate acetylcholine?

The action of 1-4 mM barium on bullfrog sympathetic ganglion cells was studied using voltage clamp. Barium imitated the action of muscarine, causing depolarization, increased input resistance, tendency to repetitive firing, and a specific inhibition of a slow small outward current termed the M current. Barium did not produce significant short-term inhibition of three other outward currents; the delayed rectifier, the calcium-dependent K current, and the A current.

Acetylcholine↗
PubMed1981

The effects of piperazine on rat sympathetic neurones.

1. The neuronal effects of the anthelmintic piperazine (Pip) on rat sympathetic ganglia were studied in vitro by means of intracellular and extracellular recording techniques. 2. Surface potential recordings indicated that Pip (0.1-10 mM as citrate, 1-30 mM as hexahydrate) produced a sustained depolarization (reversible on washing) of rat ganglia. gamma-Aminobutyric acid (GABA, 1-100 micro M) also evoked reversible depolarizations but, unlike Pip, responses to the higher doses of GABA declined during a 2 min exposure. Depolarizations produced by Pip or carbachol (but not GABA) were markedly depressed by hexamethonium but only slightly by bicuculline or picrotoxin. 3. Intracellular recordings revealed that Pip-induced depolarizations were accompanied by an increase in membrane conductance and a broadening and depression of the directly-evoked spike. 4. In the presence of hexamethonium (1 mM), the responses to Pip hexahydrate and to cholinoceptor agonists were abolished, but Pip citrate still changed the spike configuration and induced membrane hyperpolarization with a small conductance increase. These residual effects were mimicked by superfusing with Na citrate or Ca2+-free medium, suggesting that significant Ca2+ binding by the citrate anion of the Pip salt was probably responsible for the observed activity of Pip citrate in the presence of hexamethonium. 5. It is concluded that on rat ganglia Pip is a nicotinic agonist, with no detectable GABA-mimetic activity.

Animals↗
PubMed1981

Slow cholinergic and peptidergic transmission in sympathetic ganglia.

Experiments of voltage-clamped bullfrog sympathetic neurons suggest that the "slow depolarization" produced by orthodromic stimulation, by muscarinic agonists, or by the peptide luteinizing hormone-releasing hormone (LHRH), results from the suppression of a time- and voltage-dependent outward K+ current, the "M current" (IM). This current is activated between -60 and -10mV, with a half-maximal activation voltage of -35 mV, a minimum time constant (TM) of 150 ms at -35 mV, and a voltage sensitivity corresponding to a single gating particle with a minimum valency of 4.IM does not show time-dependent inactivation within its activation range and provides the sole potential-sensitive component of the steady outward membrane conductances between -60 and -25 mV. Muscarinic agonists and LHRH selectively depress IM via different receptors, without altering their voltage sensitivity. Although not dependent on external Ca2+ ion, IM is also selectively depressed by Ba2+ ions, so accounting for the cholinomimetic action of Ba2+. It is suggested that IM acts as a braking control on spike discharges and that removal of this control during slow cholinergic and peptidergic transmission provides a unique synaptic tuning mechanism.

Acetylcholine↗
PubMed1981

Voltage clamp analysis of inhibitory synaptic action in crayfish stretch receptor neurons.

Abdominal stretch receptor neurons of Procambarus clarkii were voltage clamped with two microelectrodes, and the synaptic currents set up by stimulating the inhibitory axons, or by rapid bath application of gamma-aminobutyric acid (GABA), were recorded. The inhibitory postsynaptic current (IPSC) decay was exponential, the time constant of decay being increased by membrane depolarization. The IPSC decay was prolonged by diphenylhydantoin, whereas the IPSC amplitude was depressed by picrotoxin. It is suggested that these effects may reflect slowing of the channel closing and opening rates, respectively. Step clamps applied in the presence of GABA yield currents that show inactivation in the 100 ms time range. This inactivation was shown to reflect chloride movement across the membrane. Step clamp data were used to construct dose-response curves. Diphenylhydantoin shifts the dose-response curve to the left with little change in the maximum response. Picrotoxin shifts the curve to the right with a small reduction in the maximum response. These effects are consistent with the postulated effects on channel opening and closing rates, if GABA normally opens a large portion of the channels. Suitable combinations of picrotoxin and diphenylhydantoin acting together leave the dose-response curve unmodified, as predicted.

Animals↗
PubMed1980

Intracellularly-recorded effects of glutamate and aspartate on neurones in the guinea-pig olfactory cortex slice.

The effects of bath-applied glutamate, aspartate (and some related amino acids) on neurones of the guinea pig olfactory cortex slice were recorded intracellularly. Neurones were activated either by intracellularly-applied current or orthodromically by stimulating the lateral olfactory tract. In response to orthodromic stimuli several neurones displayed a late hyperpolarizing potential (LHP) after the usual sequence of EPSP, spike and IPSP. Glutamate and aspartate evoked 3 types of response: (a) a depolarization with apparent increase in input conductance; (b) a depolarization with no detectable conductance change; and (c) a hyperpolarization with conductance increase. Some possible mechanisms by which these 3 response-types could be generated are discussed. Depolarizations evoked by the glutamate analogue, kainate, were usually irreversible. Our results emphasize that glutamate and aspartate can evoke a variety of neuronal responses from olfactory cortex neurones. Several of these responses were previously undetected in experiments based on extracellular recordings.

Animals↗
PubMed1980

Intracellular observations on the effects of muscarinic agonists on rat sympathetic neurones.

1 Responses of single neurones in isolated superior cervical ganglia of the rat to muscarinic agonists were recorded with intracellular microelectrodes. 2 (+/-)-Muscarine (1 to 10 microM) and methylfurmethide (1 to 3 microM) produced reversible membrane depolarizations (less than or equal to 15 mV) accompanied by a fall in input conductance and an increased tendency toward repetitive spike discharges. The spike configuration was unchanged. 3 Analysis of steady-state current/voltage curves revealed the most consistent muscarinic effect to be a large reduction (approximately 50% at 10 microM muscarine) in input slope conductance around rest potential. This conductance decrease diminished as the membrane was hyperpolarized, and the normal increase in slope conductance with membrane depolarization was depressed. The current/voltage curves in the between -65 and -88 mV (i.e. 9 to 28 mV hyperpolarized to rest potential). 4 Divalent cations (10 mM [Ca2+] or [Mg2+]) showed a small muscarine-like effect on the current/voltage and slope conductance/voltage curves, but did not affect the action of muscarine itself. 5 Tetraethylammonium (TEA, 5 mM) also had a small muscarine-like effect, and depressed or reversed the action of muscarine. However, TEA differed from muscarine in blocking orthodromic transmission and prolonging direct spike repolarization. 6 It is concluded that the primary effect of muscarinic agonists is to alter the rectifying properties of the cell within the potential range -80 to -40 mV.

Action Potentials↗
PubMed1980

Intraneuronal effects of inhibitory amino acids.

Injections of gamma-aminobutyric acid (GABA) into spinal motoneurons (in cats under Dial) induce a small but relatively prolonged hyperpolarization (mean - 1.7 mV, SD 2.1; n = 25) which is associated with a rise in input resistance (mean 44%, SD 122; n = 34), is not reversed by hyperpolarization, and is not potentiated by intracellular release of benzodiazepines. Muscimol sometimes has a comparable effect, but alpha-aminoisobutyric acid and glycine do not. These observations are consistent with the possibility that motoneurons have a Na+-coupled GABA transport mechanism that is electrogenic and can be reversed by an excess of intracellular GABA.

Action Potentials↗
PubMed1979

Further observations on the interaction between glutamate and aspartate on lobster muscle.

1 The ability of bath-applied L-glutamate to enhance subsequent depolarizations produced by bath-applied L-aspartate on lobster muscle was further investigated by means of intracellular recording techniques. 2. Increasing the conditioning glutamate concentration or exposure time produced a greater enhancement of aspartate responses. Enhancement was also dependent on the time interval between glutamate and aspartate doses and was not prevented by overnight storage of preparations in vitro. 3. The dose-depolarization curve for enhanced aspartate responses (measured at a fixed time following a given dose of glutamate) was displaced to the left along the abscissa scale relative to control, with no detectable change in limiting log-log slope. 4. Conditioning doses of kainate or domoate (but not quisqualate, aspartate, or KCl) also enhanced aspartate responses; however, their conditioning effect was little affected by increasing the concentration, exposure time, or time interval before applying aspartate. The rate of onset and decline of the enhanced aspartate response always resembled that of the previous conditioning agonist. 5. D and L-Aspartate were approximately equieffective depolarizing agents whereas D-glutamate was approximately 1/40 as potent as L-glutamate. After a conditioning dose of D or L-glutamate, responses to D or L-aspartate were enhanced. 6. In a Na+-free (Li+) medium, both the glutamate depolarization and the conditioning effect towards aspartate were largely abolished. With kainate however, Na+ was not apparently important either for evoking the kainate response or for producing the conditioning effect. 7. Bath-applied glutamate greatly enhanced and prolonged the time course of the iontophoretic aspartate potential with only a small effect on the glutamate potential; however, these effects were not maintained after washout of glutamate. In contrast, bath-application of aspartate depressed the aspartate potential while enhancing the glutamate potential. Some sites that were insensitive to iontophoretically-applied aspartate became clearly responsive to this agent during a bath-application of glutamate. 8. It is proposed that during conditioning with bath-applied glutamate, kainate or domoate, some agonist is trapped by extrajunctional sites and is subsequently displaced by bath-applied aspartate to produce the long-term enhancement effect.

Animals↗
PubMed1979

The GABA dose/conductance relationship on lobster muscle.

A quantitative study was made of the action of GABA, some structurally-related agonists and antagonists on the dactyl opener muscle fibres of the lobster. It was concluded that the GABA dose/conductance relationship was better described by a two independent binding-site receptor model (with KII = 30 microM) than by a single-site or a two-site high co-operativity model. The dose/conductance curves for gamma-amino-beta-hydroxybutyric acid (GABOB), delta-aminovaleric acid (DAV) and piperazine indicated 'full' agonist behaviour, whereas those for guanidoacetic acid (GuAc) indicated a partial agonist action. beta-guanidinopropionic acid (beta-GP) and gamma-guanidinobutyric acid (gamma-GB) behaved as weak competitive GABA antagonists. Bicuculline was found to antagonize GABA non-competitively on the lobster as in the crayfish, whereas picrotoxin appeared to act in a 'mixed' antagonistic fashion.

Amino Acids↗