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H L Haas

Publications and source records attributed to H L Haas.

At least 109 records · Page 6Linked to original sources
PubMed1986

Effects of histamine on hippocampal pyramidal cells of the rat in vitro.

The actions of bath applied histamine on CA1 pyramidal cells were investigated in hippocampal slices of the rat. Histamine caused a) a slight depolarization but no significant change in resting membrane conductance; b) an abbreviation of long afterhyperpolarizations after single action potentials, bursts of action potentials or TTX resistant spikes; c) a loss of accommodation of firing. In the presence of TEA or barium, histamine prolonged and increased the size and number of the slow TTX resistant spikes. A depolarizing plateau which follows such spikes was also increased by histamine, but the population spike was increased. The frequency of spontaneous chloride dependent potentials, which reflect interneurone firing, was also increased. These effects considerably outlasted histamine application and were mimicked by the H2-agonist impromidine but not the H1-agonist thiazolethylamine, and blocked by the H2-antagonists cimetidine and metiamide but not the H1-antagonists mepyramine or the beta-antagonist propranolol. It is concluded that histamine, by activating H2-receptors, antagonizes a calcium mediated potassium conductance in hippocampal pyramidal cells without affecting calcium current. By this mechanism histaminergic afferent fibres could effectively regulate cortical responsiveness by selectively potentiating large excitatory inputs of target neurones.

Animals↗
PubMed1986

Testing of prototype antiepileptics in hippocampal slices.

The effects of six prototype anticonvulsant drugs, phenytoin, carbamazepine, midazolam, phenobarbital, ethosuximide and sodium valproate, were evaluated in two different experimental models of epileptiform activity using the in vitro slice preparation from the rat hippocampus. The relative potencies of the agents were determined: a) in the complete absence of synaptic transmission by recording spontaneous burst firing from the CA 1 pyramidal cell layer in a low calcium high magnesium solution and b) during blocked synaptic inhibition by observing the activity of each drug upon orthodromically evoked population spikes in penicillin containing medium. The rank order of potencies was a) in low Ca2+: carbamazepine, phenytoin, midazolam, phenobarbital, valproate, ethosuximide; b) in penicillin containing medium: midazolam, phenobarbital, carbamazepine, phenytoin, valproate, ethosuximide. These observations illustrate that the use of multiple paradigms is warranted when examining the mechanisms of action of new anticonvulsants.

Animals↗
PubMed1986

A simple in vitro method to study the trigeminal ganglion.

This report describes a simple in vitro method to harvest and study the electrophysiological properties of the trigeminal ganglion of the rat. In suction electrode recordings from the proximal nerve end, two distinct peaks are identified in the compound action potential evoked by electrical stimulation of the distal nerve. gamma-Aminobutyric acid (GABA), added to the perfusion fluid, caused a positive shift in the DC potential (depolarization) and a partially selective decrease in the amplitude of the slow-conduction peak. Reversible antagonism of the GABA effect by picrotoxin and bicuculline suggests that both responses are receptor mediated. There was no response to carbamazepine or L-baclofen, suggesting that ganglionic polarization does not play a major role in the action of these drugs in trigeminal neuralgia.

Action Potentials↗
PubMed1986

Comparative electrophysiological investigations on oxiracetam and piracetam.

Acute effects of the two psychogeriatric agents, oxiracetam (ISF 2522) and piracetam, were studied in rat brain tissue in vivo and in vitro. In vivo, both compounds elicited a moderate activation of locus coeruleus neuronal discharge rate with doses of 1,000 mg/kg ip. Neither of the compounds however affected spontaneous firing rates of neurons of the medial septal nucleus in vivo if administered intravenously. In the hippocampal slice preparation, the two compounds elicited weak but opposite effects on extracellularly recorded field potentials if administered in high concentrations. Whereas oxiracetam elicited a moderate depressant effect on pyramidal cell excitability, piracetam increased it in a reversible fashion. Piracetam had no effect on the excitatory postsynaptic potential (epsp) evoked by stimulation of the Schaffer commissural fiber pathway but oxiracetam reversibly attenuated it at concentrations of 100 microM to 1 mM. In intracellular recordings from CA1 pyramidal neurons in vitro, piracetam had no effect on resting membrane potential, conductance or afterhyperpolarizations. Oxiracetam, however, slightly hyperpolarized six out of twelve CA1 neurons. Membrane conductance was not affected. In conclusion, electrophysiological studies with the psychogeriatrics oxiracetam and piracetam revealed that the drugs exert weak effects on rat brain tissue in acute experiments, and demonstrated that the two compounds differ in their pharmacological profile.

Animals↗
PubMed1985

The hypothalamohypophyseal system in vitro: electrophysiology of the pars intermedia and evidence for both excitatory and inhibitory inputs.

The purpose of this study was to better assess the function of catecholamine-containing nerve terminals in the pituitary pars intermedia lobe. Hypothalamohypophyseal explants, which included the intact mediobasal hypothalamus (MBH), median eminence, infundibular stalk and the neurointermediate lobe, were obtained from 2-3-week-old male and female albino rats. The tissue was placed in a perfusion chamber and maintained under physiological conditions for up to 12 h. A set of bipolar stimulating electrodes was positioned on the surface of the median eminence, infundibular stalk or the rostroventral arcuate nucleus of the MBH. A microelectrode recorded electrical activity in the pars intermedia gland. Two types of spontaneous action potentials were found; fast 2-4 ms duration neural fiber type spikes and slower 7-10 ms duration spikes probably derived from non-neural endocrine cells. Single-pulse electrical stimulation at all 3 sites evoked both kinds of potentials, while trains of stimuli (0.1-20 Hz) decreased or completely inhibited the basal firing rate of the slower ones. Application of the neuroleptic. L-sulpiride (0.01, 0.1 or 1.0 mumol), to the perfusion medium increased the spontaneous endocrine cell activity and blocked the stimulus-induced inhibition in the explants but had no effect on the activity in isolated pituitaries. Dopamine (0.1 mumol), which is known to inhibit the secretion of pro-opiomelanocortin peptides, reversibly suppressed the spontaneous endocrine cell potentials. These observations support a hypothesis for the presence of a functional tuberohypophyseal dopamine inhibitory system and a possible, but as yet unidentifiable, excitatory system in the pars intermedia. Thus, hypothalamohypophyseal explants can be used to elucidate specific information on this type of neuroendocrine axis.

Action Potentials↗
PubMed1985

Stereoselectivity of L-baclofen in hippocampal slices of the rat.

Extra- and intracellular recording from hippocampal slices of the rat revealed the following effects when baclofen (BF) (0.1-10 microM) was added to the perfusion fluid: a block of synaptic potentials evoked by stimulation of stratum radiatum; a direct hyperpolarization and a conductance increase (for potassium ions) of CA1 pyramidal cells. All this activity was found in the L- none in the D-enantiomer. D-BF did not antagonize the action of L-BF.

Animals↗
PubMed1985

Long-term potentiation and 4-aminopyridine.

Long-term potentiation (LTP) of excitatory postsynaptic potentials (epsp's) was investigated with extracellular field potential recording in hippocampal slices from rats. In the presence of 100 microM 4-aminopyridine (4-AP) the probability of eliciting LTP was unchanged or increased; the extent of potentiation was not significantly different from normal. During LTP saturation, 4-AP further enhanced the epsp. These data are inconsistent with an involvement of A-current reduction in LTP.

4-Aminopyridine↗
PubMed1985

Histamine may act through cyclic AMP on hippocampal neurones.

Bath applied histamine and 8-bromo-cyclic AMP and intracellularly injected cyclic AMP block-long-lasting after-hyperpolarizations and the accommodation of firing in CA1 pyramidal cells recorded in rat hippocampal slices. This action is due to reduction of a calcium-activated potassium conductance (gK(Ca] and leads to potentiation of excitatory signals including epileptiform discharges. The effects are further potentiated and prolonged by a phosphodiesterase inhibitor (Ro 20-1724).

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1985

Effects of caffeine on hippocampal pyramidal cells in vitro.

The effects of caffeine on the electrophysiological properties of CA1 pyramidal neurones were investigated in the rat hippocampal slice preparation in vitro. A concentration-dependent increase in both the extracellularly recorded excitatory postsynaptic potential (e.p.s.p.) and the population spike resulting from stimulation of the stratum radiatum could be evoked by caffeine with a threshold concentration of 10 microM. Intracellular recordings demonstrate a caffeine-evoked decrease in resting membrane potential, an increase in input resistance, a reduction of the long afterhyperpolarization (a.h.p.) and a decrease in accommodation. The interaction between caffeine and adenosine was investigated on the extracellularly recorded e.p.s.p. The maximal response evoked by caffeine was increased in the presence of adenosine and the adenosine concentration-response curve was shifted to the right in a parallel fashion in the presence of caffeine. It is suggested that the effects of caffeine on hippocampal neurones may be mediated by a decrease of one or more potassium conductance(s), and that adenosine and caffeine may compete for the same electrophysiologically active receptor site on these cells.

Adenosine↗
PubMed1985

Adenosine actions on CA1 pyramidal neurones in rat hippocampal slices.

Intracellular recordings with a bridge amplifier of CA1 pyramidal neurones in vitro were employed to study the mechanisms of action of exogenously applied adenosine in the hippocampal slice preparation of the rat. Adenosine enhanced the calcium-dependent, long-duration after-hyperpolarization (a.h.p.) at least in part by a reduction in the rate of decay of the a.h.p. Both the reduced rate of decay and that of the control can be described with a single exponential. Antagonism of the calcium-dependent potassium current (and as a result, the a.h.p.) by bath application of CdCl2 or intracellular injection of EGTA (ethyleneglycolbis-(beta-aminoethyl ether)N,N'-tetraacetic acid) did not reduce the adenosine-evoked hyperpolarization or decrease in input resistance. Similarly, TEA (tetraethylammonium), which antagonizes both the voltage- and calcium-sensitive, delayed, outward rectification, had no effect on the adenosine-evoked changes in resting membrane properties. Adenosine did not affect the early, transient, outward rectification. During exposure to 4-aminopyridine (4-AP) in concentrations sufficient to antagonize this early rectification, the changes in resting membrane properties evoked by adenosine were unaffected. We conclude that the enhancement of the a.h.p. and accommodation by adenosine may be mediated by a change in the regulation of intracellular calcium. However, the mechanism responsible for the hyperpolarization and decrease in input resistance evoked by adenosine is both calcium and voltage insensitive. Thus, it appears distinct from that mediating the enhancement of the a.h.p. and accommodation.

Action Potentials↗
PubMed1985

Adenosine increases synaptic facilitation in the in vitro rat hippocampus: evidence for a presynaptic site of action.

The effect of adenosine on paired synaptic responses was characterized in the CA1 region of the rat hippocampus in vitro. Adenosine increased the degree of synaptic facilitation at a 40 ms conditioning-testing interval under all conditions tested. Even when the stimulation intensity was increased so as to counteract the direct depressant effect of adenosine on synaptic transmission, its effect on facilitation was maintained. The ability of adenosine to increase synaptic facilitation was a complex function of several variables. The effect was enhanced by increasing the calcium concentration of the medium, and was most pronounced at short conditioning-testing intervals and at low response amplitudes. Adenosine was particularly efficacious in blocking the depression of synaptic responses observed in high-calcium medium at short conditioning-testing intervals. Because this depression most probably reflects depletion of the available store of releasable transmitter, one mechanism by which adenosine could reverse this effect would be by blocking the depletion of transmitter. These results suggest that adenosine diminishes transmitter release via an action at the presynaptic terminal. The reduction in the release of neurotransmitter, particularly at excitatory synapses, may be responsible for the depressant effects of adenosine upon the central nervous system.

Action Potentials↗
PubMed1984

The role of inhibitory mechanisms in hippocampal long-term potentiation.

The role of inhibitory processes in long-term potentiation (LTP) was investigated in hippocampal slices of the rat. GABAergic inhibition, tested by double shock experiments and by intracellular recording of inhibitory postsynaptic potentials, was not reduced in CA 1 pyramidal neurones after the induction of LTP. In cells recorded with caesium chloride-filled electrodes LTP could not be elicited. A reduction of intrinsic potassium-dependent inhibition may thus be responsible for LTP.

Afferent Pathways↗
PubMed1984

Adenosine enhances afterhyperpolarization and accommodation in hippocampal pyramidal cells.

Adenosine added to the perfusion fluid of rat hippocampal slices at 10 mumol X l-1 enhanced long lasting afterhyperpolarizations after single action potentials, bursts of action potentials or calcium spikes. Accommodation of firing during a depolarizing pulse was potentiated. An increase in calcium dependent potassium conductance is likely to mediate these effects. Adenosine at 50 mumol X l-1 induced a hyperpolarization accompanied by a reduction in input resistance. The hyperpolarization could be reversed at -85 mV. In TTX and TTX-barium treated slices the amplitude of the slow spike was decreased. This may result from a shunting of inward current in the dendrites due to an adenosine induced increase in potassium conductance. It is suggested that adenosine reduces pre- and postsynaptic excitatory signals principally by enhancing one or more potassium conductances. This effect is a powerful means for modulation of neuronal excitability and synaptic efficacy and can explain the antiepileptic activity of adenosine.

Adenosine↗
PubMed1984

Modulation of low calcium induced field bursts in the hippocampus by monoamines and cholinomimetics.

The influence of monoamine transmitter candidates, acetylcholine and related substances on rhythmic depolarization shifts (field bursts) in the CA 1 area of hippocampal slices from rats in low calcium (0.2 mmol X 1(-1) ) high magnesium (4 mmol X 1(-1) ) was investigated. Acetylcholine (ACh), histamine (HA) and H2-agonists, noradrenaline (NA) and beta-agonists at nano- to micromolar concentrations as well as dopamine (DA) and 8-bromo-cyclic AMP at 100 mumol X 1(-1) accelerated the field bursts. H2-antagonists blocked HA actions, beta-antagonists blocked NA actions selectively; muscarinic antagonists blocked ACh, HA and NA actions. H1-agonists, serotonin, dopamine and adenosine slowed the field bursts at micromolar concentrations. These effects parallel the action of the tested substances on afterhyperpolarizations in CA 1 pyramidal cells. High sensitivity and specificity make this response of the field bursts an excellent model to study postsynaptic transmitter actions in the central nervous system.

Animals↗
PubMed1984

Histamine potentiates neuronal excitation by blocking a calcium-dependent potassium conductance.

Histaminergic neurones send their axons to the whole forebrain. The diffuse projection is consistent with a modulatory role of these pathways. In hippocampal slices from rats a mechanism for this modulation is described, on pyramidal neurones of the CA 1 area: Strong excitations induced by intracellular current injection, ionophoretic administration of glutamate or synaptic stimulation normally restrict themselves by the activation of the calcium-dependent potassium current (gK(Ca) ). This current causes a long lasting afterhyperpolarization and an accommodation of firing. Their block by histamine and impromidine (reversed by metiamide and cimetidine) leads to a profound potentiation of excitatory signals. It is suggested that HA, through H2 receptors, accelerates the removal of intracellular free Ca++ ions.

Animals↗
PubMed1984

Low-calcium field burst discharges of CA1 pyramidal neurones in rat hippocampal slices.

Incubation of rat hippocampal slices in solutions containing low Ca2+ and increased Mg2+ rapidly blocked synaptic responses and increased spontaneous firing of all the principal neurones. More remarkably, a rhythmic and synchronous bursting discharge developed, which was restricted to the CA1 population of pyramidal neurones. These 'field bursts' or 'spreading excitation' were rapidly abolished by restoring the Ca2+ to 2 mM, by increasing the Mg2+ to 6 mM or by decreasing K+ from 6 to 3 mM. The CA1 pyramidal cells depolarized after the change to the low-Ca2+ solution by about 10-20 mV. Individual field bursts were associated with a further depolarization of 10-12 mV surmounted by a burst of action potentials at about 20/s. This transient depolarization shift, recorded extracellularly as a negative field, could be attributed to the increase of [K+]o during the bursts, reaching 9-10 mM as measured by ion-sensitive electrodes. The bursts were followed by a hyperpolarization, seen extracellularly as a small soma-positive field, which was attributed to an electrogenic pump and/or a Ca2+-activated K+ conductance. Stimulation of the tightly packed pyramidal cell axons in the alveus elicited a train of population spikes, instead of the single spike normally seen, and could trigger a full field burst. Recordings of the alvear tract volley suggested that the repeated spikes arose within the pyramidal cells. Multiple recordings from CA1 revealed that field bursts usually, but by no means always, started near the caudal (subicular) end of the area. They spread through the cell layer at 0.04-0.12 m/s. The most rapid propagation was seen when the bursts had an abrupt onset; slower propagation (1-10 mm/s) occurred when the bursts started gradually, which generally was the case near the sites of burst initiation and termination. Usually the action potentials within each burst were synchronized into population spikes which spread across CA1 at 0.04-0.15 m/s. The site of initiation and the extent of the spread of these population spikes varied during each burst, as did their amplitude. The degree of spike synchronization was enhanced by various treatments expected to increase neuronal excitability. Measurements of transmembrane potential during the burst confirmed the role in the generation of population spikes of ephaptic or field interactions between the pyramidal cells. It is proposed that the increased firing of all neurones is due to the block of tonic inhibition, depression of after-hyperpolarization and to increased membrane excitability.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1983

Analysis of carbamazepine actions in hippocampal slices of the rat.

Carbamazepine at therapeutic concentrations has a strong inhibitory effect on the spontaneous field bursts of the CA 1 region of rat hippocampal slices in low-Ca2+, high-Mg2+ solution. A reduction of excitability and synaptic transmission as well as no effect on posttetanic potentiation in the rat hippocampal slice by carbamazepine agrees with previous studies on spinal cord and peripheral nerve. Carbamazepine left synaptic inhibition and hyperpolarizing afterpotentials unaltered while these inhibitory processes were markedly enhanced by pentobarbital and adenosine, respectively. The spontaneous field bursts are, at least in part, synchronized by ephaptic transmission and may serve as a model of epilepsy and trigeminal neuralgia. The clinical effectiveness of carbamazepine in these two ailments may be explained by a suppression of this pathological synchronization.

Adenosine↗