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H L Haas

Publications and source records attributed to H L Haas.

At least 127 records · Page 7Linked to original sources
PubMed1983

Kinetics of acetylcholine-activated cation channel blockade by the calcium antagonist D-600 in Aplysia neurons.

The effects of the calcium channel blocker D-600 on the cation channels activated by acetylcholine (ACh) was studied in voltage-clamped Aplysia neurons by voltage-jump relaxation analysis. D-600 blocked the steady-state ACh current in a highly voltage-dependent manner, the degree of antagonism increasing with membrane hyperpolarization. In the presence of D-600 the current relaxations following hyperpolarizing command steps became biphasic. The time constants of ACh-induced current relaxations (tau f), which approximate the mean channel lifetime, were reduced in a voltage-dependent manner, the degree of reduction of tau f increasing with increasing membrane potential. In addition to the acceleration of tau f, a slow, inverse kinetic component (tau s) of the relaxation appeared in the presence of D-600. The rate of this inverse kinetic component was accelerated either by increasing the agonist or antagonist dose or by increasing the membrane potential. These results suggest that D-600 acts to antagonize the acetylcholine response through a blockade of the open state of the transmitter-activated cation channel. Possible kinetic schemes for this interaction are discussed.

Acetylcholine↗
PubMed1982

Cholinergic disinhibition in hippocampal slices of the rat.

In hippocampal slices of the rat maintained in vitro the addition of carbachol to the perfusion medium caused a depolarization accompanied by a conductance decrease and a block of inhibitory postsynaptic potentials in CAl pyramidal cells. During tetrodotoxin poisoning a smaller depolarization with conductance decrease was observed. Atropine blocked the effects of carbachol.

Animals↗
PubMed1982

Enhancement of synaptic transmission by 4-aminopyridine in hippocampal slices of the rat.

1. The effects of 4-aminopyridine (4-AP) on neurotransmission in hippocampal slices of the rat were studied in vitro. 2. Extracellular recordings of field potentials and intracellular recordings of excitatory and inhibitory post-synaptic potentials, action potentials and TTX-resistant spikes were obtained from the somatic and dendritic fields of CA 1 hippocampal neurones. 3. Constant perfusion with, or bolus injection of 4-AP in micromolar concentrations resulted in substantial and persistent enhancement of the amplitude of synaptic field potentials and population spikes with no alteration of the afferent input. Somatic positive waves (p-waves) were increased with local micro-application of 4-AP. 4. Intracellular recordings revealed an increase in the amplitude of e.p.s.p.s. and i.p.s.p.s. I.p.s.p.s were prolonged by 4-AP. 5. The pyramidal cells were, after an initial hyperpolarization, depolarized by up to 10 mV during exposure to 4-AP; the membrane conductance was not consistently changed. 6. Spontaneous shifts of the membrane potential were described as giant e.p.s.p.s and i.p.s.p.s. Spontaneous i.p.s.p.s were increased in frequency and amplitude. 7. Paired-pulse facilitation of e.p.s.p.s was reduced by 4-AP suggesting a presynaptic modulation of transmitter output. 8. It is concluded that 4-AP enhances transmitter release at both excitatory and inhibitory synapses in the hippocampus.

4-Aminopyridine↗
PubMed1982

Long-term potentiation of excitatory synaptic transmission in the rat hippocampus: the role of inhibitory processes.

1. The possibility that changes in inhibitory processes are responsible for long-term potentiation (l.t.p.) was examined using the rat hippocampal slice preparation.2. Inhibitory pathways were characterized using both extra- and intracellular recordings from the CA1 pyramidal cell layer. Stimulating electrodes were placed in either stratum radiatum or the alveus to allow orthodromic or antidromic activation of the pyramidal cells.3. Using extracellular recordings, inhibition was studied by applying paired pulses at interstimulus intervals of 20-500 msec through either the same or different stimulating electrodes, and quantifying the reduction in the population spike. An antidromic conditioning pulse was least effective in influencing the test response, while paired stimuli delivered through separate stimulators in stratum radiatum revealed the longest duration effects. Inhibition was either reduced or enhanced, depending upon the stimulation paradigm, with increasing stimulus intensity.4. With l.t.p., alterations in paired-pulse inhibition were observed corresponding to the changes in conditioning pulse amplitude. Reducing stimulus intensity to restore the initial conditioning pulse amplitude eliminated these effects.5. Using intracellular recordings, the effects of l.t.p. on inhibition were studied by examining changes in e.p.s.p.-i.p.s.p. sequences, i.p.s.p.s evoked by antidromic stimulation, and spontaneous depolarizing i.p.s.p.s observed with KCl-filled electrodes.6. Following l.t.p. enhanced e.p.s.p.s and slightly reduced, but prolonged, i.p.s.p.s were observed in response to orthodromic stimulation. Antidromically evoked, as well as spontaneous, i.p.s.p.s were unaffected.7 It is concluded that alterations in inhibitory processes are not responsible for l.t.p. in hippocampal subfield CA1. However, changes in the strength of inhibitory synapses as a consequence of long-term potentiation may modify the functional character of the hippocampal connexions.

Action Potentials↗
PubMed1981

Histamine hyperpolarizes hippocampal neurones in vitro.

The postsynaptic effect of histamine and impromidine, an H2-receptor agonist on CA1 pyramidal and dentate granule cells in the hippocampal slice of the rat is a hyperpolarization. Depolarizations are indirectly mediated. It is suggested that the hyperpolarization is generated by a conductance increase to potassium ions in the dendrites.

Animals↗
PubMed1981

Analysis of histamine actions by intra- and extracellular recording in hippocampal slices of the rat.

Extra- and intracellular recordings from CA1 pyramidal and dentate granule cells in hippocampal slices of the rat revealed a depressant effect of histamine which was usually accompanied by a hyperpolarization but no changes in conductance of the cell membrane. Synaptic potentials were unaffected. It is concluded that histamine has a post-synaptic action on ionic conductance in the dendrites, that allows a modulation of quick information transfer but no rapid synaptic transmission.

Action Potentials↗
PubMed1980

Effect of L-cycloserine on cortical neurons in the rat.

L-Cycloserine but not D-cycloserine, depressed the firing of neurons in the sensorimotor cortex of the rat with a relatively slow time course when administered by microionophoresis or i.p. injection. The effects of GABA applied by microionophoresis or released synaptically were not modified by i.p. injections and microionophoretic administration of L-cycloserine. It is concluded that L-cycloserine depresses cell firing not by potentiation of the action of GABA but by elevating GABA-levels.

Animals↗
PubMed1980

Do enkephalins directly affect calcium-spikes in hippocampal pyramidal cells?

Although bath application of 10(-6) g/ml tetrodotoxin abolished the fast action potentials of pyramidal cells in hippocampal slices of rats, action potentials of lower amplitude and longer duration could still be evoked by intracellular current injection. FK 33-824 (an enkephalin analogue) had no effect on the threshold or shape of these presumed calcium-spikes. These data suggest that enkephalins, which induce bursting discharges in pyramidal cells, do not exert this action by a direct effect on inward calcium movement through the pyramidal cell membrane.

Action Potentials↗
PubMed1980

Is excitation by enkephalins of hippocampal neurones in the rat due to presynaptic facilitation or to disinhibition?

1. Extracellular recordings of postsynaptic potentials (field potentials), population spikes or unitary action potentials and intracellular records of excitatory and inhibitory postsynaptic potentials were obtained from neurons in superfused slices of rat hippocampus, to study the mechanism of the excitatory effect of enkephalins. 2. Most experiments were carried out with a synthetic, stable enkephalin analogue (FK 33-824) administered either by perfusion or by local administration (ionophoresis or pressure application from micropipettes). Comparisons were made when appropriate with metenkephalin, morphine, 4-aminopyridine and bicuculline. 3. The enkephalins caused a small increase in extracellular recordings of e.p.s.p.s and a more marked increase in the amplitude and frequency of population spikes. The effect of 4-aminopyridine on the extracellular e.p.s.p. was more marked than that of enkephalins, indicating that the enkephalins may have an additional effect upon regenerative spike mechanisms in the dendrites, which is not possessed by 4-aminopyridine. The actions of the enkephalins and morphine were blocked by naloxone, which did not block the action of bicuculline or 4-aminopyridine. 4. The increase in extracellularly recorded e.p.s.p. was shown to be due to a marked increase in the e.p.s.p. amplitude recorded intracellularly in CA1 and CA3 neurones and dentate granule cells. The augmented e.p.s.p.s evoked more action potentials. 5. The increase in e.p.s.p. amplitude was not accompanied by any marked change in membrane potential or resistance. 6. The inhibition of background firing by appropriate stimulation and recorded as peristimulus histograms was not reduced by FK 33-824. There was a slight prolongation. 7. Intracellularly recorded i.p.s.p.s were not blocked by FK 33-824. There was a prolongation of the i.p.s.p.s and an apparent increase in latency due to the unmasking and prolongation of e.p.s.p.s. 8. Dendritic excitability, as tested with ionophoresis of DL-homocysteic acid locally to the dendrites was unaffected by FK 33-824. 9. It is concluded that the increase in e.p.s.p.s produced by enkephalins can be explained by an increased release of excitatory transmitter, as occurs with 4-aminopyridine.

Animals↗
PubMed1979

Inhibition by transcutaneous electrical stimulation of noxious heat elicited in human Gasserian ganglion.

During percutaneous thermocoagulation of the Gasserian ganglion for trigeminal pain, the pain perception threshold was established in a series of 25 awake patients by measuring the temperature at the electrode tip within the ganglion during slow increase of the radiofrequency current. Between 42 and 48 degress C pain perception was regularly reported by the patients. A cutaneous-stimulating system was then applied to the trigeminal area which was reported to be painful during the heating. The external stimulation attempted to preferentially stimulate the A afferent nerve fibres. When external stimulation was applied during the heating of the Gasserian ganglion, the pain perception threshold was enhanced in about half of the cases. A transcutaneous electrical stimulation of part of the body not related with the investigated pain sensation did not produce the same inhibitory action in 3 out of 5 cases.

Adult↗
PubMed1978

Hypersensitivity to histamine in the guinea-pig brain: microiontophoretic and biochemical studies.

Electrolytic lesions of the medial forebrain bundle induce a fall in histidine decarboxylase activity (the specific synthetic enzyme of brain histamine) in the ipsilateral cerebral cortex and hippocampus of the guinea pig brain; these results suggest the presence of an ascending histaminergic pathway in the guinea pig brain similar to that described in the rat. Possible alterations in the sensitivity of histaminergic receptors present in the target areas were studied following this type of lesion by combining electrophysiological and biochemical approaches. Microiontophoretic applications of histamine or noradrenaline reveal a hypersensitivity (lower ejecting currents for threshold and maximal responses) in cortical neurons ipsilateral but not contralateral to the lesion, whereas responses to iontophoretically applied GABA are not modified. In contrast the responsiveness of histamine-sensitive cyclic AMP generating systems is not modified, neither in the cerebral cortex nor in the hippocampus after this type of lesion. Similar conclusions are reached from the data obtained with specific agonists of the two classes of histaminergic receptors and measurements in the presence of a phosphodiesterase inhibitor. Several hypotheses are discussed in order to reconcile the finding of a denervation hypersensitivity revealed by iontophoresis contrasting with an unaltered responsiveness of the histaminergic receptors linked to the adenylate cyclase.

Action Potentials↗
PubMed1978

The biological activity of d- and l-baclofen (Lioresal).

Racemic d,l-baclofen and l-baclofen depressed the patellar, flexor, linguo-mandibular (0.1--30 mg/kg i.v.) and the H-reflex (1--3 mg/kg i.v.) in a dose-dependent fashion. Racemic and l-baclofen partly antagonized electroshock-induced convulsions in mice (30--60 mg/kg p.o.) and depressed the firing rate of nigral cells when applied iontophoretically. d,l-Baclofen and l-baclofen (0.1--3.0 mg/kg i.v.) moderately reduced the blood pressure in cats. Dextrorotatory baclofen, at identical doses was inactive in all these tests. It is concluded that the biological activity of baclofen resides with the l-enantiomer.

Aminobutyrates↗