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P L Herrling

Publications and source records attributed to P L Herrling.

28 records · Page 2Linked to original sources
PubMed1986

In vitro release and electrophysiological effects in situ of homocysteic acid, an endogenous N-methyl-(D)-aspartic acid agonist, in the mammalian striatum.

A potassium-induced, calcium-dependent release of endogenous homocysteic acid (HCA) from rat striatal slices was demonstrated. A precolumn derivatization high-performance liquid chromatography method was developed that allowed quantitative determination of sulfur-containing amino acids at the picomole level. Intracellular recordings from cat caudate neurons during simultaneous microiontophoretic application of drugs and electrical stimulation of the corticocaudate pathway showed that (L)-HCA evoked a depolarization pattern similar to that induced by N-methyl-(D)-aspartic acid (NMDA), and both these depolarizations could be selectively inhibited by a specific NMDA antagonist, (D)-2-amino-7-phosphonoheptanoic acid [(D)-AP-7]. A selective antagonism of (L)-HCA-induced depolarizations by (D)-AP-7 was confirmed in quantitative experiments with the frog hemisected spinal cord in vitro. Small quantities of iontophoretically applied (L)-HCA, but not of quisqualate, potentiated cortically evoked EPSPs in cat caudate neurons. These observations suggest that (L)-HCA might be a candidate as an NMDA-receptor-preferring endogenous transmitter in the caudate nucleus. One possible function for such transmitter systems could be the enhancement of EPSPs.

Animals↗
PubMed1985

Pharmacology of the corticocaudate excitatory postsynaptic potential in the cat: evidence for its mediation by quisqualate- or kainate-receptors.

Caudate neurons were recorded with intracellular electrodes in halothane anaesthetized cats during microiontophoretic application of drugs and simultaneous stimulation of the corticocaudate pathway. Application of 2-amino-7-phosphonoheptanoic acid inhibited excitations induced by the N-methyl-D-aspartic acid receptor agonists N-methyl-D-aspartic acid and quinolinic acid, but not those elicited by quisqualic acid or activation of the cortico-caudate pathway. Selective inhibition of N-methyl-D-aspartic acid induced excitations was also found in vitro in the frog hemisected spinal cord preparation where a pA2-value of 5.5 against N-methyl-D-aspartic acid was determined. The endogenous tryptophan metabolite, kynurenic acid, antagonized excitations induced by N-methyl-D-aspartic, quisqualic, L-glutamic and kainic acid as well as the excitatory postsynaptic potential (EPSP) evoked in caudate cells by stimulation of the corticocaudate pathway, while action potentials elicited by an intracellularly applied depolarizing current were only slightly affected. In vitro experiments with the frog hemisected spinal cord preparation suggested that kynurenic acid might be a competitive antagonist of both N-methyl-D-aspartate and quisqualate receptors, with pA2-values of about 4.8 and 4.0, respectively. From these results it is concluded that the three-receptor concept for excitatory amino acids are proposed by Watkins and colleagues is probably applicable to the cat caudate nucleus and that the cortically evoked monosynaptic EPSP is mediated by a non-N-methyl-D-aspartate quisqualate- or kainate-receptor.

2-Amino-5-phosphonovalerate↗
PubMed1984

Evidence for GABA as the transmitter for early cortically evoked inhibition of cat caudate neurons.

Bicuculline methochloride derived from (+) bicuculline was applied by microiontophoresis to intracellularly recorded cat caudate neurons during stimulation of the cortico-caudate pathway. This resulted in a distinct increase of the duration and amplitude of the evoked excitatory postsynaptic potentials and an increase of the delay to the following hyperpolarizations. In most cases, however, a residual hyperpolarization remained even after prolonged applications of bicuculline methochloride. Iontophoretic application of GABA usually reduced the amplitude of the cortically evoked depolarizations. Very similar effects were seen if bicuculline methochloride was applied to dorsal hippocampal neurons while the fimbria/fornix was stimulated, an augmentation of the evoked depolarizations with a concomitant reduction of the following evoked inhibition. From these observations it was concluded that GABA is very probably the transmitter for the early part of cortically evoked hyperpolarizations in cat caudate neurons and that one of its functions is to regulate the strength of cortically evoked excitation.

Animals↗
PubMed1983

Effects of excitatory amino acids and their antagonists on membrane and action potentials of cat caudate neurones.

The electrical activity of caudate neurones was recorded with intracellular electrodes in halothane anaesthetized cats. Agonists and antagonists of excitatory amino acid receptors were applied by micro-ionophoresis and their effects on membrane- and action potentials and on cortically evoked synaptic potentials evaluated. The agonists, L-aspartate (asp), L-glutamate (glu), N-methyl-DL-aspartate (NMA), quinolinate and quisqualate all depolarized the membrane, caused repetitive firing, reduced the apparent amplitude of the cortically evoked excitatory post-synaptic potentials (e.p.s.p.s) and increased the amplitude of the associated inhibitory post-synaptic potential. Two of the agonists, NMA and quinolinate, additionally caused the appearance of up to 500 ms long depolarizations (plateaus) on the falling phase of action potentials. These plateaus were seen in about two-thirds of the cells in this sample while in the other third the excitatory effects of NMA and quinolinate were indistinguishable from those of glu and quisqualate. The N-methyl-D-aspartate (NMDA) receptor antagonist D-alpha-aminoadipate (DAA) reversibly inhibited the effects of NMA and quinolinate but only on those cells where these two agents evoked action potential plateaus while on the same cells the effects of asp, glu and quisqualate were either only weakly antagonized or not affected. On cells not displaying plateaus to NMA or quinolinate none of the effects of the agonists could be antagonized by DAA. DAA applications that completely antagonized the effects of NMA never reduced the amplitudes of cortically evoked e.p.s.p.s. Cis-2,3-piperidine dicarboxylate also blocked the effects of NMA and asp at low application currents while at higher currents it enhanced the effects of glu or asp although still retaining its NMA antagonistic activity. High-frequency stimulation of the cortico-caudate pathway resulted in long-lasting depolarizations and repetitive firing, but plateaus of the type caused by NMA or quinolinate were not seen.

2-Aminoadipic Acid↗
PubMed1982

Effects of clozapine in a selective muscarinic bioassay and on single cells of the rat hippocampus.

Acetylcholine was applied to isolated crayfish hindguts and caused dose-dependent increases in its contractile force. These effects were blocked by muscarinic but not by nicotinic antagonists. Dopamine, noradrenaline, enkephalin or GABA agonists had either no effect or one distinct from the action of acetylcholine. Of a number of antischizophrenic drugs, clozapine had the strongest antimuscarinic action with a pA 2 value of 7.5, followed by thioridazine with a pA 2 value of 6.7. All other drugs of the phenothiazine, butyrophenone or benzamide type were ineffective. From these results, it was concluded that the crayfish hindgut is a very reliable and simple bioassay for muscarinic actions of drugs. Clozapine was also applied by microiontophoresis to cat hippocampal neurons and its effects on carbachol-, acetylcholine- and glutamate-induced excitations was assessed. It displayed an inhibitory action on excitations induced by the cholinergic agents, but did not visibly affect those induced by glutamate. The fact that clozapine had strong antimuscarinic effects on the crayfish hindgut as well as on hippocampal neurons of a mammalian indicates a similarity between the muscarinic receptors in both tissues.

Acetylcholine↗
PubMed1981

The membrane potential of cat hippocampal neurons recorded in vivo displays four different reaction-mechanisms to iontophoretically applied transmitter agonists.

Intracellular recordings were obtained in vivo from cat hippocampal pyramidal cells and cells in deeper layers of the hippocampal formation. Five transmitter agonists were applied to these cells by microiontophoresis. Glutamate caused depolarizations with fast onset and decay, fastest reaction times being within hundreds of msec of the beginning and the of the application. These depolarizations were accompanied by a decrease of the apparent input resistance (AIR) and an increase of the mean firing rate. Carbachol, a cholinergic agonist, caused depolarizations with slow onset and decay, reaction times were in the range of tens of seconds. The depolarizations were also accompanied by an increase in the mean firing rate. These effects are thought to be muscarinic. gamma-Aminobutyric acid elicited fast hyperpolarizations, a decrease of the AIR, mean firing rate and occasionally of the amplitude of action potentials (APs). Dopamine and norepinephrine hyperpolarized the membrane potential relatively fast, reaction times being within seconds, and reduced the mean firing rate, but this was accompanied by a marked increase of the AIR, of the size of the remaining APs and fimbria-evoked EPSPs. Inhibitory slow depolarizations of the type seen in an earlier study with dopamine in the caudate were not seen on pyramidal cells and only very rarely on non-identified cells of the deeper layers. These results indicate a partially tissue-specific effect of dopamine compared to that on caudate cells.

Animals↗
PubMed1981

Effects of opioid peptides on synaptic potentials in explants of rat hippocampus.

Bath application of 10(-8) M FK 33-824 (an enkephalin analogue) and 10(-7) M beta-endorphin reversibly induced stimulus-evoked bursting activity with depolarization shifts in cultured hippocampal pyramidal cells. Statistical analysis of the data revealed that in the majority of cells, inhibitory postsynaptic potentials were markedly decreased and excitatory postsynaptic potentials increased prior to the development of bursting activity, although some inhibition persisted in cells exposed to opioid peptides. In a minority of cells, no alteration in synaptic potentials were observed to precede the stimulus-evoked bursts induced by the opioid peptides.

Action Potentials↗
PubMed1980

Iontophoretically applied dopamine depolarizes and hyperpolarizes the membrane of cat caudate neurons.

Dopamine (DA) was applied iontophoretically on intracellularly recorded cat caudate neurons. Ejected approximately 100 micrometers away from the cell soma, it caused slow depolarizations of the membrane while the ongoing firing rate was reduced. This last effect was not due to sodium inactivation. Cortically evoked EPSP-IPSP sequences were inhibited during the depolarizations. The latency of cortically evoked action potentials was consistently increased during DA-ejections. These effects were blocked by fluphenazine, relatively selective blocker of the DA-sensitive adenylate cyclase. Nevertheless, there are serious doubts as to the specificity of these actions of DA as a number of other substances like naloxone, nicotine, acetylcholine or glutamate-diethylester occasionally had very similar effects on membrane potential, firing rate and cortically evoked EPSP-IPSP sequences. If DA was applied nearer to the soma, approximately 50 micrometers away, 70% of the recorded neurons continued to display the slow depolarizations above described, while 30% of the cells now reacted by a hyperpolarization accompanied also by a reduced firing rate. If DA was applied for prolonged periods on such cells, the initial hyperpolarization was followed by the slow depolarization. The observation that during the slow depolarization there is a decrease in firing rate and amplitude of the cortically evoked IPSP is explained by the assumption that the region of the axon hillock is hyperpolarized by DA, and that the slow depolarization is a phenomenon restricted to the distant recording site and possibly to the dendritic region. None of the 74 responsive neurons displayed an increased firing fate when DA was ejected either continuously, i.e. for more than 5 sec, or in short pulses of 50--500 msec.

Animals↗
PubMed1976

Regional distribution of three ultrastructural retinula types in the retina of Cataglyphis bicolor Fabr. (Formicidae, Hymenoptera).

The retina of Cataglyphis bicolor was investigated by electron microscopy. Three types of structurally distinct retinulae were found and mapped throughout the compound eye: Type I is composed of four unpigmented thin cells, four larger pigmented cells as well as a basal ninth cell. Its rhabdom possesses a round cross section and four microvilli directions. This type occupies most of the dorsal two-thirds of the retina. Type II consists of two thin cells, two intermediate cells and four large cells. A basal ninth cell is also present; the rhabdom is as in type I. Type II retinulae are located in the ventral third of the retina. Type III ommatidia are unique within the Hymenoptera: there are four large pigmented cells, four thinner unpigmented cells and a basal ninth cell. The rhabdom, however, has a dumb-bell shaped cross section; two small cells lie at its opposed extremities and the remaining six cells have mutually perpendicular microvilli orientations. This type of retinula is found at the dorso-medial eye margin. Serial sectioning in this region revealed a conical shaped rhabdom without any torsion along the longitudinal axis. The rhabdomere cross section was calculated from distal and proximal thin sections. Angular statistics were applied to the microvilli directions of all three ommatidial types to determine the degree of order. A possible functional significance of the structural specializations of the different eye regions is discussed.

Animals↗