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D O Carpenter

Publications and source records attributed to D O Carpenter.

At least 145 records · Page 8Linked to original sources
PubMed1986

On the transmitter at the A-to-B cell in Aplysia californica.

Cerebral A neurons make excitatory contact with cerebral B cells. While glutamate, histamine and serotonin all have excitatory receptors on B cells, the A-to-B cells synaptic potential was not found sensitive to curare, strychnine, antihistaminergic or antiserotoninergic drugs, nor did bath-perfused glutamate or serotonin cause desensitization of the synaptic response. We conclude that none of these candidates is the transmitter at this synapse.

Animals↗
PubMed1986

Enkephalin-like substance in aplysia nervous tissue and actions of leu-enkephalin on single neurons.

Extract from the abdominal ganglia of Aplysia was fractionated by high performance liquid chromatography. Several large uv absorbing peaks were found. One of these peaks from the ganglionic extract was analyzed by displacement assay with the use of Mytilus edulis membranes. The results revealed the substance in this peak was able to displace 3H-D-Ala2, met5-enkephalinamide. In electrophysiological studies of abdominal and cerebral neurons, depolarizing and hyperpolarizing responses were obtained from some neurons, including neurons in the identified cerebral B cell cluster. A smaller population of cells exhibited biphasic responses. Some of the responses could be depressed by prior naloxone treatment. In conclusion, an endogenous opioid system, using substance related to but distinct from the enkephalins, may exist in Aplysia.

Animals↗
PubMed1986

A comparison of the effects of quinolinate and N-methyl-aspartate on neurons in rat piriform cortex.

Quinolinate has been proposed to be the endogenous ligand of the N-methyl-aspartate (NMA) receptor in the mammalian central nervous system. We have compared the relative potency and pharmacologic sensitivity of quinolinate- and NMA-induced excitation on pyramidal cells in the rat piriform cortex. Quinolinate was considerably less potent than NMA, but the NMA responses were more sensitive to antagonism by NMA-receptor antagonists. These results suggest that, at least in this preparation, quinolinate and NMA are pharmacologically distinguishable and may act at different receptor sites.

2-Amino-5-phosphonovalerate↗
PubMed1986

Relaxation studies on the interaction of hexamethonium with acetylcholine-receptor channels in Aplysia neurons.

The mode of action of the cholinergic antagonist hexamethonium on the excitatory responses of voltage-clamped Aplysia neurons to acetylcholine (ACh) has been examined by voltage- and concentration-jump relaxation analysis. At steady-state concentrations of ACh hyperpolarizing command steps induced inward current relaxations to a new steady-state level (Iss). The time constants of these inward relaxations, tau f, which approximate the mean single-channel lifetime, were increased both by increasing the membrane potential and by lowering the bath temperature (Q10 = 3) but were not affected by increasing the ACh concentration over the dose range employed. In the presence of hexamethonium hyperpolarizing command steps produced biphasic relaxations of the agonist-induced current. tau f was reduced in a voltage-dependent manner, the degree of reduction increasing with hyperpolarization. Slow, inverse relaxations were also triggered in the presence of hexamethonium. The time constant of this relaxation was reduced by increasing membrane potential and hexamethonium concentration. Both the estimated association (kf = 5 X 10(4) M-1 . sec-1) and the estimated dissociation (kb = 0.24-0.29 sec-1) rate constants derived from a three-state sequential model for block by hexamethonium were independent of the membrane potential. Similar rate constants were estimated from experiments with the concentration-jump technique, which were also independent of the membrane potential over the range -50 to -110 mV. It is suggested that the voltage-dependent actions of hexamethonium may originate either from an alteration of the channel opening and closing rate constants through an allosteric interaction with the ACh receptor, rather than through an influence of the transmembrane electric field on the rate of drug binding, or through a fast reaction which is rate-limited by voltage-independent diffusion.

Acetylcholine↗
PubMed1986

Excitation of neurons in the canine area postrema by prostaglandins.

The effects of prostaglandins on electrical activity of neurons in the canine area postrema were studied using the techniques of extracellular recording with iontophoresis. Excitatory responses were obtained upon application of prostaglandins A1, B1, B2, E1, F1 alpha, and F2 alpha in between 24 and 50% of the cells studied. The excitation was very similar in pattern to that observed to apomorphine, biogenic amines, and several neuropeptides in that it had a relatively long latency, low maimal frequency, and prolonged duration. Since the area postrema is known to play a central receptive role in initiating emesis to circulating toxins, these results suggest that prostaglandins may play a role in the initiation of some forms of emesis.

Animals↗
PubMed1986

Receptors for excitatory amino acids on neurons in rat pyriform cortex.

The actions of a variety of agonists and antagonists of the excitatory amino acids on rat pyriform cortex pyramidal neurons were studied in a submerged, perfused brain slice. The order of potency for the agonists, applied by ionophoresis, was kainate greater than quisqualate greater than N-methyl-D-aspartate greater than aspartate = glutamate. The endogenous monosynaptic excitation of pyramidal neurons upon stimulation of the lateral olfactory tract was blocked post-synaptically by DL-2-amino-4-phosphonobutyric acid, although this drug did not consistently block any of the exogenous responses. The synaptic excitation was not blocked, however, by antagonists presumed specific for the quisqualate (glutamate diethyl ester), kainate, (gamma-D-glutamylglycine), or N-methyl-D-aspartate (DL-2-amino-5-phosphonovaleric acid, DL-2-amino-7-phosphonohetaonic acid) receptors. Several antagonists blocked N-methyl-D-aspartate responses at lower concentrations than those to aspartate, and other antagonists distinguished between kainate and quisqualate responses. These results suggest that 1) pyriform neurons have a variety of receptors that have properties somewhat different from those found in other preparations and 2) the endogenous transmitter activates a receptor distinct from those activated by kainate, quisqualate, and N-methyl-D-aspartate.

Animals↗
PubMed1986

Radiation-induced emesis in the dog: effects of lesions and drugs.

Dogs exposed to 8 Gy 60Co gamma mid-abdominal irradiation exhibited emesis with an average latency of 102 min and an average of 7.4 episodes over 96 min. There were no significant changes in dogs subjected to a chronic bilateral subdiaphragmatic vagotomy, but emesis was prevented by ablation of the area postrema. Indomethacin pretreatment also prevented radiation-induced emesis in two of seven dogs and in the remainder reduced the average number of episodes. Domperidone pretreatment prevented radiation-induced emesis in all of four dogs tested. In electrophysiological studies recording from the area postrema the chemosensitive neurons were found to be normally silent in anesthetized preparations but excitable by a variety of emetic agents. After irradiation of the abdomen spontaneously active neurons were found with a discharge pattern that mirrored the behavioral pattern of postirradiation emesis. These studies are consistent with radiation-induced emesis being humorally mediated in the dog and implicate dopamine and/or prostaglandins as possible mediators.

Animals↗
PubMed1985

Kainic acid responses and toxicity show pronounced Ca2+ dependence.

Responses of pyramidal neurons to ionophoretic kainate, quisqualate and N-methyl aspartate were studied in a submerged rat piriform cortex slice as a function of Ca2+ and Mg2+ concentrations. The results suggest that the channel activated by kainate is unusually influenced by Ca2+, excitotoxicity is Ca2+-dependent and a function of Ca2+ concentration, and the excitotoxic actions of various amino acid agonists are correlated with the Ca2+ dependence of their responses.

Animals↗
PubMed1985

Trifluoperazine and calcium antagonists accelerate cholinergic desensitization in Aplysia neurons.

The onset of desensitization of excitatory acetylcholine responses in isolated, voltage clamped Aplysia RB neurons to microperfused agonist was accelerated by trifluoperazine and the calcium antagonists SKF-525A and D-600. In the absence of these drugs the time course of desensitization is described as the sum of two exponentials plus a constant. All 3 compounds accelerated the fast exponential component of desensitization, but had opposite effects on the slow component: trifluoperazine and SKF-525A accelerated the slow component, whereas this phase was greatly slowed by D-600. These results provide further evidence that the two components of cholinergic desensitization may be independent and influenced by agents which may affect calcium binding to the acetylcholine receptor.

Animals↗
PubMed1985

Bicuculline and picrotoxin block gamma-aminobutyric acid-gated Cl- conductance by different mechanisms.

Using isolated, internally perfused bullfrog dorsal root ganglion cells we have studied the dose-response curves for gamma-aminobutyric acid (GABA) in the presence of internally or externally applied GABA antagonists. With external application of antagonists the inhibition of the GABA current by bicuculline was competitive and that by picrotoxin was noncompetitive. Picrotoxin but not bicuculline blocked when internally perfused.

Animals↗
PubMed1985

Dual effects of the snake venom polypeptide vipoxin on receptors for acetylcholine and biogenic amines in Aplysia neurons.

Vipoxin, a 13,000-dalton polypeptide component of Russell's viper venom, has a dual pattern of effects on the responses of voltage-clamped Aplysia neurons to acetylcholine and biogenic amines. Application of low doses of vipoxin by pressure ejection reversibly antagonized all three types of ionic response to acetylcholine and carbachol. The blockade by vipoxin of acetylcholine responses was not prevented by eserine. The order of susceptibility of acetylcholine responses to blockade by vipoxin was Na+ greater than K+ greater than Cl-. Low doses of vipoxin also produced a reversible potentiation of excitatory responses to dopamine with a slower time course of onset and recovery. Inhibitory responses to dopamine (Cl-, K+) and both excitatory and inhibitory responses to histamine and 5-hydroxytryptamine were little affected by vipoxin. Higher doses of vipoxin directly evoked current responses which were always of the same ionic type as that evoked by acetylcholine or carbachol. Responses to cholinergic agonists and vipoxin were both blocked by cholinergic antagonists but not by antagonists of biogenic amine receptors, which reversibly antagonized the responses to amines on the same cell. These results suggest that vipoxin, which has no demonstrated actions on vertebrate acetylcholine receptors, acts as a partial agonist at all three types of acetylcholine receptor in Aplysia neurons. Our observations thus provide evidence for some degree of phylogenetic difference between vertebrate and molluscan acetylcholine receptors.

Animals↗
PubMed1985

N-Acetylaspartylglutamate: possible role as the neurotransmitter of the lateral olfactory tract.

N-Acetylaspartylglutamate, an endogenous brain peptide that binds with high affinity to a subpopulation of glutamate-binding sites in rat brain, is excitatory on rat piriform cortex pyramidal cells studied in a perfused brain slice. Both the monosynaptic excitation of the pyramidal cells elicited by stimulation of the lateral olfactory tract and the response to N-acetylaspartylglutamate were blocked by DL-2-amino-4-phosphonobutyrate but not by other excitatory amino acid antagonists. Responses to glutamate and aspartate, previously considered to be candidates as the lateral olfactory tract transmitter, were unaffected by 2-amino-4-phosphonobutyrate. Three days after unilateral bulbectomy there was a significant decrease in concentrations of N-acetylaspartylglutamate as well as aspartate, N-acetylaspartate, and gamma-aminobutyrate in the pyriform cortex of the side from which the olfactory bulb had been removed. These results are consistent with the possibility that N-acetylaspartylglutamate is the endogenous transmitter of the lateral olfactory tract.

Animals↗
PubMed1985

Actions of neurotransmitters on pontine medical reticular formation neurons of the cat.

The actions of several neurotransmitters were determined on 43 antidromically identified reticulospinal neurons and 72 unidentified neurons in the paraabducens reticular formation of the anesthetized cat. All neurons were excited by glutamate and aspartate, both of which caused brief, high-frequency responses. In 80% of the reticulospinal neurons glutamate was more potent than aspartate, whereas in 61% of the unidentified neurons aspartate was more potent. Glutamate responses were reversibly antagonized by curare applied by pressure injection. Fast inhibitory responses were obtained on all neurons tested to gamma-aminobutyric acid, glycine, and norepinephrine. Some neurons showed similarly fast inhibitory responses to acetylcholine and serotonin. Acetylcholine and serotonin both acted on most neurons, but approximately equal numbers of neurons showed a relatively fast inhibition, a relatively slow and long-lasting excitation, and a biphasic combination of inhibition and slow-excitation responses. The pattern of responses to acetylcholine and serotonin is consistent with a spatial separation of excitatory and inhibitory receptors on different portions of the cell, possibly reflecting different inputs that use the same transmitter but have effects of opposite electrical and functional polarity. Although complicated by the phenomenon of excitatory and inhibitory responses to the same transmitter, these results are compatible with the Hobson-McCarley model of generation of desynchronized sleep.

Acetylcholine↗
PubMed1984

Kinetic properties of cholinergic desensitization in Aplysia neurons.

The kinetic properties of desensitization onset of excitatory cholinergic responses were studied in isolated, voltage-clamped Aplysia neurons. Desensitization of the acetylcholine (ACh)-induced current in response to microperfused acetylcholine occurred in two phases, and was best modelled as the sum of two exponential components plus a constant. Both exponential components were accelerated by increasing ACh dose. At the higher ACh doses the current decline was dominated by the fast exponential component, and the ratio of the plateau-peak current was reduced. Over the range of membrane potentials -50 to -110 mV, no change in the kinetics of desensitization onset was observed. The mean time constants of both exponential components were doubled by cooling from 20 degrees C to 5 degrees C. These results demonstrate that, as at the vertebrate neuromuscular junction, the onset of desensitization of this ACh response involves at least two processes which are dose- and temperature-sensitive. The lack of voltage dependence contrasts with results from vertebrate preparations, and indicates a fundamental difference between the properties of the excitatory ACh response in Aplysia neurons and the vertebrate neuromuscular junction.

Acetylcholine↗
PubMed1984

Action of vasopressin on CA1 pyramidal neurons in rat hippocampal slices.

The effects of arginine-vasopressin (AVP) on the excitability of 47 pyramidal cells of the CA1 region of the hippocampus were determined by using intracellular recording techniques in a submerged slice preparation. Addition of 10(-6) M AVP to the bathing medium evoked an increase in spike discharge which was slow in onset and only gradually reversible. The discharge was accompanied by an increase in excitatory postsynaptic potentials without significant change of the resting input resistance. AVP-induced excitation was found in 81% of ventral and 29% of dorsal hippocampal CA1 pyramidal cells. In low Ca2+, high Mg2+ solution this excitatory action by AVP was blocked. Microiontophoretic application of AVP onto apical or basal dendrites or the cell body did not result in excitation. These observations suggest that the action of AVP on CA1 pyramidal cells is transsynaptic and is more pronounced in ventral than dorsal CA1.

Animals↗
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

Modulation of neuronal responses to L-glutamate in Aplysia.

Potentiation of the excitatory response to L-glutamate (Glu) by L-aspartate (Asp), similar to that which has been described at the crustacean neuromuscular junction, is observed in Aplysia neurons which are glutamate sensitive. Potentiation of the inhibitory responses to ionophoretically applied Glu in neurons preconditioned with Asp permits experiments which serve to differentiate among four hypotheses previously proposed to explain the underlying mechanism of the phenomenon. The potentiation is inhibited by cooling (Q10 = 1.3 +/- 0.2) and is blocked in Na+-free seawater, where the response to Glu applied alone is increased in both amplitude and duration. These results are most consistent with the view that Glu is normally removed from the extracellular medium through an active reuptake process which is Na+ dependent, is slightly temperature sensitive, and may be blocked by Asp. Potentiation of the excitatory response to L-glutamate (Glu) by L-aspartate (Asp) has been previously described at the crustacean neuromuscular junction (Kravitz et al., 1970; Nistri and Constanti, 1979). This potentiation has been attributed to an Asp-induced change in conformation of the Glu receptor, thereby increasing its affinity for Glu (Shank and Freeman, 1975); suppression of the rate of desensitization of the Glu receptor induced by Asp (Dudel, 1977); blockade by Asp of a Glu reuptake process (Crawford and McBurney, 1977); and release, triggered by Asp, of a bound store of Glu (Constanti and Nistri, 1978).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗