Long-lasting changes of irritability in the somatosensory cortex of rabbits following tetanic stimulation of the tooth pulp]

Tetanic stimulation of the tooth pulp produced long lasting increases in potentials released by stimulation of the tooth pulp with single stimuli in the sensomotor cortex of rabbits. Stimulation with 200 impulses/sec for 5 sec produced changes of irritability that are demonstrable for 10-50 min depending on the intensity of stimulation. The lower rate limit for producing such changes is 25 impulses/sec. At a rate of 200 impulses/sec, a stimulation time of 25 msec was necessary to produce these changes. The postexcitatory depression occuring after single stimuli within 10-40 msec was increased by tetanic stimulation, whereas facilitation observed 5 msec after single stimuli was unaffected.     

A method for studying the peripheral mediators of the dental pain induced by electrical stimulation.

A useful method is described in this paper for studying the mediators released from tooth pulp of the dog during the electrical stimulation of dentine. This method is based upon the perfusion of the pulp and superfusing the return continuously over the isolated, in cascade, cat jejunum and rat stomach fundus strip. The presented evidences in this study indicate the possibility of the release of bradykinin and prostaglandin - like materials from the tooth pulp during the electrical stimulation of dentine. Possible relationship of these mediators and tooth pain due to the electrical stimulation of dentine is discussed.     

Inhibition, by electro-acupuncture, of the scalp evoked potential induced by painful stimulation of the tooth in man]

Scalp potentials evoked by electrical stimulation of the tooth pulp can be diminished in amplitude by electroacupuncture. This diminution goes generally in inverse with the increase in subjective pain threshold.     

Effect of vasopressin on neuronal responses of theNucl. Caudalis of the spinal trigeminal tract in rats

Effect of vasopressin on responses of individual neurons of thenucl. caudalis of the spinal trigeminal tract was studied on rats under urethan anesthesia; the responses were evoked by nociceptive (stimulation of the tooth pulp) or non-nociceptive (stimulation of Aa fibers of the infraorbital nerve) afferent activation. After injection of 10 nM vasopressin into the recording zone, responses evoked by stimulation of the tooth pulp were suppressed in all studied neurons of the high-threshold group; the same was true as to responses induced by stimulation of the tooth pulp and infraorbital nerve in most neurons of the convergent group. At the same time, vasopressin did not change the responses evoked by stimulation of Aa fibers of the infraorbital nerve in neurons of the low-threshold group. Possible involvement of vasopressin in the process of pain suppression is discussed.     

Modulating influence of the 2d somatosensory cortex of the cerebral cortex on the effects of electroacupuncture on the trigeminal nuclei

The effect of reversible functional inactivation of the second somatosensory cortex of the cerebral hemispheres on changes in the transmission of the afferent signals in the trigeminal nuclei after electroacupuncture was studied in acute experiments on adult cats anesthetized with hexenal (59 mg/kg i. p.). After functional inactivation of the second somatosensory cortex electroacupuncture failed to facilitate the evoked potentials in the oral trigeminal nucleus by stimulation of the tooth pulp and the lip of the mouth. In the caudal nucleus, the inhibitory effect of electroacupuncture on noxious stimulation decreased. The involvement of this brain cortex in the mechanisms of action of electroacupuncture on functionally different nuclei is discussed.     

Presynaptic potentials and facilitation of transmitter release in the squid giant synapse

Presynaptic potentials were studied during facilitation of transmitter release in the squid giant synapse. Changes in action potentials were found to cause some, but not all, of the facilitation during twin-pulse stimulation. During trains of action potentials, there were no progressive changes in presynaptic action potentials which could account for the growth of facilitation. Facilitation could still be detected in terminals which had undergone conditioning depolarization or hyperpolarization. Facilitation could be produced by small action potentials in low [Ca++]o and by small depolarizations in the presence of tetrodotoxin. Although the production of facilitation varied somewhat with presynaptic depolarization, nevertheless, approximately equal amounts of facilitation could be produced by depolarizations which caused the release of very different amounts of transmitter.     

Orotic acid biosynthesis in arginine-deficient rats.

Arginine deficiency is associated with a mild orotic aciduria. Liver slices from rats fed a purified l-amino acid diet with (control) and without arginine supplementation were used for studies of [¹⁴C]bicarbonate incorporation into orotic acid. The nanomoles of orotic acid synthesized in isolated liver slices from both control and arginine-deficient animals increased linearly with time. Orotic acid biosynthesis was significantly greater in liver slices than slices of heart, muscle, kidney, and minced spleen. The order of orotate biosynthesis from [¹⁴C]bicarbonate was liver > spleen = kidney > muscle > heart. Arginine deficiency resulted in a significant stimulation of liver orotic acid biosynthesis. This stimulation in pyrimidine biosynthesis can account for a major portion of the orotic aciduria. Orotic acid synthesis from spleens isolated from arginine-deficient rats was also enhanced compared with controls. Although the rate of orotic acid biosynthesis is small relative to liver production, the spleen may contribute slightly to increased orotic aciduria in the arginine-deficient rat. Arginine supplementation in vitro to livers from rats fed either the control of arginine-deficient diet resulted in a significant reduction in synthesis of orotic acid. Dietary arginine may play a key role in regulating mitochondrial carbamoyl phosphate utilization into both pyrimidine and urea biosynthesis.     

Effect of electro-acupuncture on the response of the trigeminal nucleus evoked by electric stimulation of dental pulp in the cat]

The potential in the spinal trigeminal nucleus evoked by electrical tooth pulp stimulation is depressed by electro-acupuncture given to the acupuncture point in the course of the nerve innervating the stimulated tooth.     

Effect of orotic acid on growth and fat synthesis in the yeastRhodotorula gracilis

Orotic acid in 0.1% concentration influenced the rate of growth ofRhodotorula gracilis in relation to the source of nitrogen nutrients. The maximum stimulation of growth (150%) was obtained on mineral medium containing asparagine. Mild stimulation of growth was also manifested in the phase of fat production. The accumulation of fat in the yeast cells was not influenced by orotic acid, but the rate of its synthesis was mildly stimulated together with growth. This phenomenon is discussed from the aspect of the effect of orotic acid on metabolic processes.     

Uracil synthesis via HCN oligomerization

Uracil is released from HCN oligomers upon acid hydrolysis in concentrations of 0.001% for 1 M HCN solutions to 0.005% for 0.1 M solutions. This yield is comparable with earlier reported, minor or nonbiological pyrimidines such as 5-hydroxyuracil and orotic acid. This is the first report of uracil itself via HCN oligomerization. Data are presented which establish that the observed uracil is not formed by decarboxylation of previously formed orotic acid, but via acid hydrolysis of at least two other precursors.     

Differential Responses of Crab Neuromuscular Synapses to Cesium Ion

Excitatory postsynaptic potentials (EPSP's) generated in crab muscle fibers by a single motor axon, differ in amplitude and facilitation. Some EPSP's are large at low frequencies of stimulation and show little facilitation; others are smaller and show pronounced facilitation. When K⁺ is replaced by Cs⁺ in the physiological solution, all EPSP's increase in amplitude, but small EPSP's increase proportionately more than large ones. Quantal content of transmission, determined by external recording at single synaptic regions, undergoes a much larger increase at facilitating synapses. The increase in quantal content of transmission is attributable to prolongation of the nerve terminal action potential in Cs⁺. After 1–2 h of Cs⁺ treatment, defacilitation of synaptic potentials occurs at synapses which initially showed facilitation. This indicates that Cs⁺ treatment drastically increases the fraction of the "immediately available" transmitter store released by each nerve impulse, especially at terminals with facilitating synapses. It is proposed that facilitating synapses normally release less of the "immediately available" store of transmitter than poorly facilitating synapses. Possible reasons for this difference in performance are discussed.     

Spatial distribution of hippocampal response to tooth pulp stimulation and acoustic stimulation

Evoked potentials (EP) and neuronal responses produced by tooth pulp stimulation and a clicking sound were recorded at different hippocampal sites using microelectrodes in unrestrained rats. Spatial distribution of EP was found to be the same for both types of stimulation. Averaged EP consisted of a high amplitude negative preceded by a low-amplitude positive component (N₁ and P₁, respectively). Latency of the N₁ wave reached its minimum (of 27 msec) at the middle third of the molecular layer of the dentate gyrus and the outer portion of the CA₃ apical dendrites. Latency of N₁ was considerably longer in the stratum radiatum layer of the CA₁. Laminar profiles of the amplitude of the N₁ componenent of EP produced in the dentate gyrus and the CA₃ by tooth pulp stimulation resemble those observed during perforant path stimulation; in the CA₁ they are similar to those evoked by stimulating the Schaffer collaterals. Maximum amplitude of the P₁ component was observed above the pyramidal layer of the CA₁ and the hilus. Neuronal discharge pattern changed in all hippocampal regions under the effects of both tooth pulp stimulation and the clicking sound. It is deduced that information can reach the hippocampus by two routes: via a "fast" (inhibitory) pathway through the fimbria and the fornix and a slower (excitatory) path through the entorhinal cortex.P. Flexig Institute for Brain Research, Karl Marx University, Leipzig, DR. Institute of Physiology, Pecs University Medical School, Pecs, Hungary. Translated from Neirofiziologiya, Vol. 19, No. 1, pp. 36–46, January–February, 1987.     

Nociceptive afferent blockade by percutaneous peripheral stimulation in the cat]

Experiments have been performed in order to study the effects of percutaneous peripheral stimulation (PCPS) both on the transmission of messages elicited by recruiting sensory units of the tooth pulp at the thalamic Centrum Medianum Level and on the jaw opening reflex (JOR). Both evoked potentials and JOR were inhibited by stimuli applied to the limbs by means of percutaneous (needle) electrodes. Observed inhibitory effects were not immediate: there was a latency period and progressive induction of these phenomena. The site of the inhibition is still unknown, nevertheless, the demonstration that PCPS was able to inhibit both evoked potentials in Centrum Medianum and JOR support the hypothesis that the analgesic effects may be due to descending inhibition blocking transmission of nociceptive information through the spinal cord.     

Dietary orotic acid accentuates the hepatic response to phenobarbital in rats.

In rats treated with phenobarbital for 3 days and simultaneously fed a semisynthetic diet containing 1.0% orotic acid, the extent of the increases in liver microsomal phosphatidylcholine, phosphatidylethanolamine, total RNA, total protein, and cytochrome P-450 were significantly greater than they were in rats treated identically with phenobarbital but without dietary orotic acid. This is attributed primarily to the stimulation of hepatic phosphatidylcholine synthesis by dietary orotic acid. In the absence of phenobarbital, orotic acid was shown to cause some increase in liver smooth endoplasmic reticulum components, but not cytochrome P-450. Orotic acid also decreased the activity of microsomal phosphatidylethanolamine N-methyltransferase, which may have contributed to the increase in the microsomal content of phosphatidylethanolamine. The hypothesis is advanced that phospholipid availability is a limiting factor in the hepatic response to phenobarbital. When more phospholipid is available to provide the structural framework for biogenesis of endoplasmic reticulum, all of the hepatic actions of phenobarbital, including induction of cytochrome P-450, are amplified.     

NMDA and non-NMDA receptors mediate responses in the primary gustatory nucleus in goldfish

Primary gustatory afferents from the oropharynx of the goldfish, Carassius auratus, terminate in the vagal lobe, a laminated structure in the dorsal medulla comparable to the gustatory portion of the nucleus of the solitary tract in mammals. We utilized an in vitro brain slice preparation to test the role of different ionotropic glutamate receptor subtypes in synaptic transmission of gustatory information by recording changes in field potentials after application of various glutamate receptor antagonists. Electrical stimulation of the vagus nerve (NX) evokes two short-latency postsynaptic field potentials from sensory layers of the vagal lobe. 6,7-Dinitroquinoxaline-2,3-dione and 6-nitro-7-sulphamoylbenzo[f]quinoxaline-2,3-dione, two non-N-methyl-D-aspartate (NMDA) ionotropic receptor antagonists, blocked these short-latency potentials. Slower potentials that were revealed under Mg2+ -free conditions, were abolished by the NMDA receptor antagonist, D(-)-2-amino-5-phosphonovaleric acid (APV). Repetitive stimulation produced short-term facilitation, which was attenuated by application of APV. These results indicate that the synaptic responses in the vagal lobe produced by stimulation of the gustatory roots of the NX involve both NMDA and non-NMDA receptors. An NMDA receptor-mediated facilitation may serve to amplify incoming bursts of primary afferent activity.     

Orotic acid biosynthesis in rat liver: studies on the source of carbamoylphosphate.

Measurements of the incorporation of radiolabeled precursors into orotic acid in tissue slices and minces provided evidence of the participation of the intramitochondrial carbamoylphosphate synthetase (CPSase-I) in the de novo biosynthesis of pyrimidines in rat liver. Ammonia, the only nitrogen source utilized by CPSase-I, markedly stimulated the incorporation of NaH¹⁴CO₃ into orotic acid in liver slices, and ornithine, which enhances the intramitochondrial consumption of carbamoylphosphate (CP) in citrulline synthesis, antagonized the stimulation by ammonia. Sensitivity of the incorporation of NaH¹⁴CO₃ into orotic acid to stimulation by ammonia was found to increase with age in concert with the emergence of CPSase-I in the liver during late fetal and neonatal development. Tissues lacking in CPSase-I activity did not exhibit the responses to ammonia and ornithine observed with the adult rat liver. While the occurrence of CPSase-I in the liver contributes extensively toward the exceptionally high capacity of that tissue for the de novo biosynthesis of orotic acid, our results also indicate that the physiological rate of orotic acid biosynthesis in rat liver is approximately one-third of capacity; the incorporation of NaH¹⁴CO₃ into orotic acid averaged 488 nmol/g of tissue in 3 h in the presence of toxic levels of ammonia, but declined to 160 nmol/g of tissue in 3 h when physiological levels of both ammonia and ornithine were provided. However, the rate of orotic acid biosynthesis observed with physiological concentrations of ammonia and ornithine could be reduced further, to about one-quarter of the physiological rate, by providing additional ornithine; thus, physiological levels of ornithine do not prevent the escape of intramitochondrial CP into the cytoplasm. Finally, over 80% of the incorporation of NaH¹⁴CO₃ into orotic acid at physiological levels of ammonia and ornithine was found to be ammonia dependent, and all but a small fraction of the ammonia-dependent incorporation could be blocked by providing ornithine in amounts in excess of physiological. These results indicate that CPSase-I is the major source of CP in the biosynthesis of hepatic pyrimidines under normal (physiological) conditions as well as in ammonia toxicity.     

Uracil synthesisvia HCN oligomerization

Uracil is released from HCN oligomers upon acid hydrolysis in concentrations of 0.001% for 1M HCN solutions to 0.005% for 0.1M solutions. This yield is comparable with earlier reported, minor or nonbiological pyrimidines such as 5-hydroxyuracil and orotic acid. This is the first report of uracil itselfvia HCN oligomerization. Data are presented which establish that the observed uracil is not formed by decarboxylation of previously formed orotic acid, butvia acid hydrolysis of at least two other precursors.     

Effect of cerebral ventricles perfusion with naloxone on trigemino-hypoglossal reflex in rats

The goal of this study was to determine whether opioid receptor antagonist naloxone abolishes the influence of periaqueductal central gray (PAG) on nociceptive evoked tongue jerks (ETJ) -- a trigemino-hypoglossal reflex induced by tooth pulp stimulation. In rats under chloralose anesthesia three series of experiments were performed. In the first two groups perfusions of lateral ventricles-cerebellomedullary cistern with McIlwain-Rodnight's solution and naloxone were carried out. In group 3 naloxone was infused through a catheter through the jugular vein. The amplitudes of tongue jerks induced by tooth pulp stimulation were recorded during subsequent 10 min perfusions. Mean amplitude of tongue movements induced by tooth pulp stimulation was regarded as the indicator of the magnitude of trigemino-hypoglossal reflex. We observed that perfusion of the cerebral ventricles with naloxone (100 nmol/ml) increased the trigemino-hypoglossal reflex up to 143%. The amplitude of ETJ was significantly reduced during PAG stimulation with a train of electrical impulses. After obtaining a significant -- 93% -- inhibition of ETJ (7% of the control), naloxone (100 nmol/ml) was added to the perfusion fluid. This led to a significant increase of the reflex up to 68%. Infusion of naloxone through the jugular vein did not affect the reflex. The above results suggest that the inhibition of ETJ due to PAG stimulation is partially reversed by naloxone and mediated via interactions with endogenous opioid systems involved in modulation of nociception.     

Characterization of the synaptic properties of olfactory bulb projections

The olfactory bulb directly projects to several diverse telencephalic structures, but, to date, few studies have investigated the physiological characteristics of most of these areas. As an initial step towards understanding the odor processing functions of these secondary olfactory structures, we recorded evoked field potentials in response to lateral olfactory tract stimulation in vivo in urethane-anesthetized Sprague-Dawley rats in the following brain structures: anterior olfactory nucleus, ventral and dorsal tenia tecta, olfactory tubercle, anterior and posterior piriform cortex, the anterior cortical nucleus of the amygdala, and lateral entorhinal cortex. Using paired-pulse stimulation with interpulse intervals of 25-1000 ms, we observed facilitation of the response to the second pulse in every structure examined, although the degree of facilitation varied among the target structures. Additionally, pulse train stimulation at three different frequencies (40, 10 and 2 Hz) produced facilitation of evoked field potentials that also varied among target structures. We discuss the potential utility of such short-term facilitation in olfactory processing.     

Analysis of frequency facilitation in neuromuscular synapses of the sartorius muscle in frogs

Changes in the quantum content of end plate potentials (EPPs) were studied in experiments on the frog sartorius muscle in the course of a gradual increase in stimulation frequency (frequency facilitation). It was shown that the frequency facilitation coefficient does not depend on the initial quantum content of EPPs but is in good agreement with the initial frequency of miniature EPPs and in bad agreement with their amplitude. The frequency facilitation is accompanied by the growth of the statistical binomial parameters P and n. The increase in P parameters is consequent of interference in P changes during the second component of facilitation after the single impulse. The growth of n is accounted for by the summation of the n increase during the first component of facilitation the time course of which is prolonged on repetitive stimulation.