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PubMed1991

Effects of L-beta-N-methylamino-L-alanine (L-BMAA) on the cortical cholinergic and glutamatergic systems of the rat.

Neurotoxic properties of L-beta-methylamino-alanine (L-BMAA) after chronic intracerebroventricular (i.c.v.) (500 micrograms/day) administration up to 60 days were investigated in the cerebral cortex of the rat. At day 16, there was a significant decrease in acetylcholinesterase (AChE) activity, 3H-QNB binding, 3H-glutamate (GLU) binding, and 3H-glutamate binding in the presence of quisqualate (QA). Choline acetyltransferase (ChAT) activity and 3H-nicotine binding were increased at day 16; however, ChAT activity decreased below control levels at days 40 and 60. 3H-Nicotine and 3H-AMPA binding were significantly lower than controls at both days 40 and 60. These significant neurochemical differences from unoperated controls were seen in both drug-injected and non-injected sides of the cortex suggesting a generalized cortical damage to glutamatergic and cholinergic systems. In the presence of bicarbonate, L-BMAA inhibited in vitro both glutamate and AMPA binding sites. L-BMAA treatment elicited behavioral changes such as splay, jerking movements, and rigidity. These symptoms were present for a period of at least 6 days after daily administration. After this period, symptoms were gradually attenuated and at day 10 the behavior of the L-BMAA-treated animals was not different from that of Na-bicarbonate injected controls. Our results are interpreted as an activation of quisqualate (AMPA) receptors by L-BMAA involving NMDA as well as non-NMDA receptors.

Acetylcholinesterase↗

PubMed1975

An evaluation of the use of intraventricularly administered [3H]5-hydroxytryptamine as a marker for endogenous brain 5-hydroxytryptamine.

Following the intraventricular injection of a small amount of [3H]5-hydroxytryptamine ([3H]5-HT), the amount of radioactivity in telencephalic structures on the injected side was 6--7 times larger than that in corresponding areas on the opposite side. Moreover, a multiphasic disappearance of [3H]5-HT from whole brain or midbrain was found after the intraventricular injection of the labeled amine. However, after the intraventricular injection of [3H]tryptophan, the levels of [3H]5-HT in midbrain declined in a monophasic manner. A significant portion of the labeled amine derived from intraventricularly administered [3H]5-HT was resistant to the depleting effect of Ro4-1284 or to that elicited by destruction of the midbrain raphe nuclei, both of which caused an almost complete loss of endogenous 5-HT and labeled 5-HT formed from tryptophan. It thus appears that the intraventricular injection of [3H]5-HT leads to the formation of artifactual pools which are not present if the amine is synthesized in vivo. Studies with 6-hydroxydopamine suggested, however, that uptake of [3H]5-HT into adrenergic neurons did not occur to any great extent.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗

PubMed1975

Biological importance of retrograde axonal transport of nerve growth factor in adrenergic neurons.

Previous studies have shown that nerve growth factor (NGF) produces a selective induction of tyrosine hydroxylase (TH) in peripheral adrenergic neurons and that NGF is transported retrogradely with a high selectivity from the adrenergic nerve terminals to the perikaryon. In order to investigate the biological importance of retrograde NGF transport, the following experiments have been performed; (a) effect of NGF on TH activity in superior cervical ganglia (SCG) after unilateral injection into the anterior eye chamber and the submaxillary gland; and (b) effect of systemic injection of NGF on TH activity in SCG after blockage of retrograde axonal transport by axotomy. After unilateral injection of NGF into the anterior eye chamber and submaxillary gland of both 8-10-day-old rats and adult mice, the increase in TH activity in the SCG was considerably larger on the injected than on the non-injected side although the adrenergic neurons supplying the two organs do not account for more than 25% of the total number of adrenergic neurons in the SCG. A direct diffusion mechanism could be excluded by the fact that unilateral local injection of [125 I] produced no significant side difference in the accumulation of radioactivity in the SCG 2 after injection whereas after 14 h there was a several-fold difference between the injected and non-injected side. Moreover, the nodose ganglia which are located very close to the SCG exhibited no statistically significant difference in the accumulation of radioactivity at any time. Forty-eight hours after subcutaneous injections of 10 mg/kg of NGF the increase in TH activity of the SCG amounted to 154% on the intact side and to 92% on the axotomized side. However, these experiments do not permit decisions about the extent the axotomy, as such, impaired the response to NGF. It is concluded that the biological effect of NGF results to a considerable extent, from the moiety which reaches the cell body by retrograde transport from the nerve terminals.

Animals↗

PubMed1978

Receptor-linked cyclic AMP systems in rat neostriatum: differential localization revealed by kainic acid injection.

Various receptor-linked cyclic AMP systems were measured in rat neostriatum 2--14 days after selective destruction of neuronal cell bodies and dendrites by micro-injection of 3 microgram of kainic acid. Basal adenylate cyclase activity was reduced by up to 56% in the injected side and the sensitivity to dopamine was abolished. Up to 84% of cyclic nucleotide phosphodiesterase activity, hydrolyzing either cyclic AMP or cyclic GMP, was destroyed by kainic acid injection. Specific binding of [3H]etorphine and [3H]spiroperidol was reduced by up to 62% in the injected side, while non-specific binding was unchanged. All of these changes were time-dependent, and were greatest 7--14 days after kainic acid treatment. On the other hand, intrastriatal kainic acid injection caused no change in the steady-state concentration of cyclic AMP in striatal slices, or in the in vivo cyclic AMP content in the striatum of rats killed by microwave irradiation. Receptor-mediated increases in cyclic AMP accumulation in striatal slices were either unchanged or markedly potentiated by kainic acid treatment. The maximum response to adenosine was unchanged, while the response to isoprenaline was increased up to 3.7-fold, the response to dopamine increased up to 6.7-fold, and the response to PGE1 increased up to 30-fold. The effect of dopamine in kainic acid-treated striatal slices was no longer blocked by fluphenazine, but was blocked by propranolol, suggesting an interaction of dopamine with a beta-adrenoceptor in kainic acid-treated slices. The results suggest differential cellular localizations of the various receptor-linked cyclic AMP systems in rat neostriatum. Some dopamine and opiate receptors, as well as most of the phosphodiesterase activity, are associated with local neuronal elements, while beta-adrenoceptor, adenosine and PGE1 alterations in cyclic AMP are not. The potentiation of the beta-adrenoceptor and PGE1 responses suggests that they may occur in glial cells. In addition, the pool of adenylate cyclase destroyed by kainic acid appears to make little contribution to normal levels of cyclic AMP in the tissue.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1990

The role of striatopallidal neurones utilizing gamma-aminobutyric acid in the pathophysiology of MPTP-induced parkinsonism in the primate: evidence from [3H]flunitrazepam autoradiography.

The GABA/benzodiazepine receptor complex in the basal ganglia of primates treated with the neurotoxin n-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been studied by semi-quantitative autoradiography with [3H]flunitrazepam ([3H]FNZ). Systemic treatment with MPTP produced a stable and lasting parkinsonian condition, with pronounced bradykinesia, akinesia and tremor. In the lateral segment of the globus pallidus (GPL) there was a significant reduction of [3H]FNZ binding compared with non-treated animals. There were no significant changes in the [3H]FNZ binding in the caudate nucleus, putamen and medial globus pallidus (GPM). This suggests that MPTP-treatment increases GABA release within the GPL exclusively. In view of the available evidence suggesting increased striatal output, and reduced unit activity within the GPL of the MPTP-treated primate, it seems likely that the striatal GABAergic output to the GPL is overactive in this model of Parkinson's disease. Furthermore, as there is no evidence for a change in GABA function within the GPM using this measure, the striatal neurones which innervate the GPM may be differentially affected by loss of dopamine innervation. In line with structural evidence and extrastriatal dopamine receptor distribution this suggests that the two striatopallidal systems are functionally heterogeneous. A hemi-parkinsonian primate model has also been used in this study. This model was produced by injection of MPTP directly into one carotid artery. The substantia nigra pars compacta (SNc) was destroyed on the injected side alone, and consequently the appearance of parkinsonian symptoms was confined to the contralateral side. [3H]FNZ binding in the GPL appears to be bilaterally reduced in this model, suggesting an interaction between the treated and non-treated side of the brain. In addition there is increased binding in the putamen and GPM with respect to the non-treated side of the brain. The increased [3H]FNZ binding in the GPM of the unilateral model may be due to the greater disruption of the nigropallidal and/or nigrostiatal dopamine neurones relative to the systemic model. The former would have the effect of uncoupling D1 dopamine receptors located on the terminals of striatal efferents from nigropallidal dopamine input, and as D1 dopamine receptors are implicated in the presynaptic control of GABA release from the terminals of striatal efferents, this would consequently reduce the level of GABA release in the GPM. The latter possibility would suggest that striatopallidal neurones projecting to GPM are more resistant to the effects of dopaminergic denervation than those projecting to GPL.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1976

Adenosine 3',5'-cyclic monophosphate as a possible mediator of rotational behaviour induced by dopaminergic receptor stimulation in rats lesioned unilaterally in the substantia nigra.

A possible involvement of c-AMP in the rotational behaviour induced by a stimulation of dopamine receptors in corpus striatum of rats was investigated. Rats were lesioned unilaterally in the substantia nigra with 6-hydroxydopamine. Intraventricular injection of dopamine, norepinephrine and apomorphine induced rotational behaviour towards the intact side as did dibutyryl c-AMP (dB-c-AMP). Dopamine, norepinephrine and apomorphine could activate adenylate cyclase in homogenates of caudate nucleus. The activation by dopamine was blocked by haloperidol. I.p. injected apomorphine increased c-AMP content bilaterally in caudate nucleus and caused turning towards the intact side; theophylline potentiated and haloperidol blocked the effect. In non-lesioned rats, dopamine and norepinephrine, when injected unilaterally into the caudate nucleus, elicited truning twoards the non-injected side if the rats were pretreated with reserpine and tranylcypromine. c-AMP and dB-c-AMP given similarly to rats pretreated with theophylline also produced turning towards the non-injected side regardless the pretreatment with reserpine and tranylcypromine. All these results emphasize the possibility that c-AMP acts as a second messenger in the central dopaminergic pathway in rats. The supersensitivity of the dopaminergic system which developed after denervation is also discussed.

Adenylyl Cyclases↗

PubMed1979

Evidence that a nigral gabaergic--cholinergic balance controls posture.

The intranigral injection of kainic acid (k.a.) (3.5 nM/s.n.) produced a lesion which resulted in a decreased muscarinic receptor binding capacity and in a decreased choline acetyl transferase (CAT) activity confined to the pars reticulata. The unilateral, intranigral injection of carbachol in the substantia nigra (s.n.) produced turning, ipsilateral to the injected side, of dose-related intensity, which was antagonized by scopolamine given either i.p. or intranigrally together with carbachol. The bilateral, intranigral injection of carbachol produced rigid catalepsy, highly resistant to apomorphine administration and antagonized by scopolamine. On the other hand, the catalepsy produced by intranigral picrotoxin was much more sensitive to apomorphine and was disrupted by systemic scopolamine administration. Intranigral scopolamine per se produced either contralateral turning or stereotyped movements consistently, when injected unilaterally or bilaterally, respectively. In addition, scopolamine injected bilaterally in the s.n. but not in the caudate nucleus (c.n.), at the concentration of 64 nM side, was able to antagonize the haloperidol-induced catalepsy and to prevent the tremors and the muscular rigidity produced by arecoline. This effect of scopolamine was surmountable with a higher dose of arecoline. Finally, intranigral muscimol (0.44 nM/s.n.) prevented the occurrence of the parkinsonian syndrome produced by systemic arecoline. It is concluded that the muscarinic receptors present in the s.n. pars reticulata play a role in the control of posture opposite to that of the nigral GABA receptors.

Animals↗

PubMed1992

Dopamine receptors in the ventral pallidum regulate circling induced by opioids injected into the ventral pallidum.

Recent reports have indicated that the ventral pallidum receives enkephalinergic and dopaminergic inputs. The present study evaluated the contribution of dopamine (DA) receptors to opioid-mediated locomotor functions of the ventral pallidum. Using circling behavior as a motor index, it was determined that injection of metabolically stable analogs of enkephalin, directly into the ventral pallidum, produced a dose-dependent, naloxone-antagonizable, increase in the number of rats rotating contralateral to the injected side, as well as the rate at which the animals turned. The frequency of the contralateral rotation, induced by intra-ventral pallidal injection of DADL (which closely mimics the endogenous enkephalin peptides, exhibiting a high affinity for the delta receptor with a moderate affinity for mu receptors), increased with intraperitoneal pretreatment with amphetamine, suggesting that enhanced release of catecholamines potentiated effects of opioids in the ventral pallidum. Systemic pretreatment with the D2-preferring antagonist haloperidol, blocked the effects of DAMGO (a mu-specific agonist) but not those mediated by DADL. In contrast, the D1-specific antagonist SCH 23390 was an effective blocker of responses to both opioid peptides. Further evidence for differential consequences of activating delta or mu opioid receptors was provided by systemic pretreatment with a cholinergic antagonist; atropine attenuated responding to DADL but not to DAMGO. To ascertain if DA receptors within the ventral pallidum were sufficient to influence mu-mediated circling, it was determined that intra-ventral pallidal injection of SCH 23390 or sulpiride (a D2 specific antagonist), at concentrations that did not produce motor effects, attenuated responding to subsequent intra-ventral pallidal injections of DAMGO. Thus, the opioid receptors and DA receptors that modify responses to activation of opioid receptors are both located within the ventral pallidum. These studies point to the critical role of DA in the ventral pallidum in motor behavior induced by stimulation of opioid receptors in the ventral pallidum.

Amphetamine↗

PubMed1979

Opposite turning effects of dainic and ibotenic acid injected in the rat substantia nigra.

Unilateral intranigral administration of kainic and ibotenic acid, two putative stimulants of glutamatergic mechanisms, elicited turning behaviour starting from doses of 10 ng. While the turning produced by kainic acid was ipsilateral, that produced by ibotenic acid was contralateral to the injected side. Previous destruction of dopaminergic neurons on the side of the intranigral injection failed to reduce the turning behaviour. Peripheral treatment with picrotoxin did not reduce the turning in response to ibotenic acid. The results might suggest the existence of excitatory and inhibitory glutamate receptors which control nigral non-dopaminergic neurons mediating turning-behaviour.

Animals↗

PubMed1989

Effects of local inhibition of locus coeruleus acetylcholinesterase by fasciculin in rats.

The inhibition of locus coeruleus (LC) acetylcholinesterase (AChE) by Fasciculin II (FAS), a novel anticholinesterase peptide from the green mamba (Dendroaspis angusticeps) venom, was studied in rats. FAS was stereotaxically injected (0.5 microliters of a 1 mg/ml solution) in the right LC. The left LC was taken as control. A group of rats received only saline injected with the same procedure. An inhibition of 80% of LC AChE activity was observed 24 h later. Monoamine and metabolite levels were assessed by high-performance liquid chromatography (HPLC) with electrochemical detection. A significant increase of noradrenaline (NA) levels was found in the injected side when compared with controls 24 h after injection. Neither dopamine, serotonin nor their metabolites or the NA metabolite 4-methoxyhydroxyphenylglycol showed any change after FAS injection. Atropine (30 mg/kg, i.p.) did not prevent the NA increase.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

Tetanus toxin alters 5-hydroxytryptamine, dopamine, and their metabolites in rat hippocampus measured by in vivo microdialysis.

Tetanus toxin is a potent neurotoxin, the mode of action of which is unknown, although it is widely considered to be mediated by loss of inhibitory neurotransmission. In the present study we have investigated the effect of a single unilateral injection of tetanus toxin in the hippocampus on extracellular concentrations of 5-hydroxytryptamine (5-HT), dopamine and their metabolites in freely moving rats. Tetanus toxin treatment caused a progressive decline in hippocampal dialysate 5-hydroxytryptamine over the 3-day period following the injection. After 3 days the level of 5-HT on the injected side was only 20% of the control side. On the second day of observation the level of dopamine was found to be elevated by more than 2-fold but this was not the case for either of the other 2 days studied. The 5-hydroxytryptamine metabolite, 5-hydroxyindoleacetic acid declined in a manner similar to that of the parent transmitter, but to a lesser extent. Of the dopamine metabolites, 3,4-dihydroxyphenylacetic acid was decreased on the second and third days of observation, whilst homovanillic acid was not significantly altered during the period of observation.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1991

Retrograde degeneration of nigrostriatal neurons induced by intrastriatal 6-hydroxydopamine injection in rats.

Quantitative receptor autoradiography was used to assess the effects of unilateral intrastriatal injections of 6-hydroxydopamine (6-OHDA) on the distribution of D1 and D2 dopamine (DA) receptors and of DA uptake sites in the mesostriatal pathway. [3H]Mazindol-labeled DA uptake sites were reduced both in the striatum (-97%) and in the substantia nigra pars compacta (SNpc) (-88%) on the injected side. There were also significant decreases of dopamine uptake sites in the nucleus accumbens (NAc) (-73%) and in the ventral tegmental area (VTA) (-70%). Changes in [3H]mazindol binding were also found within the contralateral VTA (-30%) and SNpc (-13%) but not in the contralateral-striatum. [3H]SCH23390-labeled D1 receptors were significantly reduced in the dorsomedial (-18%) and ventromedial (-14%) aspects of the striatum ipsilateral to the side of the lesions. In contrast, the concentration of [3H]spiperone-labeled D2 receptors was not altered. There were also significant decreases in D1 (-18%) and of D2 (-27%) receptors in the SNpc and of D1 (-10%) in the SN pars reticulata (SNpr). These results suggest that oxyradical-induced damage in striatal DA terminals could lead to retrograde changes in the SNpc. In addition, the data indicate that unilateral striatal damage can result in bilateral changes in the SNpc, thus confirming the interdependence of the two nigrostriatal pathways in rats.

Animals↗

PubMed1978

Stimulation of dopamine synthesis in caudate nucleus by intrastriatal enkephalins and antagonism by naloxone.

The intraventricular injection of methionine-enkephalin (50 to 100 micrograms) or [d-Ala2]-methionine-enkephalinamide (1.5 to 12 micrograms), a synthetic enkephalin analog resistant to enzyme degradation, caused a marked dose-dependent increase in dihydroxyphenylacetic acid and homovanillic acid concentrations in the rat striatum. The [d-Ala2] analog increased the accumulation of dopa in the striatum after aromatic amino acid decarboxylase inhibition, indicating that it increased dopamine synthesis. At the highest doses used both enkephalins failed to modify brain serotonin metabolism. The monolateral microinjection of the [d-Ala2]] analog (3 to 6 micrograms) into the caudate nucleus increased the concentration of dihydroxyphenylacetic acid in the injected side, whereas bilateral injection increased the concentration of this compound in both caudate nuclei and caused catalepsy. The stimulant effect of the [d-Ala2] analog on dopamine synthesis in the striatum persisted after destruction of striatal postsynaptic dopamine receptors with kainic acid. The biochemical and behavioral effects of enkephalins were prevented by naloxone, a specific narcotic antagonist. The results indicate that enkephalins stimulate dopamine synthesis by an action on opioid receptors localized on dopaminergic nerve terminals.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1990

Effects of contrast agents on the fallopian tube in a rabbit model.

The authors evaluated the effect of different iodinated contrast agents on the fallopian tube and adnexal tissue in 15 rabbits. Ethiodized oil, an oil-soluble agent, was used in five rabbits. The following water-soluble agents were used: iothalamate meglumine 30% (n = 3), iothalamate meglumine 60% (n = 3), and ioxilan (n = 4). The agents were injected through catheters placed in the fallopian tubes. Fallopian tubes and peritoneal cavities were histologically evaluated. The contralateral tube served as a control. Ioxilan and iothalamate meglumine 30% produced no pathologic response in the tube or peritoneal cavity. Iothalamate meglumine 60% was associated with mild inflammatory infiltrate, mucosal edema, giant cell reaction, and periovarian adhesions that were bilateral but more pronounced on the injected side. Use of ethiodized oil resulted in papillary fibrous adhesions on the ovarian surface, and fat granulomas were seen in the periovarian tissues. The safety of oil-based contrast agents for use in hysterosalpingography is therefore questioned. No significant differences were found among the water-soluble contrast agents.

Adnexa Uteri↗

PubMed2026

Distribution of transgene in the rodent choroid plexus after intracerebroventricular injection of adeno-associated virus.

Using adeno-associated virus to transfer genetic information to the choroid plexus has emerged as a promising route for long-term gene therapy in the brain for a variety of conditions. Overexpression of proteins has proved effective in small animal models but few attempts have been made to translate this technology to clinic, suppress the activity of a protein of interest, or further expand the limited capsid serotypes known to have choroid plexus tropism. We utilise transfer of green fluorescent protein to show choroid plexus epithelium tropism for novel AAV6 derived capsid ShH10Y445F in mouse, rat and porcine tissue explant cultures. In vivo tropism is shown in the mouse following stereotactic intracerebroventricular injection. We examined the distribution of viral transduction across the choroid plexus in all four ventricles following a single unilateral intracerebroventricular injection using both green fluorescent protein as a transgene, but also the CRISPR/Cas9 system to deliver permanent knockdown of apical water channel aquaporin-1. Quantitative immunofluorescence and SURVEYOR assay were used to statistically assess the magnitude and extent of choroid plexus knockdown across the ventricular system. We conclude that serotype ShH10Y445F targets choroid plexus epithelium in mouse, rat and pig; and when carrying the CRISPR/Cas9 system can reduce target protein expression in these cells. Transduced choroid plexus epithelial cells distribute unevenly with a bias toward the lateral ventricle on the injected side and a preferential infection of choroid plexus in the lateral over the third and fourth ventricles. Overcoming irregular distribution represents a challenge for clinical translation of this technology where clinical efficacy may require manipulation of the entire choroid plexus.

Animals↗

PubMed1976

In vivo and in vitro conjugation and metabolism of estrogens by the baboon kidney.

Labeled estrogen was injected into one of the renal arteries of baboons and urine was collected separately from each ureter via ureterostomy at various time intervals over a period of 7 h; the urinary metabolites were analyzed by DEAE-Sephadex chromatography and enzyme hydrolyses. Identification of the aglycones was made by TLC and co-crystallization upon admixture with authentic compounds. When [3H]estradiol-17beta (E2) was injected into one of the renal arteries, the major metabolites were [3H]E2-3-glucosiduronate (E2-3G) and [3H]estrone-3-glucosiduronate (E1-3G); [3H]E2-3G was excreted predominantly into the urine from the injected side during the initial 30 min after injection. Formation of [3H]E1-3G was not detectable for the first 5 min in the urine from either side. However, its excretion gradually increased and the amount was almost equal from both sides in the later hours of collection. Injection of [3H]E1 revealed ready conjugation (as E1-3G) by the kidney without significant reduction at position-17. When E2-3G, labeled with 3H at positions 6,7 and with 14C in the glucuronic moiety, was injected, it was quickly excreted in the urine of the injected side. The ratio of 3H/14C of E2-3G excreted in the urine was the same as that of the injected E2-3G. In the later periods, E1-3G, which had a slightly increased 3H/14C ratio, appeared in the urine. These results indicate that E2 and E1 are conjugated directly in the kidney to form the 3G which is excreted into the urine and that effective dehydrogenation or reduction of the steroids in vivo does not take place in the kidney. The results also show that conjugated E2 (E2-3G) is quickly excreted by the kidney of the baboon without any change in its form and that the E2-3G is dehydrogenated to E1-3G during its general circulation without significant prior removal of the glucuronic moiety. When [3H]estriol (E3) was injected, facile glucuronidation to E3-16G by the kidney was shown. Injection of an equimolar mixture of [14C]E3 and [3H]E2 showed rapid excretion of [14C]E3-16G as opposed to the slower excretion of [3H]E2-3G. These results suggested that the active sites of these conjugating enzyme systems in the kidney may be different.

Animals↗

PubMed1990

[The effect of the local anesthesia to the posterior ramus of the mandible in patients with temporomandibular joint problems].

Some clinicians in North America use anesthetic injections to differentiate the symptoms such as pain and stiffness in the facial area and neck in patients with TMJ problems. However, the effects and area which is influenced have not been studied. The purpose of this study was to study procedures and changes following administration of local anesthesia to the posterior ramus of the mandible. Twenty four patients with TMJ problems were used in this study. 0.5ml of 2% Lidocaine (epirenamine included) was injected into the most painful site upon palpation. The pain upon palpation test (following Krogh-Poulsen's method) was compared before and after 50 minutes. Results of this experiment were: 1) decrease of pain upon palpation was found not only in the site. In many cases subjective pain in the head and neck area was also reduced. 2) A significant reduction was found in the pain upon palpation test in the neck area. A highly significant reduction was seen in the Sterunoclydmastoid muscle only in the injected side. In the masticatory muscles. Also, reduction of pain upon palpation was seen in both lateral, medial pterygoid and digastric muscles in the injected side. 3) Contra side lateral pterygoid muscle and trapezius muscle also registered decreased pain upon palpation. 4) The mean values for the injected site were 5.7mm (S.D. 5.9) below the earlobe and the mean depth from the skin surface to the bony surface were 16.6 mm (S.D. 2.7mm). 5) The peak of the subjective effect were seen in one group in 20 minute later injection (early type) and in the 2nd group the peak were seen after 40 minutes (slowly type). 6) We did not experienced any paralysis of the facial nerve in this study.

Diagnosis, Differential↗

PubMed1990

[Effects of local application of 1,25 (OH)2D3 on experimental tooth movement in rats].

The purpose of the present study was to explore the effect of local application with Vitamin D metabolite, 1,25 dihydroxycholecalciferol (1,25 (OH)2D3), on experimental tooth movement in rats. 1. According to Waldo's method, a piece of orthodontic elastic band was inserted between the upper first and second molars of Wistar male rats weighing 200 g. The amount of 20 microliters of 1,25 (OH)2D3(10(-12)-10(-7) M) was injected locally in the submucosal palatal area of the root bifurcation of the right first molar. The left side was injected with vehicle. The number of osteoclasts was counted in a 700 x 1050 micron 2 area of the inter-radicular septum. The number of osteoclasts was dose-dependently increased 2-fold at 10(-10) M 1,25 (OH)2D3 compared to that in the vehicle-injected side. The maximal increase of osteoclast number was observed 3 days after local injection of 10(-10) M 1,25 (OH)2D3 on experimental tooth movement. 2. The upper first molar of Wistar male rats was moved in a buccal direction by a helical spring. The amount of 20 microliters of the local administration of 10(-10) M 1,25 (OH)2D3 was repeated every 3 days until sacrifice at day 20. The tooth movement in the 1,25 (OH)2D3-treated rats was accelerated about 2-fold compared to that in the control rats. 3. The effect of bone formation in the rats receiving experimental tooth movement was examined by fluorescent labeling and quantitative histology. Thus, the local application of 10(-10) M 1,25 (OH)2D3 tended to prevent the decrease of the mineral apposition rate of the alveolar bone following orthodontic tooth movement. 4. Serum samples of these 1,25 (OH)2D3-treated rats was obtained from abdominal aorta 3 hours after the final injection. Serious effects were not found in the values for parameters such as calcium, phosphorus and alkaline phosphatase. These findings suggested that the local use of 1,25 (OH)2D3 on experimental tooth movement in the rats caused increase in osteoclasts number and accelerated tooth movement. However, no obvious side effects were noted. 1,25 (OH)2D3 was expected to stimulate mineral apposition rate of alveolar bone on the tension side.

Alveolar Process↗