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FIGURE 9 Addition of serotonin % ; 2.5 X W'7 mol liter to the saphenous artery after an 8-minute incubation in calcium-free solution produces a brief phasic contraction, probably due to intracellularly stored calcium. The readmission of calcium IS ; 2.5 mmol liter then produces a sustained contraction which can be attributed to serotoninstimulated calcium influx. Washing is denoted by V. The contractions are reproducible, and are not affected by nimodipine up to 2.4 x 10~7 mol liter. To varying degrees, well-heeled consumers are as interested in marking out their social status by what foods they do and don’ t eat - and by what drugs they do and don’ t take - as they are in social justice, because intravenous nimodipine. Oral nimodipine likely reduces the risk of poor outcome after aneurysmal sah 25 july 2007 medwire news : patients who suffer an aneurysmal subarachnoid hemorrhage sah ; are more likely to survive and regain autonomy in their everyday activities if they receive the calcium antagonist nimodipine, a cochrane review concludes.

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Table 1. Summary of Neurosurgical Procedures Used for the Treatment of Movement Disorders, because stroke. Received each of 5 doses of mph in a counterbalanced sequenc results indicated that higher dosages are linearly related to increasing levels of hr and that these effects are dependent upon both the initial hr value and the time course of the medication.
With ramp voltage commands, it was necessary to place the voltage-activated channels in the dendrites to obtain clockwise hysteresis Fig. 3B ; . The difference between the hysteresis produced by the dendritically located LVA or HVA noninactivating currents was in the voltage of onset of the negative current slope. With the LVA channels Fig. 3Bii ; , the apparent activation voltage was 45 mV whilst with the HVA channels the activation voltage was 14 mV. On combining an LVA L-type dendritic current with an HVA L-type somatic current, both the voltage steps and ramps produced results strikingly similar to those seen experimentally, including the late-onset current, the prolonged tail current and the clockwise hysteresis with two current peaks during the hyperpolarising ramp e.g. compare Figs 1C and 3C ; . This lends support to the hypothesis that these late inward and hysteretic currents result from the activation of a noninactivating L-type conductance in the dendrites, possibly with a relatively low activation threshold. Pharmacology of the late-onset and hysteretic currents Cells displaying the late-onset currents were exposed to w-conotoxinGVIA 36 mM ; to block N-type Feldman et al., 1987 ; , w-agatoxinTK 400 nM ; to block P Q-type Teramoto et al., 1995 ; and nifedipine 20 mM ; or nimodipine 1020 mM ; to block L-type calcium channels. The L-type calcium channel activator FPL-64176 5.8 mM ; was also used to conrm the contribution of L-type channels Randall & Tsien, 1995 ; . Cells were either incubated 3070 min ; in the blockers or had the blockers acutely applied. To discriminate the effectiveness of each blocker on the late-onset currents, acute application experiments were undertaken. The lateonset currents were sensitive to both the dihydropyridines nifedipine and nimodipine seven out of seven cells; Fig. 4A ; . The current inections were completely n 2 ; or partially n 1 ; blocked by application of 20 mM nifedipine. Similarly, application of 1020 mM nimodipine completely blocked n 3 ; or reduced n 1 ; the current inections. Because sensitivity to dihydropyridines is the hallmark of L-type calcium channels, these results indicate that at least part of the lateonset conductance is mediated through L-type channels. This possibility was further tested with the application of the potent L-type channel activator FPL-64176. Application of FPL-64176 5.8 mM ; to cells with the late-onset currents caused an enhancement of these currents two out of two cells; Fig. 4B ; . In addition to the increased amplitude, this enhancement was characterized by reducing the somatic voltage at which the late current was rst seen and by producing large slowly activating currents. Similar effects of these drugs were seen with the ramp voltage commands. FPL-64176 not only had the expected effect of increasing the amplitude and shifting the peak inward current on the ascending ramp to the right, but it also increased the amplitude of the hysteretic current and delayed its deactivation, as can be seen during the hyperpolarizing ramp two out of two cells; Fig. 4C ; . This current was blocked by nimodipine 20 mM; two out of two cells; Fig. 4C ; . Given that the apparent activation voltage is more hyperpolarized in cells and noroxin. Nimodipine is approved for oral administration to improve neurological outcome after subarachnoid hemorrhage. Drug name insulin novolin, humulin ; - structure of insulin was established in 1960, leading to complete synthesis by 196 human insulin approved by fda in 198 bovine, porcine, and recombinant human insulin preparations currently available for use in diabetes worldwide; however, insulin derived from bovine tissue is no longer on us market as of 1999 because of fda concerns over transmission of bovine spongiform encephalopathy and norfloxacin, for instance, pregnancy. In reality the only defense that the drug companies have is the threat to stop doing business in that particular country. Even in patients with tsah we could not demonstrate any benefit with nimodipine and nateglinide.

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Prescriptive equivalents of dedicated products and common OCs. US Food and Drug Administrationapproved treatment consists of 2 doses taken 12 hours apart. The first dose is to be taken within 72 hours of unprotected sex for best effectiveness, although up to 120 hours afterward has been shown to result in protection. Taking both tablets of progestin-only emergency contraception in a single dose at 1 time has been shown to have equivalent efficacy. Suggested antinausea medicine: oral meclizine, 25 to 50 mg, which has 24-hour duration of action.
Message boards alternative medicine close find a drug advanced search advanced search « previous 1 2 3 next » nimotop clinical pharmacology font size a a a clinical pharmacology mechanism of action nimodipine is a calcium channel blocker and viramune. DISCUSSION These studies show that episodic alcohol intoxication of adult rats for a restricted period--either several times daily 5, 6, 12 ; or, in this report, simply once a day--produces irreversible neurodegeneration in selected olfactory and limbic cortical regions, and the damage is accompanied or preceded by electrolyte accumulation and brain edema. Also, when exposed to alcohol discontinuously rather than continuously, organotypic cerebrocortical hippocampal slice cultures exhibit statistically significant LDH release that is directly dependent on initial alcohol concentrations, thus providing a new model for in vitro studies of alcohol-induced brain damage. The alcohol concentrations producing cytotoxicity in this brain slice culture model, although high, are not unusual during alcohol detoxification 33 however, they are still lower than concentrations often needed to obtain significant neurodegeneration in dispersed neuronal tissue cultures 34, 35 ; . We suspect that alcohol's induction of cytotoxicity in the mature brain slice culture is a consequence not only of the repetitive daily exposures, but of the declining alcohol concentrations during each exposure, i.e., conditions occurring in binge intoxication. A ramification of both models' findings, consistent with observations in human subjects 36, 37 ; , is that only a limited number of severe intoxication bouts may cause selective and lasting brain deficits in alcohol abusers or heavy social drinkers. With many kinds of brain damage, neuroprotection by MK-801 is taken as evidence of involvement of the NMDA receptor. In our report showing no reductions in the entorhinal cortical damage induced by thrice-daily alcohol intoxication for 45 days using adult male rats supplied from the former Holtzman Laboratories, the MK-801 dose was 1 mgkg01day01 12 ; . In contrast, in a preliminary experiment none of the virus-free Sasco Laboratories SD rats used for studies herein ; survived beyond 5 days during oncedaily cotreatment with alcohol and a similar MK-801 dose. However, most Sasco rats did survive alcohol treatment with MK-801 at 75 mgkg01day01 a total of 600 mg kg ; over an 8-day period. Although low, the latter dose is nevertheless in a neuroprotective range; comparable acute doses 30100 mg kg ; of the potent NMDA receptor antagonist effectively reduced damage to the adult brain in other situations-- for example, soman intoxication in guinea pigs 29 ; and kainic acid treatment in rats 30 ; . We conclude that the lack of neuroprotection by MK-801 in both the once-daily or thrice-daily intoxication models and by DNQX or nimodipine in the thrice-daily model 12 ; rules against a primary pathophysiological mechanism for alcohol that involves synaptic glutamate ionotropic ; receptors or voltage-gated Ca2 channels.

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Having established that LTD can be reliably induced by pairing synaptic activity with backpropagating action potentials, we next examined the involvement of NMDA receptors in this LTD. Conditioning stimuli administered in the presence of 50 ~LM APV failed to induce depression of evoked responses 1 5 . 13.3% ; n - 6; P O.05; Fig. 6 ; . Surprisingly, the Ca 2 + transients in APV tended to be significantly smaller than those observed in normal ACSF P O.05; Fig. 6C ; in each of the three regions of the neuron. To further evaluate this effect, 5-see trains of 3-Hz stimuli were administered prior to the addition of APV in two neurons. These short trains did not alter evoked responses by themselves, but w h e APV was added to the ACSF and the trains were re-administered, Ca 2 + transients were found to be reduced in all three regions Pre: soma 16.7- + 0.4% ; proximal 15.9 3.0%; mid-radiatum 11.4- + 4.3%; Post: soma 10.0- + 0.7%; proximal 11.1 + -2.1%; midradiatum 8.1 - + 4.1% ; . Thus, NMDA receptors appear to be important for the induction of homosynaptic LTD and can greatly influence the magnitude of the Ca 2 + transients recorded during the 3-Hz stimulation. Heterosynaptic LTD in the CA1 region can be blocked by NMDA receptor antagonists and by antagonists of L-type VGCCs Abraham and Wickens 1991 ; . These findings have led to the suggestion that the activation of NMDA receptors may serve to prolong the period of postsynaptic depolarization and aid in the activation of L-type VGCCs. In addition, Hell et al. 1996 ; have shown that NMDA receptor activation in CA1 cells may persistently increase Ca 2 + influx through L-type channels following intense synaptic activity also see Chetkovich et al. 1991 ; . To determine if homosynaptic LTD is also dependent on L-type VGCC activity, nimodipine 10 p~i ; , a relatively nonphotolabile and nicotine. Effect of pretreatment of nimodipine and nitrendipine on some dopaminergically mediated behaviours in rats.
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Characterised by their sensitivity to -agatoxin IVA funnel web spider toxin FTX and are also blocked by -agatoxin IIIA and -conotoxin MVIIC. The Q-channel is blocked by -agatoxin IVA and -conotoxin MVIIC. In clinical practice, there is further selectivity of drug action at the L-channels, in part originating from the fact that there seem to be separate, but adjacent, binding sites for different chemical classes of calcium antagonists. Of the L-channel blockers, some chemical families are more active on the smooth muscle of the cardiovascular system e.g. nifedipine and most other DHPs ; whereas others are more cardioactive e.g. verapamil ; . Some further details of these differences are given under the VASODILATOR entry. This selectivity has been attributed to there being different binding sites on the 1-subunits closely located by molecular biology mutation techniques ; , for the dihydropyridines e.g. nifedipine, nitrendipine, nimodipine ; , benzothiazepines e.g. diltiazem ; , and phenylalkylamines verapamil ; groups. Latterly, further chemical groups of L-channel blockers have been developed that may afford some selectivity for uterine, gastrointestinal or airways smooth muscle including some indolizinesulfones e.g. fantofarone and mixed calcium sodium channel blockers e.g. lifarizine ; . A further factor contributing to some degree of selectivity follows from the fact that L-channel blockers show use-dependence through binding more strongly to the inactivated mode; a consequence of which might be that more electrophysiologically active and often pathological states would be more sensitive to the blocking action of some L-channel blockers, and so would to some extent be self-regulating. However, much remains to be discovered about medicinal chemistry strategies useful in designing tissueselective drugs of this type. Clinically, the main uses of the L-channel calcium channel blockers, include a direct smooth muscle relaxant action as vasodilators and for effects on heart muscle see MUSCLE RELAXANTS SMOOTH, VASODILATORS ; , leading to their widespread use as ANTIHYPERTENSIVES e.g. amlopidine, isradipine, nicardipine, nifedipine, verapamil in ANTIANGINAL AGENTS e.g. amlopidine, diltiazem, nicardipine, nifedipine, verapamil as ANTIARRHYTHMIC AGENTS e.g. verapamil ; , as VASODILATORS to treat peripheral vascular disease or Raynaud's phenomenon e.g. nifedipine in the prevention of ischaemic damage following subarachnoid haemorrhage nimodipine and as ANTIMIGRAINE AGENTS in prophylaxis against attacks e.g. nifedipine, verapamil ; . Turning to ligand-gated channels, less is known about channel blocking mechanisms. Some possible sites are outlined in the entry for CALCIUM CHANNEL ACTIVATORS. Blocking agents may work by indirect, possibly allosteric, interactions with intrinsic ion channels e.g. Ruthenium Red at the capsaicin receptor, or glycine at the NMDA glutamate receptor ; . Others work through a direct-coupled G-protein action e.g. N-type calcium channel-closure through opioid or 2-adrenoceptor activation ; . Lastly, yet other drugs affect intracellular calcium channels of the endoplasmic or sarcoplasmic reticulum e.g. inositol triphosphate receptor channels which open in response to InsP3 itself and certain other inositol phosphates antagonised by heparin. The various ryanodine receptor channels, are activated by caffeine and low concentrations of ryanodine, but antagonised by high concentrations of ryanodine, by Ruthenium Red and possibly by 8-bromo-cADP-R. The ryanodine receptor in skeletal muscle has a mutant form on an autosomal dominant gene ; which can be triggered by halothane and suxamethonium to precipitate the dangerous. Table 2. How do existing WWW based approaches cope with different attacks? and orap.

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Bay K 8644 a selective L-type VDCC agonist ; induces LTD significantly equal to RU-28362. Nimodipinf blocks its effects on LTD facilitation. Similarly, D-AP5 blocked LTD in the presence of Bay K 8644. So L-type VDCC can contribute to induction of LTD but it is still primarily dependent on NMDA receptor activation and pimozide and nimodipine.

TABLE 7A-4. PEARSON'S r CORRELATIONS n 104 ; BETWEEN THYROID HORMONES AND TSH FOR THE 14-DAY DATA OF THE SPRINGBORN LABORATORIES, INC. 1998 ; SUBCHRONIC RAT STUDY T3 T3 T4 TSH 1.00 p 0.00 T4 0.36 p 0.0001 1.00 p 0.00 TSH 0.11 p 0.27 0.20 p 0.04 1.00 p 0.00 7A-2 DRAFT-DO NOT QUOTE OR CITE.
Reference: Type: OFFER 05 SE WSIV 0CJ5 Title: A sensor for detecting damages on rental boats Abstract: A Swedish SME has developed a sensor, a black box, to detect the damage history on rental boats. A common problem when hiring out boats is the damage done to them. The box detects what has happened with the boat in a rapid, cost saving and simple way. The owner receives a SMS in real time on mobile phone with information concerning where and when the boat struck a stone. The SME is seeking partners for joint venture, manufacturing and or commercial agreement with technical assistance. Keywords: Information Technology Informatics; Internet Technologies Communication Wireless, Wi-Fi, Bluetooth Smart Appliances; Applications for Tourism; SatelliteTechnology Systems Positioning Communication in GPS Global Positioning System Applications: Other electronics related including alarm systems Other Consumer Related not elsewhere classified Leasing of railcars, buses, cars, etc.; Chemical material testing; Other transportation; Optical Technology related to measurements The biggest markets are Scandinavia, the Mediterranean and the US. - Type of partner sought: A commercial partner who can establish the product in the Mediterranean countries, e.g. licensing. - Specific area of activity of the partner: The company should be involved in the marine market and preferably have technical knowledge within the application field. Activities can include selling system solutions to boat manufacturers or to specific customers. - Task to be performed: To establish the product on the Mediterranean market and in other selected countries. The Swedish company will provide training for customer support and also support in technical consultancy, assembly and quality control and orinase. Conclusions A wide group of agents with diverse mechanisms of action have been tested in at least one Class I trial, but there is incomplete or conflicting evidence for these agents. Other strategies to slow decline in AD In one large, 2-year trial, selegiline 5 mg BID ; and vitamin E 1, 000 I.U. [alpha-tocopherol] BID ; significantly delayed the time to a composite outcome of primary measures indicative of clinical worsening, and fewer patients treated with vitamin E were institutionalized. 55 ; Importantly, there was no additive effect from selegiline plus vitamin E, neither agent improved cognitive function ADASCog ; compared with baseline values, and those on drug did not decline less than those on placebo on these types of measures. Although epidemiologic data suggest that anti-inflammatory drugs may be protective against the development of AD, 56 ; few anti-inflammatory drug trials have been reported. In one 6-month trial of indomethacin, stabilization of cognition was suggested, although the authors reported a 44% dropout rate. 57 ; A 6-month trial of diclofenac for treatment of AD reported slightly slower decline not significant ; and a 50% dropout rate because of adverse events. 58 ; A recent trial of prednisone for the treatment of AD was negative. 59 ; Epidemiologic studies suggest that estrogen may be protective against the development of AD, and from this observation, the possibility that it also might have a therapeutic effect in AD has been suggested. To date, two well designed clinical trials examining the ability of Premarin WyethAyerst, Philadelphia, PA ; to slow the rate of decline in women with AD were negative. 60, 61 ; Conclusions One study suggests a possible benefit of vitamin E or possibly selegiline for treatment of AD. The agents should not be combined. The use of anti-inflammatory agents, prednisone, and estrogen to prevent the progression of AD are not supported by prospective data. Drugs tested in mixed dementia populations or in patients with mixed dementias In one trial, propentofylline a glial-modulating agent ; produced a drugplacebo difference on a variety of cognitive and global measures, 62 ; but these findings were not adequately replicated in a second trial. Memantine, an NMDA receptor antagonist, improved cognition and global functioning in two poorly defined groups of patients with dementia. 63-65 ; Several nootropic agents including oxiracetam, 66-68 ; nicergoline, 69, 70 ; vincamine, 71 ; naftidrofuryl, 72 ; and xantinolnicotinate 73 ; have shown small degrees of improvement on some outcomes for mixed dementia populations. None of these agents has been adequately tested for specific types of dementia. One trial reported a mild benefit of fluvoxamine. 74 ; Treatment with various formulations of gingko biloba was associated with significant improvements in some but not all ; a priori parameters including a small treatmentplacebo difference on a cognitive measure not detected on a clinical global ; , 75 ; some improvement on a clinician's global assessment and an activities of daily living scale, 76 ; and increased speed on a subset of timed tasks. 77 ; Several other agents including glycosamine 78 ; nimodipine, 79 ; pyritonol, 80 ; and acetyl-L-carnitine 81 ; all have shown small improvements in overall functioning in populations with patients with mixed dementia, but none proved a treatment benefit on all the primary outcome measures. Conclusions Ginkgo biloba was safe in one Class I trial of patients with mixed dementia, but benefits fall short of those expected for clinically effective antidementia treatments e.g., a psychometric measure and a clinician's global ; . Currently there are no adequately controlled positive trials supporting the use of any pharmacologic agents in patients believed to have mixed neurodegenerative and ischemic vascular dementia, or in populations in which the specific type of dementia is not identified. Ischemic vascular multi-infarct ; dementia Few Class I trials have been performed in populations with pure ischemic vascular or multi-infarct dementia. In a single study of the nootropic oxiracetam, 82 ; improved functioning on the Blessed Functional scale was reported. Cyclandelate and flunarizine showed pre- to posttreatment benefits on a subset of measures. 83 ; Two trials of pentoxifylline were negative. 84, 85.

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BIRTH-CONTROL TABLETS ARE PACKAGED IN CARTONS OF 6 CYCLES 6 MO SUPPLY ; SUPPLY ; . THE COSTS FIGURES LISTED ARE FOR 6 CYCLES. PLEASE BE SURE YOU ARE ORDERING THE QUANTITY YOU NEED. IF YOU HAVE ANY QUESTIONS PLEASE CONTACT VAL MCDONALD OR BO SHIFFLETT AT 512-458-7500. 1. Margherita, AJ, Issues in Dancers and Gymnasts, in Buschbacher, R, Braddom, RL eds. ; , Sports Medicine and Rehabilitation: A Sport Specific Approach, 1994, pp.151-169. 2. Margherita, AJ, Sports Medicine and Injury Prevention, in deLateur, BJ, Kraft, GH eds. ; , Physical Medicine and Rehabilitation Clinics of North America, 5: 345-57, 1994.
Workshop Purpose: Three issues define national policies toward pharmaceuticals: The prices paid to pharmaceutical manufacturers, the extent of patient or third-party payment for drugs, and access to new products. Workshop Description: The price paid for pharmaceuticals is determined by health authorities, either public or private. Often a formula is used to set these prices based upon the price paid in other countries. This is called "reference pricing". The price can be set according to either of two objectives. A "Health Policy" perspective will attempt to minimize expenditures so as to contain total health care costs. A "Health Industry Policy" will also consider the effect of drug prices on the pharmaceutical research climate in the country The second issue is the question of who pays for drugs. Some health systems impose very high user fees, or cost-sharing on patients, while in other countries the cost of drugs is more heavily subsidized by the insurance program. In some countries, most notably the US, cost-sharing is part of a broader attempt to bring economic incentives into the pharmaceutical marketplace. In these programs patients face lower prices for drugs that are determined to be a particularly good value to the health plan, while consumer prices are considerably higher for products that are thought to be less cost-effective. Lastly, we consider whether, for instance, nmodipine bipolar. The leading role in osteoarthritis research is played by the National Institute of Arthritis and Musculoskeletal and Skin Diseases NIAMS ; , within the National Institutes of Health NIH ; . The NIAMS funds many researchers across the United States to study osteoarthritis. It has established a Specialized Center of Research devoted to osteoarthritis. Also, many researchers study arthritis at NIAMS Multipurpose Arthritis and Musculoskeletal Diseases Centers and Multidisciplinary Clinical Research Centers. These centers conduct basic, laboratory, and clinical research aimed at understanding the causes, treatment options, and prevention of arthritis and musculoskeletal diseases. Center researchers also study epidemiology, health services, and professional, patient, and public education. The NIAMS also supports multidisciplinary clinical research centers that expand clinical studies for diseases like osteoarthritis. For years, scientists thought that osteoarthritis was simply a disease of "wear and tear" that occurred in joints as people got older. In the last decade, however, research has shown that there is more to the disorder than aging alone. The production, maintenance, and breakdown of cartilage, as well as bone changes in osteoarthritis, are now seen as a series or cascade of events. Many researchers are trying to discover where in that cascade of events things go wrong. By understanding what goes wrong, they hope to find new ways to prevent or treat osteoarthritis. Some key areas of research are described below. Animal Models: Animals help researchers understand how diseases work and why they occur. Animal models help researchers learn many things about osteoarthritis, such as what happens to cartilage, how treatment strategies might work, and what might prevent the disease. Animal models also help scientists study osteoarthritis in very early stages before it causes detectable joint damage. Diagnostic Tools: Some scientists want to find ways to detect osteoarthritis at earlier stages so that they can treat it earlier. They seek specific abnormalities in the blood, joint fluid, or urine of people with the disease. Other scientists use new technologies to analyze the differences between the cartilage from different joints. For example, many people have osteoarthritis in the knees or hips, but few have it in the ankles. Can ankle cartilage be different? Does it age differently? Answering these questions will help us understand the disease better. Genetics Studies: Researchers suspect that inheritance plays a role in 25 to percent of osteoarthritis cases. Researchers have found that genetics may play a role in approximately 40 to 65 percent of hand and knee osteoarthritis cases. They suspect inheritance might play a role in other types of osteoarthritis, as well. Scientists have identified a mutation a gene defect ; affecting collagen, an important part of cartilage, in patients with an inherited kind of osteoarthritis that starts at an early age. The mutation weakens collagen protein, which may break or tear more easily under stress. Scientists are looking for other gene mutations in osteoarthritis. Recently, researchers found that the daughters of women who have knee osteoarthritis have a significant increase in cartilage breakdown, thus making them more susceptible to disease. In the future, a test to determine who carries the genetic defect or defects ; could help people reduce their risk for osteoarthritis with lifestyle adjustments and noroxin.
FIELDS, H. L. AND BASBAUM, A. I.: Brainstem control spinal pain-transmission neurons. Annu. Rev. Physiol. 40: 217248, 1978. HALEY, T. J. AND MCCORMICK, W. G.: Pharmacological effects produced by intracerebral injections of drugs in the conscious mouse. Br. J. Pharmacol. 12: 1215, 1957. HOKFELT, T., LJUNGEDAHL, A., TERENIUS, L., ELDE, R. AND NILSSON, G.: Immunohistochemical analysis of peptide pathway possibly related to pain and analgesia: Enkephalin and substance P. Proc. Natl. Acad. Sci. USA 74: 30813085, 1977. HOKFELT, T., TERENIUS, L., KUYPERS, H. G. J. M. AND DANN, O.: Evidence for enkephalin immunoreactive neurons in medulla oblongata projecting to the spinal cord. Neurosci. Lett. 14: 5560, 1979. HORNFELDT, C. S., SMULLIN, D. D., SCHAMBER, C. D., SUN, X. AND LARSON A. A.: Antinociceptive effects of intrathecal taurine and calcium in the mouse. Life Sci. 50: 19251934, 1992. HYLDEN, J. L. AND WILCOX, G. L.: Intrathecal morphine in mice: A new technique. Eur. J. Pharmacol. 67: 313316, 1980. JUNG, J. S., SONG, D. K., CHOI, Y. S. AND KIM, Y. H.: Effects of intraventricular injection of morphine and -endorphin on serotonin release from the spinal cord in rats. Pharmacol. Biochem. Behav. 49: 10371042, 1994. KURAISHI, Y., FUKUI, K., SHIOMI, H., AKAIKE, A. AND TAKAGI, H.: Microinjection of opioids into the nucleus reticularis gigantocellularis of the rat: Analgesia and increase in the normetanephrine level in the spinal cord. Biochem. Pharmacol. 27: 27562758, 1978. KURAISHI, Y., HARADA, Y. AND TAKAGI, H.: Noradrenaline regulation of paintransmission in the spinal cord mediated by alpha-adrenoceptors. Brain Res. 174: 333336, 1979. KURAISHI, Y., HARADA, Y., ARATANI, S., SATOH, M. AND TAKAGI, H.: Separate involvement of the spinal noradrenergic and serotonergic systems in morphine analgesia: The difference in mechanical and thermal analgesic tests. Brain Res. 273: 245252, 1983. KUZMIN, A. V., PATKINA, N. A. AND ZVARTAU, E. E.: Analgesic and reinforcing effects of morphine in mice: Influence of Bay K-8644 and nimodipine. Brain Res. 652: 18, 1994. LITCHFIELD, J. T. AND WILCOXON, F.: A simplified method of evaluating doseeffect experiments. J. Pharmacol. Exp. Ther. 96: 99113, 1949. LLINAS, R., GRUNER, J. A., SUGIMORI, M., MCGuinness, T. L. and Grrengard, P.: Regulation by synapsin I and Ca 2 ; -calmodulin-dependent protein kinase II of neurotransmitter release in squid giant synapse. J. Physiol. Lond. ; 436: 257282, 1991. LUX, F., WELCH, S. P., BRASE, D. A., DEWEY, W. L.: Interaction of morphine with intrathecally administered calcium and calcium antagonists: Evidence for supraspinal endogenous opioid mediation of intrathecal calcium-induced antinociception in mice. J. Pharmacol. Exp. Ther. 246: 500507, 1988. MALMBERG, A. B. AND YAKSH, T. L.: Voltage-sensitive calcium channels in spinal nociceptive processing: Blockade of N-type and P-type channels inhibits formalin- induced nociception. J. Neurosci. 14: 48824890, 1994. MALMBERG, A. B. AND YAKSH, T. L.: Effect of continuous intrathecal infusion of - conopeptides, N-type calcium channel blockers, on behaviour and antinociception in the formalin and hot-plate tests in rats. Pain 60: 8390, 1995. MAYER, D. J. AND PRICE, D. D.: Central nervous system mechanisms of analgesia. Pain 2: 379404, 1976. MIRANDA, H. F., BUSTAMANTE, D., KRAMER, V., PELISSIER, T., SAAVEDRA, H., PAEILE, C., FERNADEZ, E. AND PINARDI, G.: Antinociceptive effects of Ca2 channel blocker. Eur. J. Pharmacol. 217: 137141, 1992. MIZOGUCHI, H., NARITA, M., OUOCK, R. M. AND TSENG, L. F.: Involvement of Met-enkephalin and -opioid receptors in the spinal cord in antinociception induced by cold water swimming in the mouse. Soc. Neurosci. Abstr. ; 21: 1363, 1995. ROERIG, S. C. AND WEI, Z. Y.: Effects of -conotoxin on spinal morphine and clonidine antinociception. FASEB J. 9: A97, 1995. SMITH, F. L. AND STEVENS, D. L.: Calcium modulation of morphine analgesia: Role of calcium channels and intracellular pool calcium. J. Pharmacol. Exp. Ther. 272: 290299, 1995. SPAMPINATO, S., SPERONI, E., COVONI, P., PISTACCHIO, E., ROMAGNOLI, C., MURARI, G. AND FERRI, S.: Effect of omega-conotoxin and verapamil on antinociceptive, behavioral and thermoregulatory responses to opioids in the rat. Eur. J. Pharmacol. 254: 229238, 1994. SUH, H. H., COLLINS, K. A. AND TSENG, L. F.: Intrathecal cholecystokinin octapeptide attenuates the antinociception and release of immunoreactive Met-enkephalin induced by intraventricular -endorphin in the rat. Neuropeptides 21: 131137, 1992a. SUH, H. H., HONG, J. S. AND TSENG, L. F.: Intrathecal DSP-4, 6-hydroxydopamine and 5, 7-dihydroxytryptamine differentiate intracerebroventricular -endorphin- from morphine-induced antinociception in the mouse. Pharmacol. Commun. 1: 227232, 1992b. SUH, H. H., FUJIMOTO, J. M. AND TSENG, L. F.: Differential mechanisms mediating -endorphin- and morphine-induced analgesia in mice. Eur. J. Pharmacol. 168: 6170, 1989. SUH, H. H. AND TSENG, L. F.: Intrathecal -funaltrexamine antagonizes intracerebroventricular -endorphin- but not morphine-induced analgesia in mice. J. Pharmacol. Exp. Ther. 245: 587593, 1988. SUH, H. H. AND TSENG L. F.: Different types of opioid receptors mediating analgesia induced by morphine, DAMGO, DPDPE, DADLE and -endorphin in mice. Naunyn-Schmiedeberg's Arch. Pharmacol. 342: 6771, 1990a.

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