The involvement of bulbospinal serotonergic neurons in the effect of 5-hydroxytryptophan on alpha and gamma motoneurons.
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Biomedical subjects
Publications and source records attributed to N R Myslinski.
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This investigation studied the impairment of Hue, Value, and Chroma matching by color vision-defective dental personnel. Color-defective dental personnel were found to make significantly greater errors in Hue and Chroma selection than normal-vision dental personnel. Value, the component of shade selection considered the most important, was uneffected. Color-normal dental assistants were significantly more accurate in Hue and Chroma selection than color-defective dental personnel and could assist affected dentists in clinical situations.
Lysine and its metabolic intermediates were studied for their effect on pentylenetetrazol (PTZ)-induced seizures in mice. L-Lysine at dosages above 2 mmol/kg given i.p. significantly increased seizure protection and seizure latency (the time required to develop seizures after PTZ injection) with a peak effect dose at 10 mmol/kg. A pretreatment time of 15 min was required to significantly prolong seizure latency with a peak effect time of 45 min. D-Lysine at 10 mmol/kg i.p. afforded some seizure protection and significantly prolonged seizure latency but has a peak effect time of 15 min. When administered intracerebroventricularly, both L-lysine and piperidine at 0.1 mmol/kg prolonged seizure latency significantly, and increased seizure protection slightly. L-Pipecolic acid at the same dose given through the same route, however, shortened seizure latency significantly. L-alpha-Aminoadipic acid, on the other hand, had no significant effect. Lysine metabolites that prolonged seizure latency also increased seizure protection and decreased seizure death, and one that shortened seizure latency had the opposite effect. The anticonvulsant activity of lysine and its metabolites was explained on the basis of their connection with the GABAergic transmission.
Tooth pulp stimulation in the rabbit produces a complex rhythmic lick/chew response (LCR). Because of the effect of fentanyl on the afferent and efferent components of oral function we examined its effect on this response. Intravenous fentanyl attenuates the LCR in a dose dependent manner with the ED50 occurring at 0.1 mg/kg. Concurrently a different response to tooth stimulation appears consisting of a slow, non-rhythmic lateral jaw movement (LJR). The effects of fentanyl on both LCR and LJR are blocked by naloxone (0.1 mg/kg). The dopamine antagonist, chlorpromazine (10 mg/kg iv) also has the same qualitative effect as fentanyl on both responses.
This study was designed to determine the feasibility of using electromyography (EMG) to quantify muscle pain in patients suffering from chronic myofacial pain dysfunction (MPD). Ten patients were carefully selected to include those having mild to severe pain, but not any major psychological or other physiological dysfunction. Measurements of perceived pain and EMG frequency and amplitude were recorded before and after standard analgesic therapy. EMG recordings were collected bilaterally from the masseter and anterior temporalis muscles during the resting, swallowing, clenching and chewing modes of activity. Multiple regression (R) analysis indicated that changes in perceived pain are correlated with changes in the EMG and can be determined by using the following formula: delta P = (delta F) (0.405) + C where P = perceived pain level, F = EMG frequency, and C = 1.533. By computing the Phi coefficients, the highest correlation between EMG recordings and subjective pain ratings was demonstrated in the resting mode. In this mode, 64% (multiple R = 0.80) of the variance in perceived pain difference scores from pre- to post-therapy tests could be determined. A significant relationship exists between the change in perceived pain and the EMG (t = 2.525, p less than 0.05), whether pain levels increase or decrease. The implementation of this method to quantify expected changes in pain due to muscle spasm in uncomplicated individuals is discussed.
Blood-brain barrier transport of L-[1-14C]pipecolic acid was studied in the ray by single intracarotid injection using 3H2O as a diffusible internal standard. Brain uptake index (BUI) for L-[14C]pipecolic acid (0.036 mM) was found to be 18.1, 10.5, and 12.6 for the cerebral cortex, brain stem, and cerebellum, respectively which was substantially higher than that reported for its analog L-proline in the whole brain. Influx of L-pipecolic acid into the brain was concentration dependent and differed significantly between the cerebral cortex and the brain stem, and between the cerebral cortex and the cerebellum, but not between the brain stem and the cerebellum. Kinetic study of L-pipecolic acid influx revealed a low- and a high-capacity uptake mechanisms. The low-capacity saturable component has Km values ranging from 38 to 73 microM, and Vmax values ranging from 10 to 13 nmol/g/min for the three brain regions. The nonsaturable component has a Km of 4 mM, a Vmax of 200 nmol/g/min and similar diffusion constant (Kd) (0.03 to 0.06 mlg-1 min-1) for all three brain regions. A possible role of the two-component brain uptake mechanism in the regulation of the neuronal function of L-pipecolic acid was suggested.
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The effects of the 5-hydroxytryptamine (5-HT) precursors, 5-hydroxytryptophan (5-HTP) and tryptophan on alpha- and gamma-motoneuron discharges were examined in the spinal cat with a deafferented cord. The injection of 75 mg/kg of dl-5-HTP resulted in a doubling of the spontaneous discharge rate of gamma-motoneurons and the induction of spontaneous alpha-motoneuron activity. These effects of 5-HTP were reversed by the 5-HT antagonists, cinanserin (4 mg/kg) and methysergide (2 mg/kg). Tryptophan alone (100 mg/kg) exhibited minimal effects of motoneuron activity, but in animals pretreated with pargyline it significantly excited alpha- and gamma-motoneurons. Recordings of alpha- and gamma-motoneuron activity in gastrocnemius and semitendinosus nerves revealed that 5-HTP increased alpha- and gamma-motoneuron activity in both flexor and extensor nerves. Reversal of the effects of 5-HTP by 5-HT antagonists suggests that these effects were mediated by 5-HT. The fact that the 5-HTP effects were observed in preparations with an open gamma-loop indicates that the effects on the alpha-motoneurons are not mediated via the gamma-motoneuron facilitation, but results from a central activation.
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1. The responses of identified cells in the cat Clarke's column and dorsal horn to micro-electrophoretically applied cholinomimetics and anti-cholinergic substances have been investigated. 2. Both antidromically identified (DSCT neurones) and synaptically activated neurones from the region of the Clarke's column of the spinal cord were excited by ACh. However, the proportion of ACh excited cells was greater in units synaptically activated by ipsilateral dorsolateral funiculus stimulation (78%) than in DSCT neurones (50%). In addition, about 55% of neurones activated either antidromically or synaptically by ipsilateral dorsal column stimulation were excited by ACh. 3. In contrast to a relatively weak excitatory potency on the DSCT neurones (maximum firing frequency did not exceed 130% of the control activated by ipsilateral dorsolateral funiculus stimulation (maximum firing frequency reached 430% of the control level). 4. ACh has a relatively quick and rapidly reversible excitatory effect on Clarke's column neurones and some types of dorsal horn interneurones, which can be obtained also with nicotine. However, the action of nicotine is frequently delayed in onset and recovery. This excitatory action of ACh can be blocked or markedly depressed by dihydro-beta-erythroidine. These results and those obtained with acetyl-beta-methylcholine and atropine seem to suggest that the receptors mediating excitation of the cholinoceptive spinal cells activated either antidromically or synaptically by ipsilateral dorsolateral funiculus stimulation besides predominantly nicotinic have also weak muscarinic properties. 5. Desensitization with repeated applications of ACh and nicotine has been observed in both DSCT neurones and units antidromically activated by ipsilateral dorsal column stimulation. 6. About 11% of units antidromically activated by ipsilateral dorsolateral funiculus stimulation were depressed by ACh. In addition, the depressant effect of ACh was more frequently encountered in the cells unresponsive either to the dorsolateral funiculus or dorsal column stimulation. ACh depression was also seen in units activated either antidromically or synaptically by ipsilateral dorsal column stimulation. In contrast, none of the units synaptically activated by the ipsilateral dorsolateral funiculus stimulation were depressed by ACh. The same was true for spinal neurones receiving convergent peripheral inputs activated either antidromically or synaptically by ipsilateral dorsolateral or dorsal column stimulation. 7. The findings that ACh depression of all tested DSCT neurones is blocked by atropine and readily evoked by acetyl-beta-methylcholine indicates that receptors mediating the effect are of muscarinic type.
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OBJECTIVE: To review the basic and clinical pharmacology of three opioids to assist in the nursing care of postoperative patients. METHODS: The authors discuss the pharmacodynamics and pharmacokinetics of fentanyl, sufentanil, and alfentanil and compare them with other opioids. A discussion of the nursing care of patients who receive these agents both intravenously and epidurally is provided along with a nursing care plan. Common opioid-related side effects and their treatments are discussed. CONCLUSIONS: Fentanyl, sufentanil, and alfentanil are potent synthetic opioids that are used for anesthesia and postoperative analgesia. The advantages of these opioids compared with morphine are short duration of action, lack of hyperglycemic response to surgery, decrease in catecholamine levels, and high lipid solubility. The nursing care of patients receiving these opioids involves frequent assessment of the degree of analgesia and monitoring for and treatment of side effects.