Acetyl-L-Carnitine Effect on Pituitary and Plasma β-Endorphin Responsiveness to Different Chronic Intermittent Stressors

The aims of the present study were: 1) to compare the effect of two different chronic intermittent stressors i.e. cold-swimming versus ether, on the pituitary opioidergic system; 2) to evaluate the response of pituitary and plasma β-endorphin (βS-EP) to an acute stress in chronically stressed rats; and 3) to evaluate the effect of acetyl-l-carnitine treatment (10 mg/day/rat per os at night) on pituitary and plasma β-EP changes induced by two different types of chronic stress. The stressors were applied twice a day for 10 days. Rats were killed either before, during or after the last swimming or ether stress session. β-EP was measured by radioimmunoassay in anterior pituitary and in neurointermediate lobe extracts and in plasma. The following observations were made; 1) Chronic intermittent cold-swimming stress increased anterior pituitary contents and plasma β-EP levels; 2) both chronic intermittent cold-swimming stress and ether stress caused an increase of neurointermediate lobe β-EP contents; 3) as in control animals, rats exposed to chronic intermittent swimming stress reduced pituitary β-EP contents and raised plasma β-EP levels in response to the last acute swimming stress; 4) in contrast to control animals, rats exposed to chronic intermittent ether stress did not show any significant response of the pituitary-plasma opioidergic system to the last acute ether session; 5) the acetyl-l-carnitine treatment counteracted the changes evoked by chronic intermittent cold-swimming stress on the pituitary and plasma β-EP levels. The present data show that chronic intermittent ether stress impairs the capacity to respond to the acute stress and that acetyl-l-carnitine may modulate the changes of β-EP levels following chronic cold-swimming stress exposure.     

Effects of formaldehyde on the isolated phrenic nerve and the phrenic nerve-diaphragm preparation of the rat, in vitro

Formaldehyde, 0.5-4.5 mM, increased the threshold for electrical excitation of the nerve, and led to a partial and reversible inhibition of the compound action potential (cAP). The depression was not enhanced by high frequency stimulation. At 8.9 mM or higher, the depression of the nerve excitability could not be reversed. The inhibition of the nerve developed more slowly than that of the muscle, and the nerve was unaffected after 10 min exposure to 2.2 mM. Formaldehyde, 2.2 mM, caused an immediate depression of the indirectly (through the nerve) and directory (at the muscle) elicited twitch tension. After 10 min the tensions were reduced to respectively, 56% and 49% of control. However, the electromyogram was not changed, indicating that the effect was localized to the excitation-contraction coupling. Tetanic tension (100 Hz in 5 sec) was inhibited more than twitch tension during indirect stimulation, whereas the opposite was found during direct stimulation of the muscle. Thus, during high frequency stimulation, formaldehyde must have an additional effect on the neuromuscular transmission. This effect was localized presynaptically since a fall out of endplate potentials was observed in the formaldehyde-treated diaphragm. In 6.7 mM or higher concentrations the directly or indirectly induced contractions were irreversibly blocked. The resting membrane potential of the muscle cells was unchanged after exposure to formaldehyde. Formaldehyde caused myotonia-like contractions of the diaphragm, occasionally after exposure to low concentrations (2.2 mM), and always after exposure to higher concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of Dopamine D1 and D2 Receptor Agonists and Antagonists on Basal and Ethanol-Modulated β-Endorphin Secretion from Hypothalamic Neurons in Primary Cultures

In the present study, we determined the effects of dopamine receptor agonists and antagonists on basal and ethanol-modulated β-endorphin (β-EP) secretion from hypothalamic neurons in primary cultures. Treatment with various concentrations of dopamine D1 agonist SKF 38393 and D1 antagonist SCH 23390 did not affect basal IR-β-EP release. However, dopamine D2 receptor agonist LY 141865 reduced basal immunoreactive (IR)-β-EP release in a concentration dependent manner. D2 receptor antagonist, sulpiride, on the other hand, stimulated basal IR-β-EP release and blocked LY 141865-induced inhibition of IR-β-EP release in a concentration dependent manner. When the actions of these DA receptor agents on ethanol-modulated IR-β-EP release were studied, both D1 and D2 receptor agents failed to affect ethanol-modulated IR-β-EP release. These data suggest that the endogenous secretion of β-EP from hypothalamic neurons is under the influence of an inhibitory dopaminergic system involving the D2 receptor. Furthermore, ethanol's effects on β-EP secretion are not mediated by dopamine.     

Peripheral mechanisms of fatigue in muscles of normal and dystrophic mice.

We evaluated the contribution of different processes to fatigue of normal and dystrophic mouse muscles using an in vitro electromyography chamber. Fatigue was induced by repetitive nerve stimulation at 30 Hz for 0.5 s, every 2.5 s until tension decreased by about 50%. We monitored the compound nerve action potential (AP), compound muscle AP, and isometric tension responses to nerve stimulation, and compound muscle AP and tension responses to direct muscle stimulation. In normal mice, about 50% reduction in nerve-evoked tension occurred by 2.4 min in extensor digitorum longus (EDL), 4.8 min in diaphragm, and 9 min in soleus. Analysis of the responses revealed that the fatigue was caused by failure of more than one process in all muscles, and failure of nerve conduction did not contribute to fatigue in any muscle. Failure of neuromuscular transmission, muscle membrane excitation, and excitation-contraction (E-C) coupling and contractility accounted for 55, 45, and 0%, respectively, of the fatigue in EDL, for 21, 74, and 5% of the fatigue in diaphragm, and for 2, 54, and 44% of the fatigue in soleus. In dystrophic mice, while about 50% reduction in nerve-evoked tension occurred by 8.1 min in EDL and 5.6 min in diaphragm, only 29% reduction in tension occurred by 80 min in soleus. Failure of neuromuscular transmission, muscle membrane excitation, E-C coupling and contractility accounted for 22, 63 and 15% of the fatigue in EDL, for 21, 79, and 0% of the fatigue in diaphragm, and for 15, 59, and 26% of the fatigue in soleus. The proportion of slow-twitch oxidative fibers was more than normal in dystrophic EDL, but the same as normal in dystrophic diaphragm and soleus. The slower onset of fatigue was attributable to lesser failure of neuromuscular transmission in dystrophic EDL, and to lesser failure of E-C coupling and contractility in dystrophic soleus.     

Hypoglycemia-induced elevation of immunoreactive beta-endorphin level in cerebrospinal fluid in the cat

Under pentobarbital anesthesia, β-endorphin levels in cat cerebrospinal fluid (CSF) were studied by a sensitive radioimmunoassay combined with a gel column chromatograph. Immunoreactive β-endorphin (IR-β-EP) levels in cat CSF significantly increased during insulin-induced hypoglycemia along with the elevation of its peripheral plasma levels. The entry of systematically administered β-endorphin into CSF is, if of any effect, negligible in these experimental conditions. Such an increase of IR-β-EP in CSF, therefore, might reflect its release form the brain into cerebroventricular spaces during insulin-induced hypoglycemia.     

Recruitment and firing rate modulation of motor unit tension in a small muscle of the cat's foot.

Maintained contractions were elicited in the first deep lumbrical muscle of the cat's foot by electrical stimulation of the contralateral motor cortex or, reflexly, by pinching of the foot pad. The discharges of all significant motor units of the muscle were monitored by electromyography, and contractions of the various motor units were observed in isometric recordings of muscle tension. Over a wide range, muscle tension could be enhanced by an increased intensity of pad pinching or cortical stimulation. This increase in muscle tension was caused by a recruitment of new motor units as well as by an increase in the firing rate of already active motor units. The latter mechanism was clearly of great importance. Pad pinching or cortical stimulation could sometimes cause the muscle to produce a tension close to that of a maximum tetanic contraction. This was several times greater than the mean tension that would have been caused by motor unit recruitment alone (i.e. by the motor units firing at their minimum steady rate). Cortical stimulation as well as pad pinching commonly recruited weak units more easily than stronger ones of the same muscle. The recruitment order obtained in response to pad pinching often differed, however, in various details from the recruitment caused by cortical stimulation.     

Excitation frequency and muscle fatigue: mechanical responses during voluntary and stimulated contractions.

The loss of force that occurs during maximal isometric voluntary contraction (MVC) of human muscle was compared with that due to 60 s of maximal nerve stimulation at different frequencies. For the unfatigued adductor pollicis, maximal nerve stimulation at 80 Hz was required to match the force of an MVC. Prolonged stimulation at 80 Hz resulted in a faster rate of force loss than in a sustained MVC. The rate of force loss during 80 Hz tetani was also greater than during those at 20 Hz. After 20 s more force was generated by stimulating at the lower frequency. Changing from high- to low-frequency stimulation in a fatigued muscle resulted in an increase in force. When isolated curarized mouse muscle was stimulated directly in the same manner, the force changes were similar to those seen in human muscle stimulated via the nerve. In the isolated muscle a reduction of the extracellular [Na⁺] increased the rate of force loss in a similar way to increasing the stimulus frequency. We suggest that the loss of force during high-frequency fatigue may not be entirely due to neuromuscular block, but also, in part, to a reduced excitability of the muscle fiber membrane. The time course of an MVC could be imitated by a tetanus in which the stimulus frequency was initially high but then progressively reduced. We conclude that in sustained MVCs force fatigue in response to high-frequency stimulation is reduced by a progressive decline in motor neuron firing frequency.     

Desensitization of Superfused Isolated Ovine Anterior Pituitary Cells to Human Corticotropin-Releasing Factor

We have employed an in vitro system to study the time-course of β-endorphin (β-EP) immunoreactivity release from anterior pituitary cells stimulated with corticotropin-releasing factor (CRF) and whether exposure to CRF desensitizes the cells to subsequent stimulation. Ovine anterior pituitaries were enzymatically disrupted into single cells, mixed with Siegel P2 and superfused in mini-columns with carbogen-gassed medium at 37 °C. Superfusate fractions were collected at 5-min intervals and β-EP immunoreactivity in the eluate was measured by radioimmunoassay. Peaks of β-EP release that rose significantly above baseline noise were detected using the PULSAR algorithm. Unstimulated cell columns did not display any spontaneous peaks of β-EP discharge detectable by PULSAR whereas peaks were identified in the output of columns exposed to 1 nM CRF for 100 min. β-EP release increased after 10 min of stimulation and maximum stimulated output was achieved after 20 min of continuous CRF exposure. Between 20 and 60 min of CRF stimulation the rate of β-EP release declined progressively but stabilized in the last 40 min of the exposure at a level significantly above controls for baseline secretion. Peak duration did not depend on the inclusion of calcium in the superfusion medium while peak amplitude and area were significantly reduced when cells were denied extracellular calcium. Following a 100-min exposure to 1 nM CRF, pituitary cell columns were given a 30-min rest period then restimulated with either 1 nM CRF or 50 mM KCI for 20 min. The columns given prior exposure to CRF did not mount a response (detectable by PULSAR) to a subsequent dose of 1 nM CRF whereas PULSAR detected a clear response in all members of a control group that had not received prior CRF challenge. Both CRF exposed and control columns responded to 50 mM KCI although the response was significantly attenuated in the cells that had received prior CRF treatment. These results indicate that unstimulated superfused isolated ovine anterior pituitary cells do not possess an inherent rhythmicity of β-EP release that can be detected by the PULSAR algorithm while treatment of the cells with CRF results in detectable discharge. The rapid response of β-EP discharge to CRF treatment suggests the presence of intracellular β-EP stores available for rapid mobilization. Continuous exposure to 1 nM CRF can tonically amplify corticotrope output for the duration of its presence in the environment of the corticotrope, but the maximum rate of release cannot be maintained. An inrush of extracellular calcium is not essential for the corticotrope to mount a detectable response to continuous CRF exposure but the release of a maximum amount of β-EP relies on calcium entry. Long-term treatment with CRF prevents the corticotrope releasing a detectable peak of β-EP on subsequent CRF stimulation and therefore CRF exposure leaves a lasting impression on the physiological machinery of the corticotrope. The attenuation of responsiveness to 50 mM KCI after long-term CRF treatment indicates that depletion of β-EP stores may play a part in corticotrope desensitization although a reduction in CRF receptor number and an alteration in the intracellular mechanisms controlling β-EP release may also be a factor.     

The patterns of exercise-induced β-endorphin expression in the central nervous system of rats

Exercise at different intensities is able to induce different physical and psychological statuses of the subjects. The β-endorphin (β-EP) in central nervous system is thought to play an important role in physical exercise. However, its expression patterns and physiological effects in the central nuclei under different exercise states are not well understood. Five-week old male Sprague-Dawley rats were randomly divided into two groups of 21 each: Control and Exercise. Control rats were sedentary while Exercise rats were arranged to run on a treadmill (5-week adapting or moderate exercise and 2-week high-intensity exercise). Seven rats were taken from each group at day33, day42 and day49 for examination of blood biochemical parameters (lactate, Lac; blood urea nitrogen, BUN; glucose) and for detection of nuclei β-EP level with immunohistochemistry. The results showed that Lac and BUN levels were significant increased after the high intensity exercise. The five-week exercise caused a significantly increased β-EP in caudate putamen (CPu), amygdala, paraventricular thalamic nucleus (PVT), ventromedial hypothalamus nucleus (VMH) and gigantocellular reticular nucleus (Gi). The high intensity exercise induced an elevated β-EP in CPu and nucleus of the solitary tract (Sol), but a decreased β-EP in globus pallidus (GP). Compared with Control, exercise rats showed an elevated β-EP in CPu, PVT, VMH, accumbens nucleus, Gi and Sol, and a decreased β-EP in GP at day49. The β-EP levels in acurate nucleus, periadueductal gray and parabrachial nucleus were not changed at day33, 42 and 49. In conclusion, β-EP levels in different nuclei changed under the moderate and high intensity exercises, which may contribute to modifying exercise-produced psychological and physiological effects.     

Synaptic activity‐related classical protein kinase C isoform localization in the adult rat neuromuscular synapse

Protein kinase C (PKC) is essential for signal transduction in a variety of cells, including neurons and myocytes, and is involved in both acetylcholine release and muscle fiber contraction. Here, we demonstrate that the increases in synaptic activity by nerve stimulation couple PKC to transmitter release in the rat neuromuscular junction and increase the level of α, βI, and βII isoforms in the membrane when muscle contraction follows the stimulation. The phosphorylation activity of these classical PKCs also increases. It seems that the muscle has to contract in order to maintain or increase classical PKCs in the membrane. We use immunohistochemistry to show that PKCα and PKCβI were located in the nerve terminals, whereas PKCα and PKCβII were located in the postsynaptic and the Schwann cells. Stimulation and contraction do not change these cellular distributions, but our results show that the localization of classical PKC isoforms in the membrane is affected by synaptic activity. J. Comp. Neurol. 518:211–228, 2010. © 2009 Wiley‐Liss, Inc.     

Responses of intercostal muscle biopsies from normal subjects and patients with myasthenia gravis

In order to evaluate the mechanisms of weakness in muscles of patients with myasthenia gravis (MG), intercostal muscle biopsies were obtained from 9 normal subjects and 6 MG patients, and the compound muscle action potential (AP) and tension responses to nerve and muscle stimulation, and contracture responses on exposure to caffeine, were monitored in vitro. In normal muscle, on stimulation of the nerve or muscle at 30 to 100 Hz, the AP responses showed decrement in amplitude, one-third of which was attributable to failure of neuromuscular transmission and two-thirds to failure of muscle membrane excitation. On stimulation at 1 to 5 Hz, the AP responses showed very little decrement, while the contractile responses showed significant fade in tension, due to failure of E-C coupling or contractility. In muscle from patients with generalized MG, stimulation of the nerve at all frequencies (1 to 100 Hz) caused much greater decrement in APs and fade in tension responses than in normal muscle, due mainly to failure of neuromuscular transmission. However, at 100 Hz, 40% of the decrement in APs was due to failure of muscle membrane excitation, and at 1 to 5 Hz, 40% of the fade in tension was due to failure of E-C coupling or contractility, as in normal muscle. On direct stimulation the contraction and half-relaxation times were slower and the tetanic tension was smaller than in normal muscle, especially in the MG patient with thymoma. Caffeine-induced contractures were smaller in MG muscle than in normal muscle. These results indicate that while the weakness of MG muscle is due mainly to failure of neuromuscular transmission, it is also partly due to reduced E-C coupling or contractility.     

The Rosenblueth phenomenon

Rosenblueth and Luco demonstrated in 1939 that, during prolonged stimulation of a motor nerve, neuromuscular fatigue is followed by a rise of tension that has been called the Rosenblueth Phenomenon. The purpose of this work was to investigate the Rosenblueth Phenomenon in a cat neuromuscular preparation in which the nerves were severed at different levels and stimulated at 60 Hz for several hours. It was demonstrated that in the longer nerve preparation the Rosenblueth Phenomenon starts earlier and its maximal tension is higher. Acetylcholine sensitivity was studied in the superior cervical ganglion preparation and no change was observed when tested before stimulation, during fatigue, and during the Rosenblueth Phenomenon. It is concluded that the onset and amplitude of the Rosenblueth Phenomenon depend on the length of the peripheral nerve stump: the longer the stump, the earlier and higher the response. It is suggested that the Rosenblueth Phenomenon is produced by an increase in the transmitter release which would be due to axonal progression of molecules along the nerve.     

Facilitatory effects of dexamethasone on neuromuscular transmission

The beneficial effects of glucocorticoids in myasthenia gravis are attributed to their immunosuppressive actions. There are also studies reporting direct facilitatory as well as depressant effects of glucocorticoids on neuromuscular transmission. The effects of dexamethasone on neuromuscular transmission were studied by intracellular and extracellular microelectrode recording techniques in the mouse phrenic nerve-diaphragm preparation. Creatinine had to be added to the bathing media to prevent precipitation of the glucocorticoid with Ca2+ and Mg2+; creatinine had no effect. One hour of perfusion with dexamethasone (10(-4) to 10(-3) M) increased the frequency of miniature end-plate potentials (MEPPs), as well as the amplitude and quantum content of end-plate potentials (EPPs), but did not change MEPP amplitude, suggesting an increase in acetylcholine release. Dexamethasone also enhanced presynaptic facilitation and potentiation during repetitive stimulation. It had no effect on muscle resting membrane potential but increased the amplitude, overshoot, and rate of rise of muscle action potentials. The amplitudes of nerve terminal action potentials were also enhanced by dexamethasone. These findings suggest that glucocorticoids have a direct facilitatory action on neuromuscular transmission by a presynaptic action.     

帕金森病患者血浆β—内啡肽含量的变化及其临床意义

目的：探讨帕金森病（Parkinson disease,PD)患者血浆β－内啡肽（β-endorphin,β－EP）含量的变化及其临床意义。方法：采用放射免疫分析法测定35例PD患者血浆β－EP含量，并与30例正常者对照。结果：PD患者血浆β－EP含量校正常对照组明显降低（P＜0．05）；高岭、病情重及伴痴呆和抑郁的抑郁的患者血浆β－EP含量降低更显著（P＜0．05）。结论PD患者血浆β－EP含量显著降低，与PD发病密切相关，高龄、病情重及伴痴呆和抑郁的患者血浆β－EP含量低更明显，有助于对病情进展及预后进行评估。     

Multifocal motor neuropathy human sera block distal motor nerve conduction in mice

Multifocal motor neuropathy (MMN) is associated with serum autoantibodies to gangliosides, but their pathogenic role is uncertain. We have used a novel approach to study the effects of serum and plasma from 8 patients with this syndrome, 6 of whom were anti-GM1 positive. The nerve stimulus required to evoke muscle contraction and endplate potentials (EPPs) was measured in the mouse phrenic nerve—diaphragm preparation during 4 to 6 hours of direct application (plasma at 1:1 or serum 1:2 dilution) and following intraperitoneal injection of plasma (1 ml/day) for 1 to 5 days (“passive transfer”). Direct application of MMN serum or plasma produced a progressive increase in stimulus threshold, followed by complete block of nerve-evoked muscle contraction in 3 cases, and an associated decline to about 50% of the EPP amplitude followed by sudden loss of EPPs. These effects were complement independent. Even with complete block of nerve-evoked EPPs, miniature EPP (MEPP) frequency could be increased by raising external K⁺ to depolarize the nerve terminal directly. Passive transfer of 1 ml of MMN plasma (n = 5) for 3 days caused similar but less marked changes. These results demonstrate that serum factors in MMN can block nerve conduction at distal motor nerves.     

Vocalizations by a sexually dimorphic isolated larynx: peripheral constraints on behavioral expression

The clawed frog Xenopus laevis uses sexually dimorphic vocalizations, mate calling and ticking, to advertise reproductive state. The basic unit of vocalization is a brief click, produced by the movement of cartilagenous disks located within the larynx. The rate of click production in the male-specific mate call (71 Hz) is an order of magnitude faster than the rate of click production in female typical ticking (6 Hz). To determine if vocalization rate is constrained by the periphery, male and female larynges were isolated and response of the muscles to nerve stimulation was studied. Laryngeal muscle response is markedly dimorphic in the 2 sexes, both in the amplitude potentiation of electromyograms and in the rate at which discrete tension transients can be produced. At 6 Hz (ticking), both sexes generate discrete tension transients in response to each stimulus pulse. In response to nerve stimulation at 71 Hz (mate calling), male laryngeal muscle generates discrete tension transients while female laryngeal muscle does not. Since expression of sex-specific vocalizations is regulated by androgenic hormones, responses of laryngeal muscle to nerve stimulation in androgen-treated adult females and castrated adult males were also examined. The responses of laryngeal muscle from castrated and intact males are similar. Androgen-treated female larynx is partially masculinized but does not produce tension transients at the mate call rate. These physiological results are in close agreement with behavioral observations. Sounds produced by the isolated larynx were nearly identical in spectral properties to those produced by an intact male. We determined that the production of a discrete tension transient is prerequisite to click production. Thus, one reason females do not mate call, even when treated with androgens, is that female laryngeal muscle cannot produce discrete tension transients at a rapid rate.     

DENERVATION CAUSED BY TULLIDORA(Karwinskia humboldtiana)

Munoz-Martinez, E. J., Cueva J. & Joseph-Nathan P. (1983) Neuropathology and Applied Neurobiology 9, 121–134
Denervation caused by tullidora (Karwinskia humboldtiana)
Crude homogenate of the seed of the tullidora (Coyotillo, buckthorn; Karwinskia humboldtiana) fruit or a purified neurotoxin extracted from it was administered orally to male Wistar rats. Three to 5 weeks later, gait disturbances and progressive flaccid paralysis of the hindlimbs appeared in these animals which were then submitted to acute experiments. Single twitch and tetanic contractions of the soleus muscle were studied in the tullidora treated rats. The twitch tension elicited by direct stimulation of the muscle was greater than that produced by nerve stimulation. In addition, the tension of nerve-elicited twitches diminished as the stimulating electrode was moved towards the spinal cord, suggesting failure of nerve conduction. When the muscle was directly stimulated, contraction and relaxation were slower than normal and the tetanus/twitch tension ratio was subnormal. These data suggest partial denervation of the soleus muscle under the action of the toxin. Electron microscopy revealed abnormal motor-nerve endings with few synaptic vesicles and denervated end-plates. Degenerative changes of axons and myelin disturbances were frequently seen in the intramuscular branches of the soleus nerve. However, alterations of this type were less severe in the nerve sections closer to the spinal cord and no significant changes were detected at the upper portion of the sciatic nerve. It is concluded that the paralysis produced by the tullidora toxin is the result of both conduction block of the nerve impulses and muscle denervation.     

Mechanisms of fatigue in normal intercostal muscle and muscle from patients with myasthenia gravis

Fatigue mechanisms in normal intercostal muscle and muscle from patients with myasthenia gravis (MG) were evaluated by monitoring the compound muscle action potential (CMAP) and tetanic tension responses to repetitive nerve or muscle stimulation in vitro. When fatigue was induced by nerve stimulation at 30 Hz for 0.5 s every 2.5 s, about half of the original tension decreased after 30 min in normal muscle and 5 min in MG muscle. Analysis of the changes in area of CMAPs and tension indicated that impairment of neuromuscular transmission, muscle membrane excitation, and excitation-contraction (E-C) coupling and contractility accounted for 40%, 29%, and 31% of fatigue in normal muscle, and 83%, 0%, and 17% of fatigue in MG muscle. When fatigue was induced by muscle stimulation at 30 Hz, tension declined by a quarter after 30 min in normal muscle, but by a half after 17 min in MG muscle. Impairment of muscle membrane excitation and E-C coupling and contractility accounted for 58% and 42% of fatigue in normal muscle, and 22% and 78% of fatigue in MG muscle. Thus, fatigue of normal muscle is caused by impairment of at least four processes, and enhanced fatigue of MG muscle is caused by greater impairment of neuromuscular transmission, E-C coupling, and contractility. © 1993 John Wiley & Sons, Inc.     

Contralateral reinnervation in Bell's palsy. A case report.

Congenital lesion of the left facial nerve trunk has been investigated in a 30-year-old woman. Upon stimulation of the left facial nerve, no response was evoked in any of the mimic muscles. The patient was able to perform voluntary contractions of the left corrugator glabellae muscle and of the left corner of the orbicular oral muscle; these contractions were recorded electromyographically. The stimulation of the right facial nerve elicited responses in the referred left mimic muscles. This circumstance indicated their activity to be due to contralateral reinnervation by the intact facial nerve. The blink reflex examination evoked no response on the left side, while the blinik reflex on the right side was elicited with both its components, both upon ipsi- and contralateral stimulation.     

Modulation of humoral immune response by central administration of leucine-enkephalin: Effects of μ, δ and κ opioid receptor antagonists

The effect of leucine-enkephalin (Leu-Enk) on primary humoral immune response was investigated following intracerebroventricular (i.c.v.) administration of the peptide in the rat. Leu-Enk stimulated plaque-forming cell (PFC) response in rats i.c.v. injected with 0.1 and 1 μg/kg, whereas doses of 20 and 50 μg/kg exerted immunosuppressive effects. I.c.v. treatment of rats with δ opioid receptor antagonist ICI 174864 and κ opioid receptor antagonist nor-binaltorphimine (nor-BNI) blocked stimulation and suppression of PFC response induced by Leu-Enk, respectively. The μ opioid receptor antagonist β-funaltrexamine (β-FNA) reversed both immunomodulatory effects produced by Leu-Enk. Since β-FNA alone had no effect on PFC response (unlike ICI 174 864 and nor-BNI), these data showed that central effects of Leu-Enk on PFC response were mediated by brain μ opioid receptors, and suggested a possible involvement of δ and κ opioid receptors.