Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In rats, recovery of sensory-motor function following a crush lesion of the sciatic or tibial nerve was monitored by measuring foot reflex withdrawal from a local noxious stimulation of the foot sole. 2. Putative neurotrophic compounds were tested on this functional recovery model: melanocortins (peptides derived from ACTH (corticotropin) and alpha-MSH (melanotropin], gangliosides and nimodipine were effective whereas isaxonine and TRH (thyrotropin releasing hormone) were not. 3. Structure-activity studies with melanocortins revealed a similar effectiveness of alpha-MSH, [N-Leu4, D-Phe7]-alpha-MSH, desacetyl-alpha-MSH and the ACTH analogue ORG 2766, questioning the validity of the previously suggested notion that the melanotrophic properties of these peptides are responsible for their neurotrophic effect. 4. As recovery of function after peripheral nerve damage follows a similar time course in hypophysectomized (five days post operation) and sham-operated rats, effective melanocortin therapy does not mimic an endogenous peptide signal in the repair process from pituitary origin. 5. Subcutaneous treatment with ORG 2766 (7.5 micrograms kg-1 48 h-1) facilitates recovery of function following peripheral nerve damage in young (6-7 weeks old), mature (5 month old) and old (20 month old) rats. 6. In view of the diversity in structure of the effective neurotrophic factors and the complexity of nerve repair, the present data support the notion that peripheral nerve repair may be facilitated by different humoral factors likely to be active on different aspects of the recovery process.
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PMID:Putative neurotrophic factors and functional recovery from peripheral nerve damage in the rat. 167 80

The functional recovery from impaired motor activity caused by 6-OHDA lesions in the nucleus accumbens is accelerated by the ACTH-related peptides ACTH-(4-10), alpha-MSH (ac-Ser1-ACTH-(1-13)NH2), ACTH-(7-10) and the ACTH-(4-9) analog ORG 2766. The peptides ACTH-(4-7) and Phe-D-Lys-Phe were not effective in this respect. This indicates that this effect of ACTH-derived peptides is located in the 7-10 part of the molecule whereas for the effect of ORG 2766 a bigger part of the molecule may be required. ORG 2766 was effective after intra-accumbal, subcutaneous and oral administration. The differences in potencies between the 3 routes of administration (ED50 0.76 ng/kg, 28.5 ng/kg and 80.6 micrograms/kg, respectively) suggest that the peptide exerts its effect by facilitating recovery processes at the lesion site. Studies with ORG 2766 showed that treatment during the first days following the induction of the lesion is essential for the facilitating action of the peptide on spontaneous recovery from brain damage.
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PMID:Functional recovery after destruction of dopamine systems in the nucleus accumbens of rats. III. Further analysis of the facilitating effect of the ACTH-(4-9) analog ORG 2766. 215 94

Rats with 6-OHDA lesions in the nucleus accumbens which were treated intra-accumbally with control serum during the first week following the lesion showed a similar level of motor activity 3 weeks after the lesion as sham-lesioned rats treated with control serum. In 6-OHDA-lesioned rats that were identically treated with antiserum against alpha-MSH or the ACTH-(4-9) analog ORG 2766 motor activity was decreased 3 weeks after the lesion. Intra-accumbal treatment with the antisera did not affect motor activity of sham-lesioned rats. The increased motor activity after apomorphine injection into the nucleus accumbens of control serum-treated 6-OHDA-lesioned rats was not observed in 6-OHDA-lesioned rats treated with the antisera. Furthermore, [3H]haloperidol binding studies showed that the changes in the DA receptor systems in the nucleus accumbens of 6-OHDA-lesioned rats treated with control serum, which may reflect denervation supersensitivity, were not observed in 6-OHDA-lesioned rats treated with the antisera. The present data indicate that the functional recovery and the concurrent development of supersensitive DA receptor systems in the nucleus accumbens of 6-OHDA-lesioned rats are delayed by intra-accumbal treatment with ORG 2766 or alpha-MSH antiserum. This suggests that endogenous ACTH/MSH-like factors may be mediating the recovery processes.
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PMID:Functional recovery after destruction of dopamine systems in the nucleus accumbens of rats. IV. Delay by intra-accumbal treatment with ORG 2766- or alpha-MSH antiserum. 215 96

The motor functional recovery after sciatic nerve crush was measured in rats treated with daily injections of (a) thyrotropin-releasing hormone (2.0 mg/kg, (b) alpha-melanocyte-stimulating hormone (0.07 mg/kg/48 h), or (c) testosterone propionate (4.4 mg/kg). The recovery of the motor function of the sciatic nerve was indicated by using the return of the toe-spreading response. None of the treatments differed significantly from saline controls in the time needed for recovery. The same procedure (without injections) was carried out with castrated and noncastrated male rats in order to test the effect of the lack of testosterone on recovery time after sciatic crush. The groups did not differ significantly as to their recovery times. The same method was used to study the effect of spermine (10.0 mg/kg/day) on the recovery of motor function. Spermine seemed to reduce the time needed for recovery from a mean value of 15.7 to 11.0 days (P less than 0.01). We also studied the effect of daily injections of spermine (13.0 mg/kg) on the sensory division of the peripheral nerve using the foot-flick test. The time needed for recovery after crush in the sciatic notch was reduced from 13.7 to 7.7 days (P less than 0.005). These results do not support the hypothesis that alpha-melantocyte-stimulating hormone, thyrotropin-releasing hormone, or testosterone enhance functional recovery of severed motor axons. Our results confirm a previous observation that spermine reduces the time needed for recovery after trauma in peripheral motor neurons. The result of the foot-flick test suggests that spermine enhances both motor and sensory recovery.
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PMID:Putative stimulants for functional recovery after neural trauma: only spermine was effective. 282 13

The efficacy of melanocortins (alpha-MSH and an ACTH-(4-9) analog, Org.2766) in accelerating functional recovery from sciatic nerve damage following various types of subcutaneous and oral administration was assessed in the rat. Furthermore, the effectiveness of the local delivery of melanocortins to the site of injury was examined. An accelerated recovery was evident following subcutaneous constant delivery of Org.2766 from an osmotic mini-pump and from biodegradable polymere microspheres, and was as effective as repeated subcutaneous injections of alpha-MSH or Org.2766. Oral administration of Org.2766 was ineffective. Local application of Org.2766, achieved by wrapping a peptide-impregnated biodegradable gelatine foam matrix around the site of injury, facilitated recovery as well. The biodegradable microspheres and gelatine foam matrix may be of importance in eventual clinical use as effective vehicles for administration of melanocortins in the treatment of peripheral nerve damage.
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PMID:alpha-MSH and Org.2766 in peripheral nerve regeneration: different routes of delivery. 283 94

Rats were subjected to nigro-striatal hemitransection and then intracerebroventricularly infused with the potent and long-acting alpha-MSH analogue, (Nle4, D-Phe7)alpha-MSH, at two different doses (15 or 30 ng/h/rat), or with saline (0.6 microliter/h/rat), continuously for 14 days starting on day 2 after lesion. (Nle4, D-Phe7)alpha-MSH dose-dependently improved the sensorimotor deficit (postural asymmetry, impaired limb reflexes and coordinated limb use, signs of cortical and pyramidal lesion), reduced turning behaviour induced by apomorphine, and increased spontaneous motility in the open field. 3H-Spiperone binding showed that (Nle4, D-Phe7)alpha-MSH treatment caused a down regulation of the striatal DA receptors in the lesioned side, contrary to the supersensitivity developed by the corresponding receptors of saline treated rats. These results indicate that melanopeptides improve the functional recovery of nigro-striatally hemitransected rats, by an action at CNS level.
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PMID:Improved recovery of nigro-striatally hemitransected rats induced by (Nle4, D-Phe7)alpha-MSH: a central effect. 283 66

The effects of chronic treatment with the ACTH-(4-9) analogue Org 2766, alpha-MSH, and gamma 2-MSH were studied on T-maze reversal learning and on behavior assessed on the basis of open-field and other gross behavioral activities, grasping responses, inspection of various reflexes and electrical footshock sensitivity of rats with parafascicular lesions or sham-lesions. Repeated administration of Org 2766 and alpha-MSH to parafascicular area-lesioned rats resulted in functional recovery of impaired T-maze reversal learning. The structurally related neuropeptide gamma 2-MSH was without any effect. The alpha-MSH effect did not depend on time after lesioning as treatments during the first or second post-operative week were equally effective. Chronic peptide treatments did not change disturbed motor functions of parafascicular-lesioned rats, as measured by open-field activity, other gross behavioral activities and grasping responses. Since acute peptide treatments did not affect the impaired reversal learning performance of lesioned rats, the beneficial effect of Org 2766 and alpha-MSH could not be explained as a short-term effect on attention and motivation. It was more likely to be an accelerated recovery of cognitive function as a result of long-term neurotropic influences.
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PMID:Beneficial effect of chronic treatment with Org 2766 and alpha-MSH on impaired reversal learning of rats with bilateral lesions of the parafascicular area. 299 19

The effect of alpha-melanocyte-stimulating hormone on peripheral nerve regeneration was studied by monitoring functional recovery and quantifying histologic changes that follow crush lesion of the rat sciatic nerve. The results showed that such treatment of rats with a crushed sciatic nerve resulted in a reduction of the recovery period and in an increase in the number of regenerating nerve fibers.
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PMID:Alpha-melanocyte-stimulating hormone stimulates the outgrowth of myelinated nerve fibers after peripheral nerve crush. 395 75

ACTH4-10, a fragment of the adrenocorticotropic hormone (ACTH) molecule, has marked effects on the compensation process following unilateral labyrinthectomy. In Rana temporaria ACTH4-10-treatment (5-250 micrograms/kg) influences both the acquisition and the maintenance of the compensated state. The compensation process is slowed down by hypophysectomy but can then be restored by the administration of ACTH4-10. It is concluded that ACTH-like neuropeptides might physiologically be involved in the plastic processes underlying functional recovery from CNS lesions.
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PMID:Effects of ACTH4-10 on vestibular compensation. 628 90

The possible role of endogenous opioids in the pathophysiology of spinal cord injury was evaluated utilizing a variety of experimental models and species. In the cat, we have shown that beta-endorphin-like immunoreactivity was increased in plasma following traumatic spinal injury; such injury was associated with a decrease in spinal cord blood flow (SCBF) which was reversed by the opiate receptor antagonist naloxone. Naloxone treatment also significantly improved functional neurological recovery after severe injury. Thyrotropin-releasing hormone (TRH), possibly through its "anti-endorphin" actions, was even more effective than naloxone in improving functional recovery in the cat. In a rat model, utilizing a similar trauma method, TRH proved superior to naloxone in improving SCBF after injury. In addition, naloxone at high doses attenuated the hindlimb paralysis produced by temporary aortic occlusion in the rabbit. The high doses of naloxone required to improve neurological function after spinal injury suggest that naloxone's actions, if opiate receptor mediated, may be mediated by non-mu receptors. Dynorphin, an endogenous opioid with a high affinity for the kappa receptor, produced hindlimb paralysis following intrathecal administration in rats. Taken together, these findings suggest that endogenous opioids, possibly acting at kappa receptors in the spinal cord, may serve as pathophysiological factors in spinal cord injury.
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PMID:Neuropeptides in spinal cord injury: comparative experimental models. 665 11


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