beta-endorphin and Central-Nervous-System-Diseases

A 100 plaque forming unit (pfu) dose of a temperature-sensitive (ts) mutant of vesicular stomatitis virus (VSV), tsG31 KS5, engendered a slowly progressive paralytic central nervous system (CNS) disease that killed all BALB/c nude mice within 28 days. Reconstitution of nude mice with 10(7) syngeneic splenocytes 24 h before intracerebral inoculation with tsG31 KS5 VSV, however, protected 92% of the animals from death. When these reconstituted animals were injected intracerebroventricularly with 14 pmol of beta-endorphin 24 h after reconstitution with splenocytes and 24 h before inoculation with tsG31 KS5 VSV, only 72% of the animals survived. Furthermore, whereas 40% of the afflicted reconstituted nude mice given intracerebroventricular injections of sterile water were able to recover from the symptoms of disease, those surviving animals which received beta-endorphin were unable to do so. A single intravenous injection of 14 pmol beta-endorphin, or repeated postinfection administration of 28 pmol of beta-endorphin intravenously into nude mice reconstituted with syngeneic splenocytes, which were pretreated with beta-endorphin, did not alter the course of CNS disease induced by tsG31 KS5 VSV. The effect induced by intracerebroventricular injection of beta-endorphin was antagonized by naloxone, but not by the neuropeptide fragment beta-endorphin-(1-27). A simultaneous intracerebroventricular injection of reconstituted nude mice with 1220 pmol of naloxone and 14 pmol of beta-endorphin resulted in a 89% survival rate, and 33% of the afflicted animals were able to overcome the symptoms of the disease induced by tsG31 KS5 VSV. Intracerebroventricular injection of reconstituted nude mice with 330 pmol of beta-endorphin-(1-27) and 14 pmol of beta-endorphin resulted in a 72% survival rate and the surviving animals were unable to improve appreciably the clinical status of their disease. Injection of reconstituted nude mice with either 1220 pmol of naloxone or 330 pmol of beta-endorphin-(1-27) alone did not alter the course of the CNS disease in any way. A single intracerebroventricular injection of 29 pmol of another psychoactive peptide, [Des-Tyr]-endorphin, 24 h after reconstitution of nude mice with splenocytes and 24 h prior to infection with virus, resulted in 74% survival; and 39% of the afflicted animals were able to recover from the clinical symptoms.

Topics: Animals; beta-Endorphin; Central Nervous System Diseases; Injections, Intraventricular; Mice; Mice, Inbred BALB C; Mice, Nude; Spleen; Temperature; Vesicular stomatitis Indiana virus

A single intracerebroventricular injection of 100 ng of beta-endorphin altered the course of the central nervous system (CNS) infection of a temperature-sensitive mutant of vesicular stomatitis virus (VSV), tsG31-KS5. When mice were administered beta-endorphin and then 24 h later infected intracerebrally with tsG31-KS5 VSV, 70% of the animals died within 8 days of infection. In comparison, less than 10% of the animals had died after 21 days when infected with tsG31-KS5 VSV alone. When mice were injected with beta-endorphin and tsG31-KS5 VSV simultaneously, or with beta-endorphin 21 days after infection, the more aggressive clinical disease was not observed. Superficially, the more lethal disease induced by beta-endorphin appeared to be a result of a mild hypothermia caused by the neuropeptide. beta-Endorphin, however, did not influence the disease in nude (nu/nu) mice even though their core temperatures were reduced to an extent similar to that of BALB/c (+/+) mice, implicating the involvement of T lymphocytes in the alteration of the course of infection in normal mice.

Topics: Animals; beta-Endorphin; Central Nervous System Diseases; Injections, Intraventricular; Mice; Mice, Inbred BALB C; Mice, Nude; Vesicular stomatitis Indiana virus; Virus Diseases

Using radioimmunoassay the authors studied concentrations of beta-endorphine and metenkephalin in the cerebrospinal fluid (CSF) of 65 patients with various diseases of the central nervous system (CNS)--hereditary extrapyramidal disorders, disseminated sclerosis (DS), lateral amyotrophic sclerosis (LAS), spinal tumours, senile dementia, some CNS impairments of inflammatory nature. Patients with spinal tumours showed a 4-14-fold elevation in metenkephalin levels along with a comparatively high content of beta-endorphine. In senile dementia, the concentration of both peptides was lowered. In hereditary extrapyramidal diseases, the levels of beta-endorphine were also low, while there was no concomitant decrease in the metenkephalin concentration.

Topics: Amyotrophic Lateral Sclerosis; beta-Endorphin; Central Nervous System Diseases; Chronic Disease; Dementia; Endorphins; Enkephalin, Methionine; Humans; Multiple Sclerosis; Radioimmunoassay; Spinal Cord Neoplasms

beta-Endorphin, leucine enkephalin and methionine enkephalin, were measured in 41 samples of human lumbar cerebrospinal fluid (CSF) of patients with different neurological diseases. beta-Endorphin-like immunoreactivity (beta-ELI) was present in concentrations between 10 and 150 fmol/ml CSF, and in 30 of the 41 samples studied the levels ranged from 10 to 40 fmol/ml. Methionine enkephalin-like immunoreactivity (MELI) measured 1-85 pmol/ml CSF, with 24 of the 41 samples having values between 3 and 4 pmol/ml. CSF concentrations of leucine enkephalin-like immunoreactivity (LELI) ranged from 0.1 to 12.5 pmol/ml, and in 31 of the 41 CSF samples studied LELI was present in concentrations of 0.1-0.25 pmol/ml. No significant relationship exists between the concentrations of beta-endorphin in CSF and sex and age of patients, CSF protein, CSF IgG and CSF leukocytes. No interrelationship could be found between beta-ELI, MELI and LELI concentrations.

Topics: Adolescent; Adult; Aged; beta-Endorphin; Central Nervous System Diseases; Endorphins; Enkephalin, Leucine; Enkephalin, Methionine; Female; Humans; Male; Middle Aged