Effects of electrical stimulation on teh enkephalinsin guinea-pig small intestine

When myenteric plexus-longitudnal muscle preparations of the guinea-pig small intestine are simulated electrically in the presence of cycloheximide there is a decrease in teh content of enkephalins which is taken to be due to their release. With supramaximal stimuli, the release per pulse is similar at 1 and 10 Hz but it is lower with submaximal than with maximal stimuli. Met-enkephalin is more readily released than Leu-enkephalin.     

Effect of Acute Ethanol Administration on the Release of Opioid Peptides From the Midbrain Including the Ventral Tegmental Area

Background:  Experimental evidence suggests that ethanol alters the activity of the endogenous opioid peptide systems in a dose and brain-region dependent manner. These alterations may influence the processes of ethanol reward and reinforcement. Thus, it was the objective of this study to investigate the response of the 3 major opioid peptide systems (endorphins, enkephalins, and dynorphins) to acute ethanol administration, at the level of the midbrain including the ventral tegmental area (midbrain/VTA), a region important for drug, including ethanol reinforcement.
Methods:  Using the in vivo microdialysis technique coupled with specific solid-phase radioimmunoassay for β-endorphin, met-enkephalin, and dynorphin A_1–8, changes in the extracellular concentration of theses peptides at the level of midbrain/VTA were determined at distinct time points following the administration of 0.0 (saline), 0.8, 1.2, 1.6, 2.0, and 2.4 g ethanol/kg B.Wt.
Results:  A biphasic effect of ethanol on β-endorphin release was found, with low to medium (1.2, 1.6, and 2.0 g) but not high (2.4 g) doses of ethanol, inducing a significant increase in the dialysate content of β-endorphin. A late increase in the dialysate content of dynorphin A_1–8 was observed in response to the 1.2 g ethanol dose. However, none of the ethanol doses tested significantly altered the content of met-enkephalin in the dialysate.
Conclusions:  The present findings suggest that the ethanol-induced increase of β-endorphin release at the level of midbrain/VTA may influence alcohol reinforcement.     

In Utero Ethanol Exposure Increases Proenkephalin, a Precursor of a Neuropeptide That Is Inhibitory to Neuronal Growth

BACKGROUND: One of the effects of fetal alcohol syndrome (FAS) is altered motor function. In an attempt to elucidate a potential cause of this ethanol-associated damage, we investigated the effects of in utero ethanol exposure on the production of proenkephalin (PE). METHODS: PE is the precursor of met- and leu-enkephalin, two neuropeptides that inhibit the proliferation of neurons and astrocytes. PE mRNA and PE peptide were measured in the striatum and nucleus accumbens because of the importance of these brain regions to motor function, their sensitivity to the effects of in utero ethanol exposure, and their high concentration of PE mRNA and PE peptide. RESULTS: The present studies demonstrated that in utero ethanol exposure is associated with increased PE mRNA in the striatum and nucleus accumbens. Of specific interest is the elevation in PE mRNA in the nucleus accumbens in 5-, 12-, and 19-day-old ethanol-exposed offspring and the fact that this change persists for at least 19 days after the last exposure to ethanol. Further studies of postnatal day 19 (PN19) offspring localized the abnormality in the nucleus accumbens to the core region, an area that contains enkephalinergic projections to another motor area-the substantia nigra. In the nucleus accumbens, the increased PE mRNA was associated with a greater proportion of PE-expressing neurons that have 41% to 60% of the cell area covered by grains associated with PE mRNA. CONCLUSIONS: Although we were not able to detect a change in the concentration of the PE peptide in the nucleus accumbens or striatum, we cannot rule out the possibility that the increase in PE mRNA was reflective of a functional abnormality.     

Influence of halothane and methoxyflurane on regional brain and spinal cord concentrations of methionine-enkephalin in the rat

Rats were exposed to either oxygen (controls), 1.5% halothane in oxygen, or methoxyflurane (0.5%) in oxygen over a period of 2 h, then sacrificed at the end of exposure (2-h group), 4 h after removal from environmental chamber (4-h group), or at 24 h following anesthetic exposure (24-h group). Pituitary (excluding the neural lobe, Pit), brain, and spinal cord areas were isolated and processed with Met-enkephalin tissue concentrations determined. In halothane-exposed animals, Met-enkephalin concentrations in pit and across CNS areas studied were significantly lower at 2 h following anesthetic exposure than in control animals. Concentrations of Met-enkephalin in many areas of CNS and Pit of 4-h group approached control levels. Concentrations of Met-enkephalin in all areas studied except spinal cord returned to basal levels by 24 h following halothane exposure. Exposure to methoxyflurane resulted in less dramatic changes in Met-enkephalin concentrations across CNS regions examined. Exposure to methoxyflurane resulted in significant decreases in Met-enkephalin levels in olfactory bulb, thalamus, and hippocampus only. Met-Enkephalin levels did not change significantly in other areas of the central nervous system following methoxyflurane exposure. These results indicate that halothane and methoxyflurane may have differential effects on the endogenous opioid system.     

The neurotoxic actions of ibotenic acid on cholinergic and opioid peptidergic systems in the central nervous system of the rat

The neurotoxic effects produced by ibotenic acid (IA) induced chemical lesions of the central nervous system (CNS) cholinergic system were examined on the opioid peptidergic system in adult rats. Forebrain cholinergic systems were bilaterally lesioned by the infusion of IA (1 or 5 micrograms/site) into the nucleus basalis magnocellularis (NBM). One week after the injections, the animals were sacrificed, and activities of acetylcholinesterase (AChE), choline acetyltransferase (ChAT) and concentrations of beta-endorphin (beta-End) and Met-enkephalin (Met-Enk) were measured in different brain regions. Animals treated with IA showed a decrease in the activity of ChAT (-24%), AChE (-36%) and beta-End level (-33%) in the frontoparietal cortex (FC). For the first time we report that these changes were associated with a compensatory increase in the activity of ChAT (+27%), AChE (+25%), beta-End level (+66%) in the remaining part of the cortex, i.e. cortex devoid of frontal cortex (C-FC). Met-enkephalin level increased by 59% in the frontoparietal cortex and did not change in the cortex devoid of frontal cortex upon IA treatment. These results suggest that IA treatment results in changes in the activity of cortical ChAT and AChE, and beta-End level in the same direction. Injection of IA in the NBM did not cause a change in the activity of ChAT or AChE in other brain regions such as hippocampus, striatum or midbrain. In addition to cortex devoid of frontal cortex, midbrain also showed a significant increase in the beta-End level in the IA treated animals. However, pituitary beta-End decreased in the neurotoxin treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Met-enkephalin levels in midbrain dopamine regions of inbred mouse strains which differ in the number of dopamine neurons

The Met-enkephalin content in tissue micropunches of the substantia nigra zona compacta, ventral tegmental area and the caudate nucleus in BALB/c and CBA mouse strains was measured by radioimmunoassay. The CBA strain had significantly higher Met-enkephalin levels in all 3 regions than the BALB/c strain. These differences should be taken into account when relating the intensity of dopamine-induced behaviors to the number of dopamine neurons.     

Inhomogeneity of the putaminal lesion in striatonigral degeneration

Summary An immunohistochemical topographic study was carried out in the putamen from three patients with striatonigral degeneration (SND) using antibody to calcineurin (CaN), a neurochemical marker for the striatal medium-size spinous neurons. In patients with SND, there was significant depletion of CaN immunoreactivity in the putamen with the caudal and lateral portion of the putamen being consistently and severely affected. In addition, the SND patients showed an inhomogeneous distribution pattern of residual CaN staining in the putamen, where remaining CaN immunoreactivity appeared as a characteristic patchwork of islands resembling the striosomes observed by the tyrosine hydroxylase or Met-enkephalin immunostaining in the putamen from normal individuals. This finding may account for the fact that there are subregional and compartmental differences in susceptibility of the medium-sized spinous neurons in the putamen with SND.     

Release of met-enkephalin and its modulation through acetylcholine receptors in the rabbit superior colliculus

Summary This report presents evidence for the depolarization-dependent release of met-enkephalin from the superior colliculus of the rabbit. Collicular tissue was placed in superfusion chambers and met-enkephalin accumulation in the superfusate was measured by radioimmunoassay. Exposure to high potassium concentrations (30 mM and 56 mM) increased met-enkephalin release. This is the fourth transmitter shown to be released from collicular tissue. Furthermore, we have obtained the first evidence that suggests that metenkephalin release is susceptible to muscarinic modulation. While the depolarization-dependent release of met-enkephalin was depressed in the presence of atropine (1 M), hexamethonium (100 M) did not block the increase of met-enkephalin release induced by high potassium.     

Hormonal (ACTH, Cortisol, β-Endorphin, and Met-Enkephalin) and Cardiovascular Responses to Hyperthermic Stress in Chronic Alcoholics

Chronic alcohol drinking causes profound alterations in hypothalamic-pituitary function. In the present study, endocrine [corticotropin (ACTH), β-endorphin, cortisol, and met-enkephalin] and cardiovascular (blood pressure) changes in response to hyperthermic stress (sauna at 90°C for 30 min) were evaluated in 25 normal men (25 to 50 years old) and in 48 male alcoholic subjects (34 to 56 years old) after 5 weeks of abstinence. Significantly lower increments in systolic blood pressure were observed in alcoholics than in control subjects. Furthermore, alcoholics showed lower ACTH, β-endorphin, and cortisol increments in response to sauna than normal controls. In contrast, sauna-induced hyperthermia did not change significantly the circulating met-enkephalin levels in either normal controls or chronic alcoholics. These data suggest that an impairment in the adaptive response to stress affects alcoholic men even after a few weeks of abstinence from alcohol.     

Evidence for the coexistence of glutamate decar☐ylase and Met-enkephalin immunoreactivities in axon terminals of rat ventral pallidum

Evidence for the coexistence of glutamate decarboxylase (GAD) and Met-enkephalin (Met-Enk) in axon terminals of ventral pallidum was demonstrated by colocalization of anti-GAD and anti-Met-Enk immunoreactivities in alternate adjacent 1 micron serial sections. Conventional electron microscopy of immunostained ventral pallidum confirmed that the immunoreactive structures were boutons which made predominantly symmetrical synapses on ventral pallidal cell bodies and dendrites.