MORPHINE INDUCED CALCIUM DEPLETION IN DISCRETE REGIONS OF RAT BRAIN 1

It was confirmed that morphine administration in vivo produced a selective decrease in the calcium content of synaptosomal fractions prepared from rat cerebral cortices. This effect was prevented by naloxone. After morphine or naloxone, there were no changes in the sodium, potassium and magnesium contents of any of the seven subcellular fractions tested. Since the selective calcium loss was found to occur from fractions similar to those reported to exhibit opiate receptor binding, it is concluded that calcium may play a role in the action of narcotic agonist drugs.

Section: Preparation Ofsubcellularfractionssupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Section: Preparation Ofsubcellularfractionsmentioning

confidence: 99%

See 1 more Smart Citation

Calcium Depletion of Synaptosomes After Morphine Treatment

Cardenas

Ross

1976

“…This blockade is not achieved through interference with impulse conduction in nerve terminals (Kosterlitz & Wallis, 1964), nor by depression due to blockade of uptake of catecholamines into synaptic vesicles (Blosser & Catravas, 1974). The analgesic effects of morphine are suppressed by intracistemal administration of Ca (Kakunga, Kaneto & Nano, 1966), whilst the tissue Ca of rat brain is decreased by morphine (Cardenas & 0007-1188/80/060185-07 $01.00 Ross, 1975). This effect is due to a decrease in the Ca levels found in synaptic terminals (Ross, Lynn & Cardenas, 1976;Harris, Yamamoto, Loh & Way, 1976;Yamamoto, Harris, Loh & Leon Way, 1978), and may be associated with alteration by morphine of the binding of Ca ions to phospholipids within the presynaptic membrane (Mule, 1969).…”

Section: Introductionmentioning

confidence: 99%

An Electrophysiological Analysis of the Effects of Morphine on the Calcium Dependence of Neuromuscular Transmission in the Mouse Vas Deferens

Bennett

Lavidis

1980

1 The effects of morphine on the Ca-dependence of the synaptic potential amplitude in the mouse vas deferens have been determined.2 The synaptic potential increased with a power factor of 2.4 for [Ca]. between 0.7 mm and 1.8 mm.Morphine (40 nM) decreased the synaptic potential, without altering the second power relationship between the synaptic potential and [Ca]0. 3 Morphine reversed the depression in the synaptic potential which develops during a short highfrequency (10 Hz) train of impulses to facilitation. Consequently the synaptic potential beyond the tenth impulse was unaffected by morphine. 4 Morphine did not alter the facilitation of the synaptic potential which develops during a short low-frequency (<2 Hz) train of impulses in normal [Ca]0. Consequently morphine decreased the synaptic potential for each impulse by about the same percentage amount. 5 Morphine increased the small facilitation in the synaptic potential which occurs during a short low-frequency (< 2 Hz) train of impulses in high [Ca]0. This facilitation approximated the predictions based on the assumption that each impulse leaves residual Ca ions bound to receptors involved in transmitter release from the nerve terminal.

“…The striatum, hypothalamus and pons/medulla were dissected by the method of Glowinski & Iversen (1966) (Willis, 1960). Brain calcium was also measured by atomic absorption spectrophotometry using the method of Cardenas & Ross (1975).…”

Section: Methodsmentioning

confidence: 99%

Brain and Serum Calcium Concentrations Following Electroconvulsive Shock or Bicuculline‐induced Convulsions in Rats

Bowdler

Green

Rawle

1980

I A single electroconvulsive shock (ECS; 125 V, 1 s, 50 Hz) given to rats anaesthetized with halothane produced little change in either serum or regional brain calcium concentrations, compared to rats anaesthetized with halothane, either 5 min or 24 h after the convulsion. Both anaesthetic and ECS-treated rats showed an elevated serum concentration 5 min after the ECS. 2 When 5 ECS were given spread out over 10 days there were no significant calcium concentration changes in either serum or brain except for an increase in the pons/medulla. 3 A single convulsion produced by bicuculline (0.375 mg/kg i.v.) resulted in a marked increase in the calcium concentration in serum, but not brain, 5 min later. Diazepam pretreatment (10 mg/kg i.v.) prevented both the convulsion and the serum calcium change. 4 Results are discussed in relation to clinical data on calcium changes following electroconvulsive therapy (ECT) and the enhanced monoamine-mediated behaviours which follow ECS administration to rats.