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. 1994 Sep;113(1):121–128. doi: 10.1111/j.1476-5381.1994.tb16183.x

Hyperpolarization by opioids acting on mu-receptors of a sub-population of rat periaqueductal gray neurones in vitro.

B Chieng 1, M J Christie 1
PMCID: PMC1510059  PMID: 7812601

Abstract

1. The actions of opioids on membrane properties of rat periaqueductal gray neurones were investigated using intracellular recordings from single neurones in brain slices. Morphological properties and anatomical location of each impaled neurone were characterized by use of intracellular staining with biocytin. The present paper primarily considers neurones which were directly hyperpolarized by opioids. The accompanying paper considers inhibition of synaptic transmission by opioids. 2. Met-enkephalin (10-30 microM) hyperpolarized 29% (38/130) of neurones. The hyperpolarization was fully antagonised by naloxone (1 microM, n = 3). The response to Met-enkephalin was not affected by agents which block synaptic neurotransmission (1 microM tetrodotoxin, and 0.1 microM tetrodotoxin + 4 mM Co2+, n = 3). 3. The specific mu-receptor agonist, D-ala-met-enkephalin-glyol (3 microM, n = 17) produced hyperpolarizations of similar amplitude to those produced by Met-enkephalin (10-30 microM). The EC50 of D-ala-met-enkephalin-glyol was 80 nM and the maximum response was achieved at 1-3 microM. The delta-receptor (D-Pen-D-Pen-enkephalin, 3 microM, n = 7) and kappa-receptor (U50488H, 3 microM, n = 5) agonists had no effect on the membrane properties of these neurones. 4. The opioid-induced hyperpolarization was associated with an increased potassium conductance. Hyperpolarizations were accompanied by a significant decrease in membrane resistance between -70 and -80 mV, and a significantly greater decrease between -110 and -140 mV (n = 16). Hyperpolarizations reversed polarity at -111 +/- 3 mV (n = 16), close to the expected equilibrium potential for potassium ions.(ABSTRACT TRUNCATED AT 250 WORDS)

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