Diminished response to beta‐bungarotoxin in neonatal rat diaphragm.

Gundersen, Cameron B.

doi:10.1113/jphysiol.1981.sp013697

Cited by 6 publications

(1 citation statement)

References 19 publications

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“…The toxin has a high affinity and saturable binding capcity toward isolated brain membranes of rat (Oberg and Kelly, 1976) and chick (Rehm and Betz, 1982). It reduces the levels of amino acid neurotransmitters in brain synaptosomes (Wernicke et al, 1974;Smith et al, 1980), but stimulates the synthesis and accumulation of acetylcholine (ACh) in rat phrenic nerve (Gundersen, 1981; Gundersen et al, 1981). It has also been demonstrated that 6-BT inhibits the high-affinity choline (Ch) transport in Torpedo electric organ (Dowdall et al, 1977).…”

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In Vivo Effects of β‐Bungarotoxin on the Acetylcholine System in Different Brain Areas of the Rat

Gulya¹,

Budai²,

Kása³

et al. 1984

Journal of Neurochemistry

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The in vivo effects of beta-bungarotoxin (beta-BT) on the acetylcholine (ACh) system were studied in the whole cerebrum and in different brain regions. The effect of beta-BT on cerebral ACh and choline (Ch) contents was time-dependent. The results show that a single intracerebroventricular injection of 1 microgram toxin increased both the ACh and Ch contents in the cortex, hippocampus, and cerebellum, while in the striatum the ACh level was decreased. Ten nanograms of toxin injected into the lateral ventricle twice, on the first and third days, led to a reduced ACh level 2 days after the last treatment. In animals treated with the same dose three times, on the first, third, and fifth days, and sacrificed 2 days after the last injection, the choline acetyltransferase and acetylcholinesterase activities were reduced and the number of muscarinic acetylcholine receptors was decreased. A biphasic effect of the toxin was therefore demonstrated. It is suggested that in the first phase of the toxin effect the increased levels of ACh and Ch may be due to the inhibition of neuronal transmission, while in the second phase, when the elements of the ACh system are reduced, the neuronal degenerating effect of beta-BT plays a significant role.

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