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Autonomic control mechanisms in the brush possum (Trichosorus vulpecula).


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McLeod, Lyndsay James 1977 , 'Autonomic control mechanisms in the brush possum (Trichosorus vulpecula).', PhD thesis, University of Tasmania.

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The autonomic influences on some organ systems in the possum
(Trichosurus vulpecula) have been studied. The work has also included
aspects of possible mechanisms for the modulation of autonomic function
by endogenous prostaglandins and lipids.
Noradrenaline has been identified by pharmacological methods. The
chemical method used was not sensitive enough to identify noradrenaline
positively in the splenic tissue and in the venous effluent of the
electrically stimulated spleen. Support for noradrenaline being the
neurotransmitter at sympathetic nerve endings comes from indirect evidence.
Phenoxybenzamine blocks the effect of sympathetic nerve stimulation in
the hind limb vascular bed. Phentolamine blocks the contracture of the
nictitating membrane when the preganglionic nerve is stimulated and it
also blocks part of the effect induced by sympathetic nerve stimulation
of the possum gut. Propranolol blocks a component of the reflex changes
in heart rate induced by a variety of methods.
Less direct support for noradrenaline being the adrenergic transmitter
is supplied from the findings that adrenoceptors exist in a number of
isolated tissues. Application of exogenous noradrenaline produces
contracture of the nictitating membrane, an increased rate and force of
beating of the isolated heart, a decreased blood flow in the skeletal
muscle and skin of the hind limb and a reduced amplitude and tone of the
spontaneously active isolated gut. The identity of the adrenoceptors
has been determined by using specific pharmacological blocking agents.
The receptors in the nictitating membrane and the skin are α-adrenoceptors
because they are blocked by phenoxybenzamine or phentolamine. The
receptors in the heart are β-receptors because they are blocked by
propranolol. Both α- and β-adrenoceptors exist in skeletal muscle vessels, because both α- and β-antagonists are necessary to block the effects of
intra-arterial adrenaline. The possum gut reacts to catecholamines in
a qualitatively similar way to the guinea pig and rabbit guts. A mixed
α and β block, produced by the simultaneous use of phentolamine and
propranolol, is necessary to inhibit the response from adrenaline,
noradrenaline and isoprenaline on the possum gut.
In the hind limb vascular bed maximal decrease in blood flow is
achieved by sympathetic stimulation at frequencies of 15-20 Hz. At
frequencies 40-100 Hz there is'a reduced response which indicates an
inhibitory mechanism acting rapidly to prevent excessive sympathetic
outflow at higher frequencies. Compared with the cat and dog there is
a relatively small amount of noradrenaline released when the sympathetic
splenic nerves of the possum are electrically stimulated. This may be
due to the modulating influence of a large plasma concentration of
prostaglandin F 2a . Prostaglandin E2 which is released when the splenic
nerve is stimulated may also be a component for reducing noradrenaline
As well as prostaglandins in the possum plasma there is also an
unstable phospholipid with vasoconstrictor properties, but its function
is unknown. 14 C arachidonate studies indicate that there may be some
biosynthetic relationship between arachidonic acid, prostaglandins and
the unknown phospholipid.
There is indirect support for the role of acetylcholine as a
transmitter substance in the possum. Atropine blocks the effects of
exogenous acetylcholine on the isolated heart and the isolated intestine,
and also blocks a component of the reflex changes in heart rate induced
by different methods. Acetylcholine appears to be the transmitter at the superior cervical ganglion. The ganglion is stimulated by close
arterial injection of acetylcholine and nicotine and these effects and those
of preganglionic stimulation are blocked by hexamethonium.
There are no sympathetic cholinergic vasodilator fibres to the possum
hind limb. However, the hind limb vascular bed dilates under the
influence of intra-arterial acetylcholine and the response is blocked by
atropine. It appears therefore that the muscarine receptors in the hind
limb are not innervated. They are about 1/5 as sensitive to acetylcholine
as comparable tissue in the cat.
Possible mechanisms are discussed for the "playing dead" reaction
and for the relatively poor noradrenaline overflow when sympathetic
nerves are stimulated.

Item Type: Thesis - PhD
Authors/Creators:McLeod, Lyndsay James
Keywords: Opossums, Marsupials, Neurophysiology
Copyright Holders: The Author
Additional Information:

Thesis (Ph.D.) -- University of Tasmania, 1977. Bibliographical references

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