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Biomedical subjects

W F Riker

Publications and source records attributed to W F Riker.

34 records · Page 2Linked to original sources
PubMed1977

Glucocorticoid effects on the edrophonium responsiveness of normal and degenerating mammalian motor nerve terminals.

An intensive short-term triamcinolone regimen in cats preserves the prejunctional actions of edrophonium in degenerating motor nerves. These edrophonium actions include the induction of a stimulus-dependent afterdischarge and the initiation of fasciculations. The relationship between fasciculations and stimulus-dependent afterdischarge is discussed. The glucocorticoid preservation of these edrophonium effects is like that previously reported for the preservation of posttetanic facilitation in motor nerves equally compromised. The results therefore show that glucocorticoid and facilitatory drug actions synergize to increase facilitation in degenerating but still functional motor nerves. This drug synergy is comparable to that which occurs in normal motor nerves. This interaction may provide a basis for effectively combining glucocorticoid and facilitatory drugs in the treatment of myasthenia gravis.

Animals↗
PubMed1975

Glucocorticoids and mammalian motor nerve excitability.

Short-term treatment of cats with high doses of triamcinolone and related steroids strikingly increased the capacity of soleus motoneurons to generate posttetanic stimulus-bound repetition (SBR) and the obligatory postetanic potentiation (PTP) of muscle. The edrophonium chloride (Tensillon)-induced SBR and twitch potentiation were likewise augmented. These effects reflect an increase in the excitability of the motoneuron. This glucocorticoid effect suggests that the motoneuron is the site of the antimyasthenic action of the hormone. Certainly, the enhanced SBR is a neuronal representation of the adverse epileptogenic action of the glucocorticoids. The glucocorticoid effect on motoneuron outlasts the dosing period, suggesting an underlying alteration in the neuron. Other glucocorticoids caused the same effects, but varied in their potencies. Mineralocorticoids were less effective. The single androgen that was tested proved to be minimally effective.

Animals↗
PubMed1975

Motor nerve terminal response to edrophonium in delayed DFP neuropathy.

A localized peripheral neuropathy was induced in cats with di-isopropyl fluorophosphate (DFP). Soleus nerve-muscle preparations, and the motor nerve terminals in particular, were evaluated for responsiveness to edrophonium (200 mug/kg i.v.). Potentiation of contractile strength was absent 24 hr after DFP, and showed a trend toward recovery 7-14 days post-DFP; it then fell to about 25% of normal 3 weeks following DFP administration. During the ensuing 5 weeks this aspect of edrophonium responsiveness was largely regained. The underlying post-drug repetition which gives rise to the potentiated responses was not demonstrable in either the nerve or muscle 3 weeks after DFP, but was again observed 8 weeks after poisoning. These findings suggest a delayed peripheral neuropathy indicative of a trophic deprivation and further illustrate a motor nerve terminal deficit as the initial function alteration in DFP neuropathy.

Action Potentials↗
PubMed1971

Destruction of mammalian motor nerve terminals by black widow spider venom.

Black widow spider venom selectively poisons motor nerve endings. A progressive and irreversible failure of neuromuscular transmission occurs in the cat. Electron microscopy of the poisoned nerve-muscle junction shows a sequence of motor nerve ending damage that culminates in disruption of the prejunctional membrane and loss of all organelles, including synaptic vesicles. The postjunctional membrane was morphologically unaffected. After complete poisoning, the contractile response to exogenous acetylcholine was severely impaired, an indication that the prejunctional site is chiefly involved in the contractile response produced by exogenous acetylcholine and that the pre- and postjunctional effects of acetylcholine were separated.

Acetylcholine↗
PubMed1969

Motor nerve terminals as the site of initial functional changes after denervation.

For the cat soleus nerve-muscle system, motor nerve section 48 hr prior to in situ experiment causes certain characteristic transmission losses. Responses to repetitive stimulation are sharply altered: The capacity to transmit iterative stimulation is severely reduced; post-tetanic potentiation and the post-tetanic repetition of soleus nerve terminals responsible for it are also greatly impaired; a phenomenon of post-tetanic depression was frequently observed. However, function of the extramuscular axons appears normal and single impulse transmission is usually not seriously affected. The loss of reactivity to repetitive stimulation has been traced to soleus motor nerve terminals. In view of these data and the known absence of denervation hypersensitivity at this time, the earliest functional failure may be said to occur in the unmyelinated terminals. This subacutely denervated preparation therefore offers a simple means of evaluating motor nerve terminal responsiveness.

Action Potentials↗
PubMedDate not supplied

A benzodiazepine-anticholinergic drug synergism in the prevention of stress-induced gastric mucosal erosion in mice.

Chlordiazepoxide and clidinium each, as a function of dose, prevent stress-induced gastric mucosal erosion in mice. Clidinium was 2.5 times more potent than chlordiazepoxide. When used in a combination of 2 parts chlordiazepoxide and 1 part clidinium, the protective effect was nearly five times greater than that produced by clidinium alone. Furthermore, the combination dosing proved nearly three times more potent than the potency that was predicted from simple additivity of the individual drug effects. This potentiation appears related to the number of ways in which the combination treatment can decrease autonomic input to the gastric mucosa. Thus, the peripheral cholinergic blockade by clidinium may be potentiated by a central chlordiazepoxide suppression of both sympathetic and parasympathetic activities. Therefore, the combined use of these drugs in the therapy of stress-induced gastric disorder appears to have a rational pharmacologic basis.

Animals↗
PubMedDate not supplied

In vivo reversal of depolarizing neuromuscular blockade.

The antagonism of depolarizing blockers, principally succinylcholine and decamethonium, by tetraethyl- and tetrabutylammonium ions in an in vivo neuromuscular preparation in anesthetized cats is described; possible mechanisms for these effects are discussed. Tetraethyl- (50-100 mg/kg, i.v.) and tetrabutylammonium (1-5 mg/kg, i.v.) produced sharp reversals of 95-99% succinylcholine and decamethonium blocks. These reversals were effective and sustained at any point during the course of the blockades. Tetraethyl- or tetrabutylammonium, administered 2-3 min before succinylcholine or decamethonium, prevented blockade, an effect compatible with an earlier reported in vitro investigation. The studies of others disclose the interaction of depolarizing blockers with acetylcholine receptors, leading to channel opening, channel entry and binding therein of these blockers. The present studies support this in showing the prevention of succinylcholine and decamethonium block by the prior administration of tetraethylammonium, which also interacts with acetylcholine receptors. It is proposed that a possible mechanism for tetraethylammonium reversals of succinylcholine and decamethonium blocks may be attributable to the tetraethylammonium reversal of a K+ current block by quaternary ammonium ions such as succinylcholine and decamethonium. Tetraethyl- and tetrabutylammonium ions proved to be effective antagonists of succinylcholine block following inactivation of plasma cholinesterases by hexafluorenium.

Action Potentials↗