Recurrent inhibition

Sastry, B. S. R., and Sinclair, J. G. (1976) Tonic inhibitory influence of a supraspinal mono-aminergic system on recurrent inhibition of extensor monosynaptic reflex. Brain Res., 117 69— 76. 

Dyer RS, Boyes WK. 1984. Trimethyltin reduces recurrent inhibition in rats. Neurobehavioral Toxicol Teratol 6 369-371. 

Modeling in the brain is mainly targeted to the general qualitative principles underlying various phenomena such as epileptic seizures [574], and not to quantitative assessment and forecasting as one would expect to achieve in simpler systems. For example, in [479], recurrent inhibition and epilepsy are studied and also penicillin is considered as a q-aminobutyric acid inhibitor. 

Langmoen, I. A., and Dingledine, R., 1979, On the time course of recurrent inhibition in hippocampal pyramidal cells in vitro, Acta Physiol. Scand. 105 40-41A. 

Certain intemeurons located in the anterior horn in close association with the motor neurons constitute the Renshaw inhibitory system, which causes inhibition of neurons surrounding the motor neuron carrying a given excitatory impulse. This phenomenon is known as recurrent inhibition. The function of the Renshaw inhibitory system is to sharpen the signal of the motor rmit It prevents the signal from diffusing into adjacerrt nerve fibers, which wotrld weaken the signal. 

The antiviral mechanism of action of acyclovir has been reviewed (72). Acyclovir is converted to the monophosphate in herpes vims-infected cells (but only to a limited extent in uninfected cells) by viral-induced thymidine kinase. It is then further phosphorylated by host cell guanosine monophosphate (GMP) kinase to acyclovir diphosphate [66341 -17-1], which in turn is phosphorylated to the triphosphate by unidentified cellular en2ymes. Acyclovir triphosphate [66341 -18-2] inhibits HSV-1 viral DNA polymerase but not cellular DNA polymerase. As a result, acyclovir is 300 to 3000 times more toxic to herpes vimses in an HSV-infected cell than to the cell itself. Studies have shown that a once-daily dose of acyclovir is effective in prevention of recurrent HSV-2 genital herpes (1). HCMV, on the other hand, is relatively uninhibited by acyclovir. 

One of the oldest antiepileptic drugs, bromide, has been repotted to boost inhibition by an unknown mechanism. Bromide is still in use in certain cases of tonic-clonic seizures and in pediatric patients with recurrent febrile convulsions and others. The mechanism of action may include a potentiation of GABAergic synaptic transmission, although the precise target is not known. 

Stimulation of mAChRs also results in the activation or inhibition of a large number of ion channels [5]. For example, stimulation of Mi receptors leads to the suppression of the so-called M current, a voltage-dependent Recurrent found in various neuronal tissues. M2 receptors, on the other hand, mediate the opening of cardiac Ikcacii) channels, and both M2 and M4 receptors are linked to the inhibition of voltage-sensitive calcium channels [5]. 

Acyclovir (Zovirax) and penciclovir (Denavir) are the only topical antiviral dragp currently available These dragp inhibit viral replication. Acyclovir is used in the treatment of initial episodes of genital herpes, as well as heqies simplex virus infections in immunocompromised patients (patients with an immune system incapable of fighting infection). Penciclovir is used for the treatment of recurrent herpes labialis (cold sores) in adults. 

Denileukin diftitox is a combination of the active sections of interleukin 2 and diphtheria toxin. It binds to high-affinity interleukin 2 receptors on the cancer cell (and other cells), and the toxin portion of the molecule inhibits protein synthesis to result in cell death. The pharmacokinetics of denileukin diftitox are best described by a two-compartment model, with an a half-life of 2 to 5 minutes and a terminal half-life of 70 to 80 minutes. Denileukin diftitox is used for the treatment of persistent or recurrent cutaneous T-cell lymphoma whose cells express the CD25 receptor. Side effects include vascular leak syndrome, fevers/chills, hypersensitivity reactions, hypotension, anorexia, diarrhea, and nausea and vomiting. 

The answer is b. (Hardman, p 1203.) Trifluridine inhibits viral activity in HSV types 1 and 2, CMV, vaccinia, and perhaps adenovirus. It acts as a viral DNA synthesis inhibitor by irreversibly blocking thymidylate synthetase. Trifluridine triphosphate is a competitive inhibitor of thymidine triphosphate accumulation into DNA It is used in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis caused by HSV 1 and 2. 

Li+ is currently administered topically for the relief of HSV and, in addition, it has been demonstrated that the recurrence of HSV infection is inhibited in Li+-treated patients, indicating another potential prophylactic effect of Li+ [245]. Ointment containing 8% lithium succinate has been shown to reduce the severity and the incidence of recurrent genital HSV infection in man [246]. It has also been proposed that Li+ might be efficacious in treating HIV-infected patients, although any benefits have not yet been demonstrated [247]. While HTV is a RNA virus and as such might not be predicted to be affected by Li+, it is a retrovirus and utilizes a DNA intermediate for its replication and it uses a DNA polymerase. 

Protein S The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors Villa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH]... 

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