Central depressants interaction

There are some clinically important pharmacodynamic drug-drug interactions to be mentioned. Antipsychotics will potentiate the central depressant effects of sedatives and of alcohol. They will also increase the risk of respiratory-depressant effects of opiates. Inducers of drug metabolic enzymes like for example rifampicin and several antiepileptics, may increase the elimination rate of antipsychotic agents and thus decrease their efficacy. 

An excellent brief article on buprenorphine treatment has been provided by Taikato et al. (2005), which notes the common possible side-effects (headaches, nausea and vomiting, sweating, constipation, etc.) and drug interactions. The limited central depressant effect of buprenorphine may be compounded by alcohol and antidepressants, while the metabolism of buprenorphine can be enhanced by anticonvulsants, with therefore possibly reduced efficacy. There have been some case reports of liver toxicity from buprenorphine that is reversible if the medication is stopped (Herve et al. 2004), and often clinical guidelines will recommend that liver function tests are included in buprenorphine treatment, as they definitely should be with naltrexone. 

Interactions. All potentiate the effects of alcohol and other central depressants, and all are likely to exacerbate breathing difficulties where this is already compromised, e.g. in obstructive sleep apnoea. 

Tricyclic drug interactions (Table 30-3) include additive depression of the CNS with other central depressants, including ethanol, barbiturates, benzodiazepines, and opioids. Tricyclics may also cause reversal of the antih)pertensive action of guanethidine by blocking its transport into sympathetic nerve endings. Less commonly, tricyclics may interfere with the antihypertensive actions of methylnorepinephrine (the active metabolite of methyl-dopa) and clonidine. 

Drug interactions. BDZs have additive or synergistic effects with other central depressants such as alcohol, barbiturates and antihistamines. 

The neuropeptide Y (NPY) belongs to a family of peptides that includes peptide YY and pancreatic polypeptide, and it is associated with several diseases such as asthma, immune system disorders, inflammatory diseases, anxiety, depression and diabetes mellitus. NPY is found in the central and peripheral nervous system, and its biological functions are mediated by interactions with five receptor sub-types, i.e. Yl, Y2, Y4, Y5 and Y6. Several studies indicate that the feeding behavior is influenced by interactions between NPY and Yl and Y5. Deswal and Roy used Cerius descriptors and genetic function approximation QSAR to investigate the structural determinants for the inhibition potency of 24 compounds with the general structure 4 for the NPY Y5 receptor [31]. The best QSAR (H = 0.720,... 

It has been hypothesized that depression could arise from a pathological enhancement of 5-HT2 receptor function. This view would concur with the observations that the functional activity of 5-HT2 receptors on the platelet membrane is enhanced in depression and the increase in the density of 5-HT2 receptors in the frontal cortex of brains from suicide victims. It is possible that enhanced 5-HT2 receptor function is associated primarily with anxiety, a common feature of depression, and that the increased activity of the 5-HT2 receptors results in an attenuation of the functioning of S-HT receptors thereby resulting in the symptoms of depression. Whether this change in the activity of S-HT receptors is due to direct effects of the altered 5-HT2 receptor function is uncertain. There is evidence that hypercortisolaemia, which is a characteristic feature of depression, reduces the activity of these receptors probably through central glucocorticoid type 2 receptors. Clearly further research is needed to determine the precise interaction between the 5-HT2 and 5-HTi receptor types. 

Ginseng interacts with phenelzine, a drug used to treat depression, stimulating the central nervous system. 

Cydobenzaprine (Flexeril) [Skeletal Muscle Relaxant/ANS A nt] Uses Relief of muscle spasm Action Centrally acting skeletal muscle relaxant reduces tonic somatic motor activity Dose 5-10 mg PO bid-qid (2-3 wk max) Caution [B, ] Shares the toxic potential of theTCAs urinary hesitancy, NAG Contra Do not use concomitantly or w/in 14 d of MAOIs hyperthyroidism heart failure arrhythmias Disp Tabs SE Sedation anticholinergic effects Interactions t Effects of CNS d ression W/ CNS dqjressants, TCAs, barbiturates, EtOH t risk of HTN convulsions W/MAOIs EMS Use caution w/ other CNS depressants concurrent EtOH use can t CNS d ession OD May cause N/V,... 

Methocarbamol (Robaxin) [Skeletal Muscle Relaxant/ Centrally Acting] Uses Relief of discomfort associated w/ painful musculoskeletal conditions Action Centrally acting skeletal muscle relaxant Dose Adults. 1.5 g PO qid for 2-3 d, then 1-g PO qid maint therapy IV form rarely indicated Peds. 15 mg/kg/dose IV, may repeat PRN (OK for tetanus only), max 1.8 g/mVd for 3 d Caution Sz disorders [C, +] Contra MyG, renal impair Disp Tabs, inj SE Can discolor urine drowsiness, GI upset Interactions T Effects Wf CNS depressant, EtOH EMS May cause blurred vision and orthostatic hypotension use caution w/ CNS depressants concurrent EtOH use can T CNS depression OD May cause drowsiness, light-headedness, syncope, and slow shallow breathing symptomatic and supportive... 

Clearly, a single neurotransmitter theory does not suffice to explain all known evidence. As a result, models that include two or more systems have been developed to encompass their modulatory interactions. One of the most cogent is the permissive hypothesis, which proposes that a decreased function in central serotonin transmission sets the stage for either a depressive or manic phase ( 60). This circumstance itself is not sufficient to produce the mood disturbance, however, with superimposed aberrations in NE function required to determine the phase of an affective episode (i.e., decreased 5-HT and decreased NE subserves depression decreased 5-HT and increased NE subserves mania). Data from animal studies to support this theory include the following ... 

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