Antidepressants administration

Nibuya M., Nestlr E. J., Duman R. S. (1996). Chronic antidepressant administration increases the expression of cAMP response element binding protein (CREB) in rat hippocampus. J. Neurosci. 16, 2365-72. 

There likely remains a role for pharmacotherapy for some AN patients during the maintenance phase of treatment. Appetite stimulants, prokinetics, and anxiolytics should be tapered and discontinued at the conclusion of the acute phase of treatment. However, early evidence suggests that continued antidepressant administration may help to sustain remission. The appropriate duration for maintenance pharmacotherapy in AN has not been well studied and remains open to debate. 

Malberg, J.E., Eissch, A.J., Nestler, E.J., and Duman, R.S. (1999) Chronic antidepressant administration increases granule cell neurogenesis. Soc Neurosci Abstr 25 1029. 

Michelson, D., Bancroft, J., Targum, S., Kim, Y., and Tepner, R. (2000) Female sexual dysfunction associated with antidepressant administration a randomized, placebo-controlled study of pharmacologic intervention. Am J Psychiatry 157 239—243. 

In contrast to minimal risks for long-term antidepressant administration, the risks of treatment discontinuation are profound, attributable to the greatly increased risk of recurrence. With each new episode, the patient is likely to have increased risk of occupational dysfunction, job loss, social impairment, problems with interpersonal relationships, marital discord, separa-... 

Nemeroff CB, Krishnan KRR, Reed D, et al Adrenal gland enlargement in major depression a computed tomographic study. Arch Gen Psychiatry 49 384-387, 1992 Nestler EJ, Terwilliger RZ, Duman RS Chronic antidepressant administration alters the subcellular distribution of cyclic AMP-dependent protein kinase in rat frontal cortex. J Neurochem 53 1644-1647, 1989 Nestor PC, Parasuraman R, Haxby JV, et al Divided attention and metabolic brain dysfunction in mild dementia of the Alzheimer s type. Neuropsychologia 29(5) 379-387, 1991... 

Hensler JG. Regulation of 5-HT1A receptor function in brain following agonist or antidepressant administration. Life Sci 2003 72(15) 1665-1682. 

Other models include the olfactory bulbectomy model (Song and Leonard, 2005). Lesions of the olfactory bulb cause behavioral changes, inteipreted to result from disturbed function of the limbic system. These behaviors are reversed by chronic antidepressant administration. 

As previously described, practically all antidepressants increase the monoamine concentration in the synaptic cleft. This effect is acute and it is probably not associated with direct antidepressive action. The chain of intra- and intercellular events following chronic antidepressant administration corresponds chronologically to the resolution of depression, which takes between 4 and 8 weeks to develop. ... 

Chronic antidepressant administration causes a chain of events, which begins with receptor targeting, intracellular second-messenger activation, gene expression, and the production of neurotrophic brain factors. These events modulate the neuroplasticity vital for the maintenance of normal mood and the resolution of the depressive mood. This chain of events corresponds chronologically to the resolution of depression, which usually takes at least 4 weeks. ... 

Antidepressants are small heterocyclic molecules entering the circulation after oral administration and passing the blood-brain barrier to bind at numerous specific sites in the brain. They are used for treatment of depression, panic disorders, generalized anxiety disorder, social phobia, obsessive compulsive disorder, and other psychiatric disorders and nonpsychiatric states. 

Administration of atropine with meperidine (Demerol), flurazepam (Dalmane), diphenhydramine (Benadryl), phenothiazines, and the tricyclic antidepressants may increase the effects of atropine. There is a decreased effectiveness of haloperidol when administered with the anticholinergic dragp. 

The amphetamines and the anorexiants should not be given during or within 14 days after administration of monoamine oxidase inhibitors (see Chap. 31) because the patient may experience hypertensive crisis and intracranial hemorrhage. When guanethidine is administered with the amphetamines or the anorexiants, the antihypertensive effect of guanethidine may decrease. Coadministration of the amphetamines or the anorexiants with the tricyclic antidepressants may decrease the effects of the amphetamines or the anorexiants. 

Use of die MAOIs must be discontinued 2 weeks before the administration of die SSRIs. When the SSRIs are administered witii die tricyclic antidepressants, tiiere is an increased risk of toxic effects and an increased tiierapeutic effect. When sertraline is administered witii a MAOI, a potentially fatal reaction can occur. Sjymptoms of a serious reaction include hyper-tiiermia, rigidity, autonomic instability witii fluctuating vital signs and agitation, delirium, and coma Sertraline blood levels are increased when administered witii cimetidine. 

The expected outcomes of die patient depend on die reason for administration of an antidepressant but may... 

Explains the reason for drug therapy, including the type of antidepressant prescribed, drug name, dosage, and frequency of administration. 

The hypotensive effects of most antihypertensive dru are increased when administered with diuretics and other antihypertensives. Many dnigp can interact with the antihypertensive drugs and decrease their effectiveness (eg, antidepressants, monoamine oxidase inhibitors, antihistamines, and sympathomimetic bronchodilators). When the ACE inhibitors are administered with the NSAIDs, their antihypertensive effect may be decreased. Absorption of the ACE inhibitors may be decreased when administered with the antacids. Administration of potassium-sparing diuretics or potassium supplements concurrently with the ACE inhibitors may cause hyperkalemia. When the angiotensin II receptor agonists are administered with... 

NEUROBIOLOGICAL CHANGES INDUCED BY CHRONIC ADMINISTRATION OE ANTIDEPRESSANTS... 

There is a good deal of evidence that the therapeutic effects of antidepressants could involve adaptive changes in 5-HTia receptors. Postsynaptic 5-HTia receptor responses became implicated because the hyperpolarisation of hippocampal CA3 pyramidal neurons that follows ionophoretic administration of 5-HT was found to be increased after chronic treatment with most (but not all) antidepressants (Chaput, de Montigny and Blier 1991). Others suggested that antidepressants attenuate postsynaptic 5-HTja responses because the hypothermia, evoked by their activation, is diminished by antidepressants (Martin et al. 1992). 

More importantly for this discussion is the finding that chronic administration of an antidepressant produces a similar increase in the concentration of extracellular 5-HT in the terminal field together with recovery of neuronal firing. Presumably this is because the prolonged elevation of extracellular 5-HT around the neurons in the Raphe causes progressive desensitisation of the somatodendritic 5-HTia receptors. At this point, inhibition of their firing does not occur and so more 5-HT is released in the cortex (see Hervas et al. 1999). 

Table 20.7 Neurochemical changes generally found after chronic administration of antidepressant drugs or repeated electroconvulsive shock...

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