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(1): Daily injections during 6 days

(2): Single injection

(3): Daily injections during 5 weeks

(4): Daily injections during 3 weeks

(5): Daily per os during 4 weeks

(1): Daily injections during 6 days

(2): Single injection

(3): Daily injections during 5 weeks

(4): Daily injections during 3 weeks

(5): Daily per os during 4 weeks

1996). An inhibitory effect of monoamine reuptake inhibitors on immune activation has also been found in rats with experimental allergic neuritis (Bengtsson, Zhu,Thorell, Olsson, Link, & Walinder, 1992; Zhu, Bengtsson, Mix,Thorell, Olsson, & Link, 1994). Moreover, olfactory bulbectomy in rats, a classic animal model of depression (Jancsar & Leonard, 1983), increased a-l-acid glycoprotein 5 to 9 weeks after surgery (Arnold & Meyerson, 1990), and this increase of acute phase proteins response was reversed by treatment with selective 5-HT reuptake inhibitors (Song & Leonard, 1994). In addition, acute treatment with fluoxetine (a 5-HT reuptake inhibitor) and clomipramine (a tricyclic antidepressant) reduced the inflammation induced by carrageenin or brewer's yeast in rats (Bianchi, Sacerdote, & Panerai, 1994 a, b; Bianchi, Rossoni, Sacerdote, Panerai, & Berti, 1995). However, different mechanisms appear to be involved in mediating the effects of these compounds, which belong to two different families. The anti-inflammatory activity of fluoxetine in inflammation induced by brewer's yeast is associated with activation of the HPA axis (Bianchi et al., 1994a), whereas activity of clomipramine in carrageenin-induced inflammation may be due to an inhibition of substance P production (Bianchi et al., 1995). Moreover, clomipramine depressed the migration of rat macrophages both in vivo and in vitro (Sacerdote, Bianchi, & Panerai,

1997). Clomipramine also reduced human polymorphonuclear cell chemiotaxis in vitro (Sacerdote, Bianchi, & Panerai, 1994), whereas non-tricyclic antidepressants like fluoxetine had no effect on this chemiotaxis. These results indicate that the antiinflammatory activities of tricyclic antidepressants are independent of their antidepressive activity and result from a particular effect linked to their molecular structure. The anti-inflammatory effects of tricyclic antidepressants partly result from the inhibition of NA reuptake induced by these drugs. Indeed, this anti-inflammatory effect can be attenuated by pharmacological inhibition of catecholamine synthesis or medullo-adrenalectomy (Arrigoni Martelli, Toth, Segre, & Corsico, 1967). In addition, chronic (28 days), but not acute treatment with different antidepressants (imipramine, fluvox-amine, and maprotiline) administered per os, induces a marked increase of both IL-ip and IL-lra mRNA expression in different brain stuctures, including the hypothalamus, hippocampus, frontal cortex, and brain stem (Suzuki, Shintani, Kanba, Asai, & Nakaki, 1996). It is noteworthy that the increase of the expression of IL-lra, the natural antagonist for IL-1, is more intense than that of IL-1, and its time-profile in response to antidepressants coincides with the time required for therapeutic efficiency. These interesting results suggest that antidepressants may either inhibit cytokine production at the periphery or block the central action of IL-1 via the increase of brain IL-lra.

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