INVESTIGADORES
GENARO Ana Maria
artículos
Título:
Altered expression of autonomic neurotransmitter receptors and proliferative responses in lymphocytes from a chronic mild stress model of depression: effects of fluoxetine.
Autor/es:
VALERIA AYELLI-EDGAR; GRACIELA A CREMASCHI; LEONOR STERIN-BORDA; ANA MARÍA GENARO
Revista:
BRAIN BEHAVIOR AND IMMUNITY
Editorial:
ACADEMIC PRESS INC ELSEVIER SCIENCE
Referencias:
Lugar: United States; Año: 2002 vol. 16 p. 333 - 350
ISSN:
0889-1591
Resumen:
We studied b-adrenergic and muscarinic cholinergic receptor (MR) expression and proliferative
response in lymphocytes from animals under chronic mild stress (CMS) model
of depression (CMS animals). Animals were subjected to CMS (periods of food or water
deprivation, changes in lighting conditions, tilted cage, etc.) for 12 weeks. CMS lymphocytes
showed an altered mitogen-induced proliferation. CMS-B and -T lymphocytes
showed an increment on b-adrenoceptor number and on intracellular responses to a b-
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
response in lymphocytes from animals under chronic mild stress (CMS) model
of depression (CMS animals). Animals were subjected to CMS (periods of food or water
deprivation, changes in lighting conditions, tilted cage, etc.) for 12 weeks. CMS lymphocytes
showed an altered mitogen-induced proliferation. CMS-B and -T lymphocytes
showed an increment on b-adrenoceptor number and on intracellular responses to a b-
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
response in lymphocytes from animals under chronic mild stress (CMS) model
of depression (CMS animals). Animals were subjected to CMS (periods of food or water
deprivation, changes in lighting conditions, tilted cage, etc.) for 12 weeks. CMS lymphocytes
showed an altered mitogen-induced proliferation. CMS-B and -T lymphocytes
showed an increment on b-adrenoceptor number and on intracellular responses to a b-
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
response in lymphocytes from animals under chronic mild stress (CMS) model
of depression (CMS animals). Animals were subjected to CMS (periods of food or water
deprivation, changes in lighting conditions, tilted cage, etc.) for 12 weeks. CMS lymphocytes
showed an altered mitogen-induced proliferation. CMS-B and -T lymphocytes
showed an increment on b-adrenoceptor number and on intracellular responses to a b-
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
b-adrenergic and muscarinic cholinergic receptor (MR) expression and proliferative
response in lymphocytes from animals under chronic mild stress (CMS) model
of depression (CMS animals). Animals were subjected to CMS (periods of food or water
deprivation, changes in lighting conditions, tilted cage, etc.) for 12 weeks. CMS lymphocytes
showed an altered mitogen-induced proliferation. CMS-B and -T lymphocytes
showed an increment on b-adrenoceptor number and on intracellular responses to a b-
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.
b-adrenoceptor number and on intracellular responses to a b-
agonist. CMS-T cells showed higher MR expression and lower cGMP responses than normal
lymphocytes. MR were not detectable in normal B cells while CMS-B cells showed
both MR expression and cGMP response. Beta and muscarinic stimulation influenced lymphocyte
proliferative responses, in accordance with cAMP and cGMP responses. After 12
weeks of the CMS procedure, animals were treated with fluoxetine while the CMS procedure
continued. Fluoxetine treatment reverted the alterations induced by CMS. These findings
suggest a possible mechanism for the immune alterations found in depressive disorders
and for the effect of fluoxetine treatment on immune response.