Sustained activation of microglia in the hypothalamic PVN following myocardial infarction
- Authors: Dworak, Melissa , Stebbing, Martin , Kompa, Andrew , Rana, Indrajeetsinh , Krum, Henry , Badoer, Emilio
- Date: 2012
- Type: Text , Journal article
- Relation: Autonomic Neuroscience Vol. 169, no. 2 (August 2012 2012), p. 70-76
- Full Text: false
- Reviewed:
- Description: Microglia are the immune cells in the central nervous system and can produce cytokines when they are activated by an insult or injury. In the present study, we investigated in detail the time frame of the activation of microglia in the hypothalamic paraventricular nucleus (PVN) following myocardial infarction in rats. Morphological changes and immunohistochemistry to detect CD11b (clone OX-42) were used to identify activated microglia. Compared to rats that had undergone sham surgical procedures, there was a significant increase of between 40 and 50% in the proportion of activated microglia in the PVN 4–16 weeks following myocardial infarction (P < 0.001, One way ANOVA). At 24 h or 1 week post myocardial infarction, however, there was no significant increase in the proportion of activated microglia. Echocardiography and haemodynamic parameters after myocardial infarction indicated significantly reduced left ventricular function. In conclusion, following myocardial infarction, activation of microglia in the PVN does not occur immediately but once manifested, activation is sustained. Thus, activated microglia may contribute to the chronic elevation in cytokine levels observed following myocardial infarction. Since cytokines elicit sympatho-excitatory effects when locally microinjected into the PVN, activated microglia may contribute to the mechanisms mediating the chronic increase in sympathetic nerve activity in animals with reduced left ventricular function induced following myocardial infarction.
- Description: C1
Microglia activation in the hypothalamic PVN following myocardial infarction
- Authors: Rana, Indrajeetsinh , Stebbing, Martin , Kompa, Andrew , Kelly, Darren , Krum, Henry , Badoer, Emilio
- Date: 2010
- Type: Text , Journal article
- Relation: Brain Research Vol. 1326, no. (April 2010 2010), p. 96-104
- Full Text: false
- Reviewed:
- Description: Following a myocardial infarction (MI), inflammatory cytokines are elevated in the brain, as well as in plasma, indicating that inflammation is occurring in the brain in addition to the periphery. Microglia are the immune cells in the central nervous system and can produce cytokines when they are activated by an insult or injury. In the present study, we investigated whether MI in rats induces activation of microglia in the brain. We used immunohistochemistry to detect CD11b (clone OX-42) and morphological changes to identify activated microglia. Compared to control rats that had undergone sham surgical procedures, there was a significant increase in activated microglia in the hypothalamic paraventricular nucleus (PVN) following myocardial infarction. Activated microglia were not observed in the ventral hypothalamus, adjacent to the PVN, nor in the cortex, indicating the response was not the result of a generalized inflammatory reaction in the brain. Echocardiography and haemodynamic parameters after myocardial infarction indicated that reduced left ventricular function but congestive heart failure had not developed. In conclusion, microglia are activated in the PVN but not in the adjacent hypothalamus following myocardial infarction. The activated microglia may contribute to the increased local production of pro-inflammatory cytokines observed in the PVN after myocardial infarction and resulting in reduced left ventricular function.
- Description: C1