PMID- 25697594
OWN - NLM
STAT- MEDLINE
DCOM- 20160225
LR  - 20150309
IS  - 1873-3360 (Electronic)
IS  - 0306-4530 (Linking)
VI  - 54
DP  - 2015 Apr
TI  - Microemboli alter the acute stress response and cause prolonged expression of 
      MCP-1 in the hippocampus.
PG  - 71-7
LID - S0306-4530(15)00037-2 [pii]
LID - 10.1016/j.psyneuen.2015.01.023 [doi]
AB  - Microvascular ischemia is linked to cardiovascular disease pathology, as well as 
      alterations in mood and cognition. Ischemia activates the 
      hypothalamic-pituitary-adrenal (HPA) axis and through chronic activation, alters 
      HPA axis function. Dysregulation of the HPA axis can lead to the chronic release 
      of glucocorticoids, a hyper-inflammatory cerebral response, cell damage, and 
      changes in behavior. Although the interactions between injury and HPA axis 
      activity have been established in global ischemia, HPA-related repercussions of 
      diffuse ischemic damage and subsequent inflammation have not been assessed. The 
      current study used a rat model of microsphere embolism (ME) ischemia to test the 
      hypothesis that microvascular ischemia would lead to long term alterations in HPA 
      axis function and inflammatory activity. Furthermore, given the pro-inflammatory 
      nature of chronic stress, we assessed the implications of chronic stress for gene 
      expression of inflammatory factors and key components of the glucocorticoid 
      receptor response, following microvascular ischemia. Results indicated that ME 
      altered the response to an acute stress fourteen days following ME injury and 
      increased hippocampal expression of monocyte chemoattractant protein 1 (Mcp-1) as 
      long as 4 weeks following ME injury, without concomitant effects on gene 
      expression of the glucocorticoid receptor or its co-chaperones. Furthermore, no 
      exacerbative effects of chronic stress exposure were observed following ME injury 
      beyond the effects of ME injury alone. Together, these results indicate that ME 
      injury is sufficient to alter both HPA axis activity and cerebral inflammation 
      for a prolonged period of time following injury.
CI  - Copyright (c) 2015 Elsevier Ltd. All rights reserved.
FAU - Nemeth, Christina L
AU  - Nemeth CL
AD  - Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA, 
      United States; Department of Physiology, Emory University, Atlanta, GA, United 
      States.
FAU - Neigh, Gretchen N
AU  - Neigh GN
AD  - Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA, 
      United States; Department of Physiology, Emory University, Atlanta, GA, United 
      States. Electronic address: gretchen.neigh@emory.edu.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150204
PL  - England
TA  - Psychoneuroendocrinology
JT  - Psychoneuroendocrinology
JID - 7612148
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Receptors, Glucocorticoid)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Corticosterone/metabolism
MH  - Disease Models, Animal
MH  - Gene Expression
MH  - Hippocampus/*blood supply/metabolism/*physiopathology
MH  - Hypothalamo-Hypophyseal System/*physiopathology
MH  - Intracranial Embolism/genetics/metabolism/*physiopathology
MH  - Ischemia/etiology/genetics/metabolism/*physiopathology
MH  - Male
MH  - Pituitary-Adrenal System/*physiopathology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Glucocorticoid/genetics/metabolism
MH  - Stress, Physiological/genetics/*physiology
OTO - NOTNLM
OT  - HPA axis
OT  - Inflammation
OT  - Ischemia
OT  - Stress
OT  - Vasculature
EDAT- 2015/02/24 06:00
MHDA- 2016/02/26 06:00
CRDT- 2015/02/21 06:00
PHST- 2014/10/21 00:00 [received]
PHST- 2015/01/05 00:00 [revised]
PHST- 2015/01/27 00:00 [accepted]
PHST- 2015/02/21 06:00 [entrez]
PHST- 2015/02/24 06:00 [pubmed]
PHST- 2016/02/26 06:00 [medline]
AID - S0306-4530(15)00037-2 [pii]
AID - 10.1016/j.psyneuen.2015.01.023 [doi]
PST - ppublish
SO  - Psychoneuroendocrinology. 2015 Apr;54:71-7. doi: 10.1016/j.psyneuen.2015.01.023. 
      Epub 2015 Feb 4.