PMID- 16689670
OWN - NLM
STAT- MEDLINE
DCOM- 20060803
LR  - 20071114
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 23
IP  - 5
DP  - 2006 May
TI  - Postinjury administration of pituitary adenylate cyclase activating polypeptide 
      (PACAP) attenuates traumatically induced axonal injury in rats.
PG  - 686-95
AB  - Pituitary adenylate cyclase activating polypeptide (PACAP) has several different 
      actions in the nervous system. Numerous studies have shown its neuroprotective 
      effects both in vitro and in vivo. Previously, it has been demonstrated that 
      PACAP reduces brain damage in rat models of global and focal cerebral ischemia. 
      Based on the protective effects of PACAP in cerebral ischemia and the presence of 
      common pathogenic mechanisms in cerebral ischemia and traumatic brain injury 
      (TBI), the aim of the present study was to investigate the possible protective 
      effect of PACAP administered 30 min or 1 h postinjury in a rat model of diffuse 
      axonal injury. Adult Wistar male rats were subjected to impact acceleration, and 
      PACAP was administered intracerebroventricularly 30 min (n = 4), and 1 h after 
      the injury (n = 5). Control animals received the same volume of vehicle at both 
      time-points (n = 5). Two hours after the injury, brains were processed for 
      immunohistochemical localization of damaged axonal profiles displaying either 
      beta-amyloid precursor protein (beta-APP) or RMO-14 immunoreactivity, both 
      considered markers of specific features of traumatic axonal injury. Our results 
      show that treatment with PACAP (100 microg) 30 min or 1 h after the induction of 
      TBI resulted in a significant reduction of the density of beta-APP-immunopositive 
      axon profiles in the corticospinal tract (CSpT). There was no significant 
      difference between the density of beta-APP-immunopositive axons in the medial 
      longitudinal fascicle (MLF). PACAP treatment did not result in significantly 
      different number of RMO-14-immunopositive axonal profiles in either brain areas 2 
      hours post-injury compared to normal animals. While the results of this study 
      highlighted the complexity of the pathogenesis and manifestation of diffuse 
      axonal injury, they also indicate that PACAP should be considered a potential 
      therapeutic agent in TBI.
FAU - Tamas, Andrea
AU  - Tamas A
AD  - Department of Anatomy (Neurohumoral Regulations Research Group of the Hungarian 
      Academy of Sciences), University of Pecs, Medical Faculty, Pecs, Hungary. 
      andrea.tamas@aok.pte.hu
FAU - Zsombok, Andrea
AU  - Zsombok A
FAU - Farkas, Orsolya
AU  - Farkas O
FAU - Reglodi, Dora
AU  - Reglodi D
FAU - Pal, Jozsef
AU  - Pal J
FAU - Buki, Andras
AU  - Buki A
FAU - Lengvari, Istvan
AU  - Lengvari I
FAU - Povlishock, John T
AU  - Povlishock JT
FAU - Doczi, Tamas
AU  - Doczi T
LA  - eng
GR  - 1-R03-TW0131302A1/TW/FIC NIH HHS/United States
GR  - NS20193/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Neurotransmitter Agents)
RN  - 0 (Pituitary Adenylate Cyclase-Activating Polypeptide)
SB  - IM
MH  - Amyloid beta-Protein Precursor/drug effects/metabolism
MH  - Animals
MH  - Axons/*drug effects/pathology
MH  - Brain Injuries/*drug therapy/metabolism/pathology
MH  - Image Processing, Computer-Assisted
MH  - Immunohistochemistry
MH  - Injections, Intraventricular
MH  - Male
MH  - Neurotransmitter Agents/*administration & dosage
MH  - Pituitary Adenylate Cyclase-Activating Polypeptide/*administration & dosage
MH  - Pyramidal Tracts/drug effects/metabolism/pathology
MH  - Rats
MH  - Time Factors
EDAT- 2006/05/13 09:00
MHDA- 2006/08/04 09:00
CRDT- 2006/05/13 09:00
PHST- 2006/05/13 09:00 [pubmed]
PHST- 2006/08/04 09:00 [medline]
PHST- 2006/05/13 09:00 [entrez]
AID - 10.1089/neu.2006.23.686 [doi]
PST - ppublish
SO  - J Neurotrauma. 2006 May;23(5):686-95. doi: 10.1089/neu.2006.23.686.