PMID- 15296847
OWN - NLM
STAT- MEDLINE
DCOM- 20041027
LR  - 20131121
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 189
IP  - 1
DP  - 2004 Sep
TI  - Repeated episodic exposure to ethanol affects neurotrophin content in the 
      forebrain of the mature rat.
PG  - 173-81
AB  - Chronic exposure to ethanol can cause deficits in learning and memory. It has 
      been suggested that withdrawal is potentially more damaging than the ethanol 
      exposure per se. Therefore, we explored the effect of repeated episodic exposure 
      to ethanol on key regulators of cortical activity, the neurotrophins. Rats were 
      exposed to ethanol via a liquid diet for 3 days per week for 6-24 weeks. Control 
      rats were pair-fed an isocaloric liquid diet or ad libitum fed chow and water. 
      The concentrations of nerve growth factor (NGF), brain-derived neurotrophic 
      factor (BDNF), and neurotrophin-3 (NT-3) were determined using enzyme-linked 
      immunosorbant assays (ELISAs). Five telencephalic structures were examined: 
      parietal cortex, entorhinal cortex, hippocampus, the basal nucleus, and the 
      septal nuclei. All five areas expressed each of the three neurotrophins; BDNF was 
      most abundant and NGF the least. The parietal cortex was susceptible to ethanol 
      exposure, NGF and BDNF content increased, and NT-3 content fell, whereas no 
      changes were detectable in the entorhinal cortex. In the hippocampus, the amount 
      all three neurotrophins increased following episodic ethanol exposure. 
      Neurotrophin content in the two segments of the basal forebrain was affected; NGF 
      and NT-3 content in the basal forebrain was reduced and NGF and BDNF content in 
      the septal nuclei was increased by ethanol exposure. In many cases where ethanol 
      had an effect, the change was transient so that by 24 weeks of episodic exposure, 
      no significant changes were evident. Thus, the effects of ethanol are site- and 
      time-dependent. This pattern differs from changes caused by chronic ethanol 
      exposure, hence, neurotrophins must be vulnerable to the effects of withdrawal. 
      Furthermore, the ethanol-induced changes do not appear to fit a model consistent 
      with retrograde regulation, rather they suggest that neurotrophins act through 
      autocrine/paracrine systems.
FAU - Miller, Michael W
AU  - Miller MW
AD  - Department of Neuroscience and Physiology, State University of New York-Upstate 
      Medical University, Syracuse, NY 13210, USA. millermw@upstate.edu
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Central Nervous System Depressants)
RN  - 0 (Nerve Growth Factors)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Animals
MH  - Brain/anatomy & histology/drug effects/metabolism
MH  - Central Nervous System Depressants/*pharmacology
MH  - Drug Administration Schedule
MH  - Eating/drug effects
MH  - Enzyme-Linked Immunosorbent Assay/methods
MH  - Ethanol/*pharmacology
MH  - Male
MH  - Nerve Growth Factors/*metabolism
MH  - Prosencephalon/*drug effects/metabolism
MH  - Rats
MH  - Rats, Long-Evans
MH  - Time Factors
EDAT- 2004/08/07 05:00
MHDA- 2004/10/28 09:00
CRDT- 2004/08/07 05:00
PHST- 2004/01/20 00:00 [received]
PHST- 2004/04/16 00:00 [revised]
PHST- 2004/05/20 00:00 [accepted]
PHST- 2004/08/07 05:00 [pubmed]
PHST- 2004/10/28 09:00 [medline]
PHST- 2004/08/07 05:00 [entrez]
AID - S0014488604002122 [pii]
AID - 10.1016/j.expneurol.2004.05.026 [doi]
PST - ppublish
SO  - Exp Neurol. 2004 Sep;189(1):173-81. doi: 10.1016/j.expneurol.2004.05.026.