PMID- 10377368
OWN - NLM
STAT- MEDLINE
DCOM- 19990715
LR  - 20220309
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 19
IP  - 13
DP  - 1999 Jul 1
TI  - Actions of brain-derived neurotrophic factor in slices from rats with spontaneous 
      seizures and mossy fiber sprouting in the dentate gyrus.
PG  - 5619-31
AB  - This study examined the acute actions of brain-derived neurotrophic factor (BDNF) 
      in the rat dentate gyrus after seizures, because previous studies have shown that 
      BDNF has acute effects on dentate granule cell synaptic transmission, and other 
      studies have demonstrated that BDNF expression increases in granule cells after 
      seizures. Pilocarpine-treated rats were studied because they not only have 
      seizures and increased BDNF expression in granule cells, but they also have 
      reorganization of granule cell "mossy fiber" axons. This reorganization, referred 
      to as "sprouting," involves collaterals that grow into novel areas, i.e., the 
      inner molecular layer, where granule cell and interneuron dendrites are located. 
      Thus, this animal model allowed us to address the effects of BDNF in the dentate 
      gyrus after seizures, as well as the actions of BDNF on mossy fiber transmission 
      after reorganization. In slices with sprouting, BDNF bath application enhanced 
      responses recorded in the inner molecular layer to mossy fiber stimulation. 
      Spontaneous bursts of granule cells occurred, and these were apparently generated 
      at the site of the sprouted axon plexus. These effects were not accompanied by 
      major changes in perforant path-evoked responses or paired-pulse inhibition, 
      occurred only after prolonged (30-60 min) exposure to BDNF, and were blocked by 
      K252a. The results suggest a preferential action of BDNF at mossy fiber synapses, 
      even after substantial changes in the dentate gyrus network. Moreover, the 
      results suggest that activation of trkB receptors could contribute to the 
      hyperexcitability observed in animals with sprouting. Because human granule cells 
      also express increased BDNF mRNA after seizures, and sprouting can occur in 
      temporal lobe epileptics, the results may have implications for understanding 
      temporal lobe epilepsy.
FAU - Scharfman, H E
AU  - Scharfman HE
AD  - Neurology Research Center, Helen Hayes Hospital, West Haverstraw, New York 
      10993-1195, USA.
FAU - Goodman, J H
AU  - Goodman JH
FAU - Sollas, A L
AU  - Sollas AL
LA  - eng
GR  - R01 NS037562/NS/NINDS NIH HHS/United States
GR  - R01 NS037562-03/NS/NINDS NIH HHS/United States
GR  - R56 NS037562/NS/NINDS NIH HHS/United States
GR  - NS 37562/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (GABA Antagonists)
RN  - 0 (Neuropeptide Y)
RN  - 0 (Receptor, Ciliary Neurotrophic Factor)
RN  - 0 (Receptors, GABA)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 01MI4Q9DI3 (Pilocarpine)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
SB  - IM
MH  - Action Potentials/drug effects
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/analysis/*pharmacology
MH  - Cell Size/drug effects
MH  - Epilepsy/chemically induced/metabolism/pathology
MH  - Excitatory Postsynaptic Potentials/drug effects
MH  - GABA Antagonists/pharmacology
MH  - In Vitro Techniques
MH  - Male
MH  - Mossy Fibers, Hippocampal/chemistry/drug effects/pathology/*physiopathology
MH  - Neuropeptide Y/analysis
MH  - Pilocarpine/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism
MH  - Receptor, Ciliary Neurotrophic Factor
MH  - Receptors, GABA/physiology
MH  - Receptors, N-Methyl-D-Aspartate/agonists/antagonists & inhibitors/physiology
MH  - Receptors, Nerve Growth Factor/antagonists & inhibitors/metabolism
MH  - Seizures/chemically induced/metabolism/*pathology
MH  - Status Epilepticus/chemically induced/metabolism/pathology
MH  - Synapses/drug effects/physiology
MH  - Synaptic Transmission/*drug effects
PMC - PMC2504498
MID - NIHMS59826
EDAT- 1999/06/23 00:00
MHDA- 1999/06/23 00:01
PMCR- 2000/01/01
CRDT- 1999/06/23 00:00
PHST- 1999/06/23 00:00 [pubmed]
PHST- 1999/06/23 00:01 [medline]
PHST- 1999/06/23 00:00 [entrez]
PHST- 2000/01/01 00:00 [pmc-release]
AID - 3167 [pii]
AID - 10.1523/JNEUROSCI.19-13-05619.1999 [doi]
PST - ppublish
SO  - J Neurosci. 1999 Jul 1;19(13):5619-31. doi: 10.1523/JNEUROSCI.19-13-05619.1999.