PMID- 11730978
OWN - NLM
STAT- MEDLINE
DCOM- 20020307
LR  - 20190901
IS  - 0167-0115 (Print)
IS  - 0167-0115 (Linking)
VI  - 102
IP  - 2-3
DP  - 2001 Dec 15
TI  - Glutamate release from adult primary sensory neurons in culture is modulated by 
      growth factors.
PG  - 69-79
AB  - The aim of this study was to examine possible modulatory effects of some trophic 
      molecules, i.e. nerve growth factor (NGF), brain-derived neurotrophic factor 
      (BDNF) and basic fibroblast growth factor (bFGF), on potassium (K(+))-, 
      bradykinin (BK)- or capsaicin (CAPS)-evoked release of glutamate (GLU) from 
      dorsal root ganglion (DRG) neurons in vitro. BK (0.5 and 1 microM) induced a 
      dramatic and significant increase in glutamate release. Neither CAPS nor K(+) (60 
      mM) produced any significant increase of GLU release vs. basal levels during a 
      5-min stimulation. The BK-evoked release of GLU was almost completely blocked by 
      HOE 140, a selective BK2-receptor antagonist at high doses. Basal release of GLU 
      was significantly reduced in cultures grown in the presence of bFGF, whereas BDNF 
      and NGF had no significant effect. Incubation with growth factors generally 
      decreased the BK-stimulated GLU release, an effect most pronounced for bFGF, 
      which completely blocked BK-stimulated release. The rise in intracellular 
      [Ca(2+)] following stimulation with BK (100 nM-1 microM), potassium (60 mM) or 
      ATP (10 microM) was also studied using a Ca(2+)-sensitive indicator, Fura-2, in 
      cultures grown in basal medium with or without bFGF. None of the bFGF-treated 
      cells exhibited strong Ca(2+) responses to BK or ATP stimulation, while 10-20% of 
      the responding cells grown in basal medium exhibited strong responses. The 
      K(+)-induced increase of [Ca(2+)] did not vary between the different groups. The 
      present findings suggest that sensory neurotransmission involving glutamate may 
      be modulated by growth factors and that regulation of intracellular Ca(2+) 
      homeostasis may be a contributing factor.
FAU - Rydh-Rinder, M
AU  - Rydh-Rinder M
AD  - AstraZeneca, S-151 85 Sodertalje, Sweden.
FAU - Kerekes, N
AU  - Kerekes N
FAU - Svensson, M
AU  - Svensson M
FAU - Hokfelt, T
AU  - Hokfelt T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Regul Pept
JT  - Regulatory peptides
JID - 8100479
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Growth Substances)
RN  - 0 (Neuroprotective Agents)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - RWP5GA015D (Potassium)
RN  - S07O44R1ZM (Capsaicin)
RN  - S8TIM42R2W (Bradykinin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Bradykinin/pharmacology
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Calcium/metabolism
MH  - Capsaicin/pharmacology
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Fibroblast Growth Factor 2/pharmacology
MH  - Ganglia, Spinal/cytology
MH  - Glutamic Acid/*metabolism
MH  - Growth Substances/*pharmacology
MH  - Immunohistochemistry
MH  - Male
MH  - Microscopy, Fluorescence
MH  - Nerve Growth Factor/pharmacology
MH  - Neuroglia/cytology/drug effects/metabolism
MH  - Neuronal Plasticity
MH  - Neurons, Afferent/cytology/*drug effects/metabolism
MH  - Neuroprotective Agents/pharmacology
MH  - Potassium/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sciatic Nerve/cytology
EDAT- 2001/12/04 10:00
MHDA- 2002/03/08 10:01
CRDT- 2001/12/04 10:00
PHST- 2001/12/04 10:00 [pubmed]
PHST- 2002/03/08 10:01 [medline]
PHST- 2001/12/04 10:00 [entrez]
AID - S016701150100297X [pii]
AID - 10.1016/s0167-0115(01)00297-x [doi]
PST - ppublish
SO  - Regul Pept. 2001 Dec 15;102(2-3):69-79. doi: 10.1016/s0167-0115(01)00297-x.