PMID- 16928864
OWN - NLM
STAT- MEDLINE
DCOM- 20060928
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 26
IP  - 34
DP  - 2006 Aug 23
TI  - Corticosterone-sensitive monoamine transport in the rat dorsomedial hypothalamus: 
      potential role for organic cation transporter 3 in stress-induced modulation of 
      monoaminergic neurotransmission.
PG  - 8758-66
AB  - Glucocorticoid hormones act within the brain to alter physiological and 
      behavioral responses to stress-related stimuli. Previous studies indicated that 
      acute stressors can increase serotonin [5-hydroxytryptamine (5-HT)] 
      concentrations in the dorsomedial hypothalamus (DMH), a midline hypothalamic 
      structure involved in the integration of physiological and behavioral responses 
      to stress. The current study tests the hypothesis that rapid, stress-induced 
      accumulation of 5-HT is attributable to the inhibition of 5-HT transport via 
      organic cation transporters (OCTs). OCTs are a family of high-capacity, 
      bidirectional, multispecific transporters of organic cations (including 5-HT, 
      dopamine, and norepinephrine) only recently described in brain. In peripheral 
      tissues, organic cation transport via some OCTs is inhibited by corticosterone. 
      We examined the expression and function of OCTs in the periventricular medial 
      hypothalamus of male Sprague Dawley rats using reverse-transcriptase (RT)-PCR, 
      immunohistochemistry, and in vitro transport assays. RT-PCR revealed expression 
      of OCT3 mRNA, but not OCT1 or OCT2 mRNA, in the medial hypothalamus. OCT3-like 
      immunoreactivity was observed in ependymal and glial-like cells in the DMH. 
      Acutely prepared minces of rat medial hypothalamic tissue accumulated the OCT 
      substrates [3H]-histamine and [3H]-N-methyl-4-phenylpyridinium ([3H]-MPP+). 
      Consistent with the pharmacological profile of OCT3, corticosterone, 5-HT, 
      estradiol, and the OCT inhibitor decynium22 dose-dependently inhibited histamine 
      accumulation. Corticosterone and decynium22 also inhibited efflux of [3H]-MPP+ 
      from hypothalamic minces. These data support the hypothesis that 
      corticosterone-induced inhibition of OCT3 mediates stress-induced accumulation of 
      5-HT in the DMH and suggest that corticosterone may acutely modulate 
      physiological and behavioral responses to stressors by altering serotonergic 
      neurotransmission in this brain region.
FAU - Gasser, Paul J
AU  - Gasser PJ
AD  - School of Life Sciences, Arizona State University, Tempe, Arizona 85287-4501, 
      USA. paul.gasser@bristol.ac.uk
FAU - Lowry, Christopher A
AU  - Lowry CA
FAU - Orchinik, Miles
AU  - Orchinik M
LA  - eng
GR  - Wellcome Trust/United Kingdom
GR  - RCDF 068558/Z/02/Z/WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-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 (Biogenic Monoamines)
RN  - 0 (Organic Cation Transport Proteins)
RN  - 0 (solute carrier family 22 (organic cation transporter), member 3)
RN  - 820484N8I3 (Histamine)
RN  - R865A5OY8J (1-Methyl-4-phenylpyridinium)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - 1-Methyl-4-phenylpyridinium/pharmacokinetics
MH  - Animals
MH  - Biogenic Monoamines/*metabolism
MH  - Biological Transport/drug effects
MH  - Corticosterone/*pharmacology
MH  - Histamine/pharmacokinetics
MH  - Hypothalamus/*metabolism
MH  - Male
MH  - Organic Cation Transport Proteins/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Stress, Physiological/*physiopathology
MH  - *Synaptic Transmission
MH  - Tissue Distribution
PMC - PMC6674371
EDAT- 2006/08/25 09:00
MHDA- 2006/09/29 09:00
PMCR- 2007/02/23
CRDT- 2006/08/25 09:00
PHST- 2006/08/25 09:00 [pubmed]
PHST- 2006/09/29 09:00 [medline]
PHST- 2006/08/25 09:00 [entrez]
PHST- 2007/02/23 00:00 [pmc-release]
AID - 26/34/8758 [pii]
AID - 3142480 [pii]
AID - 10.1523/JNEUROSCI.0570-06.2006 [doi]
PST - ppublish
SO  - J Neurosci. 2006 Aug 23;26(34):8758-66. doi: 10.1523/JNEUROSCI.0570-06.2006.