PMID- 23785079
OWN - NLM
STAT- MEDLINE
DCOM- 20131028
LR  - 20211021
IS  - 1522-1490 (Electronic)
IS  - 0363-6119 (Print)
IS  - 0363-6119 (Linking)
VI  - 305
IP  - 4
DP  - 2013 Aug 15
TI  - Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular 
      neurosecretory neurons in heart failure rats.
PG  - R414-22
LID - 10.1152/ajpregu.00160.2013 [doi]
AB  - An enhanced glutamate excitatory function within the hypothalamic supraoptic and 
      paraventricluar nuclei is known to contribute to increased neurosecretory and 
      presympathetic neuronal activity, and hence, neurohumoral activation, during 
      heart failure (HF). Still, the precise mechanisms underlying enhanced 
      glutamate-driven neuronal activity in HF remain to be elucidated. Here, we 
      performed simultaneous electrophysiology and fast confocal Ca(2)(+) imaging to 
      determine whether altered N-methyl-d-aspartate (NMDA) receptor-mediated changes 
      in intracellular Ca(2)(+) levels (NMDA-DeltaCa(2)(+)) occurred in hypothalamic magnocellular 
      neurosecretory cells (MNCs) in HF rats. We found that activation of NMDA 
      receptors resulted in a larger DeltaCa(2)(+) in MNCs from HF when compared with sham 
      rats. The enhanced NMDA-DeltaCa(2)(+) was neither dependent on the magnitude of the 
      NMDA-mediated current (voltage clamp) nor on the degree of membrane 
      depolarization or firing activity evoked by NMDA (current clamp). Differently 
      from NMDA receptor activation, firing activity evoked by direct membrane 
      depolarization resulted in similar changes in intracellular Ca(2)(+) in sham and HF 
      rats. Taken together, our results support a relatively selective alteration of 
      intracellular Ca(2)(+) homeostasis and signaling following activation of NMDA 
      receptors in MNCs during HF. The downstream functional consequences of such 
      altered DeltaCa(2)(+) signaling during HF are discussed.
FAU - Stern, Javier E
AU  - Stern JE
AD  - Department of Physiology, Georgia Regents University, Augusta, Georgia.
FAU - Potapenko, Evgeniy S
AU  - Potapenko ES
LA  - eng
GR  - R01 HL-090948/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130619
PL  - United States
TA  - Am J Physiol Regul Integr Comp Physiol
JT  - American journal of physiology. Regulatory, integrative and comparative 
      physiology
JID - 100901230
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 6384-92-5 (N-Methylaspartate)
SB  - IM
MH  - Action Potentials
MH  - Animals
MH  - *Calcium Signaling/drug effects
MH  - Disease Models, Animal
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Feedback, Physiological
MH  - Heart Failure/*metabolism/physiopathology
MH  - Hypothalamus/drug effects/*metabolism/physiopathology
MH  - Male
MH  - Microscopy, Confocal
MH  - N-Methylaspartate/pharmacology
MH  - Neurons/drug effects/*metabolism
MH  - Patch-Clamp Techniques
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, N-Methyl-D-Aspartate/agonists/*metabolism
MH  - Time Factors
PMC - PMC3833393
OTO - NOTNLM
OT  - Ca2+
OT  - NMDA
OT  - glutamate
OT  - supraoptic
OT  - vasopressin
EDAT- 2013/06/21 06:00
MHDA- 2013/10/29 06:00
PMCR- 2014/08/15
CRDT- 2013/06/21 06:00
PHST- 2013/06/21 06:00 [entrez]
PHST- 2013/06/21 06:00 [pubmed]
PHST- 2013/10/29 06:00 [medline]
PHST- 2014/08/15 00:00 [pmc-release]
AID - ajpregu.00160.2013 [pii]
AID - R-00160-2013 [pii]
AID - 10.1152/ajpregu.00160.2013 [doi]
PST - ppublish
SO  - Am J Physiol Regul Integr Comp Physiol. 2013 Aug 15;305(4):R414-22. doi: 
      10.1152/ajpregu.00160.2013. Epub 2013 Jun 19.