PMID- 22723672
OWN - NLM
STAT- MEDLINE
DCOM- 20130111
LR  - 20211021
IS  - 1522-1598 (Electronic)
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 108
IP  - 6
DP  - 2012 Sep
TI  - Rapid fluctuations in extracellular brain glucose levels induced by natural 
      arousing stimuli and intravenous cocaine: fueling the brain during neural 
      activation.
PG  - 1669-84
LID - 10.1152/jn.00521.2012 [doi]
AB  - Glucose, a primary energetic substrate for neural activity, is continuously 
      influenced by two opposing forces that tend to either decrease its extracellular 
      levels due to enhanced utilization in neural cells or increase its levels due to 
      entry from peripheral circulation via enhanced cerebral blood flow. How this 
      balance is maintained under physiological conditions and changed during neural 
      activation remains unclear. To clarify this issue, enzyme-based glucose sensors 
      coupled with high-speed amperometry were used in freely moving rats to evaluate 
      fluctuations in extracellular glucose levels induced by brief audio stimulus, 
      tail pinch (TP), social interaction with another rat (SI), and intravenous 
      cocaine (1 mg/kg). Measurements were performed in nucleus accumbens (NAcc) and 
      substantia nigra pars reticulata (SNr), which drastically differ in neuronal 
      activity. In NAcc, where most cells are powerfully excited after salient 
      stimulation, glucose levels rapidly (latency 2-6 s) increased (30-70 muM or 6-14% 
      over baseline) by all stimuli; the increase differed in magnitude and duration 
      for each stimulus. In SNr, where most cells are transiently inhibited by salient 
      stimuli, TP, SI, and cocaine induced a biphasic glucose response, with the 
      initial decrease (-20-40 muM or 5-10% below baseline) followed by a reboundlike 
      increase. The critical role of neuronal activity in mediating the initial glucose 
      response was confirmed by monitoring glucose currents after local microinjections 
      of glutamate (GLU) or procaine (PRO). While intra-NAcc injection of GLU 
      transiently increased glucose levels in this structure, intra-SNr PRO injection 
      resulted in rapid, transient decreases in SNr glucose. Therefore, extracellular 
      glucose levels in the brain change very rapidly after physiological and 
      pharmacological stimulation, the response is structure specific, and the pattern 
      of neuronal activity appears to be a critical factor determining direction and 
      magnitude of physiological fluctuations in glucose levels.
FAU - Kiyatkin, Eugene A
AU  - Kiyatkin EA
AD  - In-Vivo Electrophysiology Unit, Behavioral Neuroscience Branch, National 
      Institute on Drug Abuse-Intramural Research Program, NIH, DHHS, 333 Cassell Dr., 
      Baltimore, MD 21224, USA. ekiyatki@intra.nida.nih.gov
FAU - Lenoir, Magalie
AU  - Lenoir M
LA  - eng
GR  - Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
DEP - 20120620
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 4Z8Y51M438 (Procaine)
RN  - I5Y540LHVR (Cocaine)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Administration, Intravenous
MH  - Animals
MH  - Arousal/*physiology
MH  - Brain/metabolism
MH  - Cocaine/administration & dosage/*pharmacology
MH  - Extracellular Space/chemistry/metabolism
MH  - Glucose/analysis/*metabolism
MH  - Glutamic Acid/pharmacology
MH  - Male
MH  - Neurons/physiology
MH  - Nucleus Accumbens/*metabolism/physiology
MH  - Procaine/pharmacology
MH  - Rats
MH  - Rats, Long-Evans
MH  - Social Environment
MH  - Substantia Nigra/*metabolism/physiology
MH  - Touch
PMC - PMC3544950
EDAT- 2012/06/23 06:00
MHDA- 2013/01/12 06:00
PMCR- 2013/09/15
CRDT- 2012/06/23 06:00
PHST- 2012/06/23 06:00 [entrez]
PHST- 2012/06/23 06:00 [pubmed]
PHST- 2013/01/12 06:00 [medline]
PHST- 2013/09/15 00:00 [pmc-release]
AID - jn.00521.2012 [pii]
AID - JN-00521-2012 [pii]
AID - 10.1152/jn.00521.2012 [doi]
PST - ppublish
SO  - J Neurophysiol. 2012 Sep;108(6):1669-84. doi: 10.1152/jn.00521.2012. Epub 2012 
      Jun 20.