Opposite membrane potential changes induced by glucose deprivation in striatal spiny neurons and in large aspiny interneurons

Paolo Calabresi, Carlos Magarinos Ascone, Diego Centonze, Antonio Pisani, Giuseppe Sancesario, Vincenza D'Angelo, Giorgio Bernardi

Research output: Contribution to journalArticle

Abstract

We have studied the electrophysiological effects of glucose deprivation on morphologically identified striatal neurons recorded from a corticostriatal slice preparation. The large majority of the recorded cells were spiny neurons and responded to aglycemia with a slow membrane depolarization coupled with a reduction of the input resistance. In voltage- clamp experiments aglycemia caused an inward current. This current was associated with a conductance increase and reversed at -40 mV. The aglycemia- induced membrane depolarization was not affected by tetrodotoxin (TTX) or 6- cyano-7-nitroquinoxaline-2,3-dione plus aminophosphonovalerate, antagonists acting respectively on AMPA and NMDA glutamate receptors. Also, the intracellular injection of bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetic acid, a calcium (Ca2+) chelator, and low Ca2+/high Mg2+-containing solutions failed to reduce this phenomenon. Conversely, it was reduced by lowering external sodium (Na+) concentration. A minority of the recorded cells had the morphological characteristics of large aspiny interneurons and the electrophysiological properties of 'long-lasting afterhyperpolarization (LA) cells.' These cells responded to aglycemia with a membrane hyperpolarization/outward current that was coupled with an increased conductance. This current was not altered by TTX, blockers of ATP-dependent potassium (K+) channels, and adenosine A1 receptor antagonists, whereas it was reduced by solutions containing low Ca2+/high Mg2+. This current reversed at -105 mV and was blocked by barium, suggesting the involvement of a K+ conductance. We suggest that the opposite membrane responses of striatal neuronal subtypes to glucose deprivation might account for their differential neuronal vulnerability to aglycemia and ischemia.

Original languageEnglish
Pages (from-to)1940-1949
Number of pages10
JournalJournal of Neuroscience
Volume17
Issue number6
Publication statusPublished - Mar 15 1997

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Corpus Striatum
Interneurons
Membrane Potentials
Neurons
Glucose
Membranes
Tetrodotoxin
Adenosine A1 Receptor Antagonists
6-Cyano-7-nitroquinoxaline-2,3-dione
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
Ethane
Potassium Channels
Glutamate Receptors
Barium
N-Methyl-D-Aspartate Receptors
Acetic Acid
Ischemia
Adenosine Triphosphate
Sodium
Injections

Keywords

  • aglycemia
  • excitatory amino acids
  • interneurons
  • ischemia
  • neuronal death
  • striatum

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Opposite membrane potential changes induced by glucose deprivation in striatal spiny neurons and in large aspiny interneurons. / Calabresi, Paolo; Magarinos Ascone, Carlos; Centonze, Diego; Pisani, Antonio; Sancesario, Giuseppe; D'Angelo, Vincenza; Bernardi, Giorgio.

In: Journal of Neuroscience, Vol. 17, No. 6, 15.03.1997, p. 1940-1949.

Research output: Contribution to journalArticle

Calabresi, Paolo ; Magarinos Ascone, Carlos ; Centonze, Diego ; Pisani, Antonio ; Sancesario, Giuseppe ; D'Angelo, Vincenza ; Bernardi, Giorgio. / Opposite membrane potential changes induced by glucose deprivation in striatal spiny neurons and in large aspiny interneurons. In: Journal of Neuroscience. 1997 ; Vol. 17, No. 6. pp. 1940-1949.
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