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Volume 17, Number 6,
Issue of March 15, 1997
pp. 1940-1949
Copyright ©1997 Society for Neuroscience
Opposite Membrane Potential Changes Induced by Glucose
Deprivation in Striatal Spiny Neurons and in Large Aspiny
Interneurons
Received Oct. 21, 1996; revised Jan. 2, 1997; accepted Jan. 7, 1997.
Paolo Calabresi1,
Carlos Magarinos Ascone1,
Diego Centonze1,
Antonio Pisani1, 2,
Giuseppe Sancesario1,
Vincenza D'Angelo1, and
Giorgio Bernardi1, 2
1 Clinica Neurologica, Dip. Sanitá,
Universitá di Roma Tor Vergata, 00173 Rome, Italy, and
2 IRCCS Ospedale S. Lucia, Via Ardeatina, Rome, Italy
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.
Key words:
aglycemia;
ischemia;
excitatory amino acids;
neuronal
death;
striatum;
interneurons
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