Relative Resistance of Striatal Neurons Containing Calbindin or Parvalbumin to Quinolinic Acid-Mediated Excitotoxicity Compared to Other Striatal Neuron Types

Mar 17, 1998Experimental neurology

Striatal neurons with calbindin or parvalbumin show more resistance to quinolinic acid damage than other striatal neurons

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Abstract

Calbindin-rich striatal neurons showed significantly enhanced survival just outside the lesion center after excitotoxic insult.

Parvalbumin-rich and calbindin-rich neurons exhibited a comparable gradient of loss following the injection of the excitotoxin quinolinic acid.
Striatal interneurons containing somatostatin-neuropeptide Y were more vulnerable to the excitotoxic effects than the other neuron types studied.
Calbindin does not entirely prevent vulnerability to excitotoxicity in striatal projection neurons.
Cholinergic striatal interneurons were noted to be highly resistant to the excitotoxic insult despite lacking calcium buffering proteins.
The findings suggest that calbindin may provide some protection against moderate excitotoxic insults, possibly explaining increased vulnerability in neurons low in calbindin.

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To evaluate the relative ability of those striatal neuron types containing calbindin or parvalbumin to withstand a Ca(2+)-mediated excitotoxic insult, we injected the NMDA receptor-specific excitotoxin quinolinic acid (QA) into the striatum in mature adult rats and 2 months later examined the relative survival of striatal interneurons rich in parvalbumin and striatal projection neurons rich in calbindin. To provide standardization to the survival of striatal neuron types thought to be poor in Ca2+ buffering proteins, the survival was compared to that of somatostatin-neuropeptide Y (SS/NPY)-containing interneurons and enkephalinergic projection neurons, which are devoid of or relatively poorer in such proteins. The various neuron types were identified by immunohistochemical labeling for these type-specific markers and their relative survival was compared at each of a series of increasing distances from the injection center. In brief, we found that parvalbuminergic, calbindinergic, and enkephalinergic neurons all showed a generally comparable gradient of neuronal loss, except just outside the lesion center, where calbindin-rich neurons showed significantly enhanced survival. In contrast, striatal SS/NPY interneurons were more vulnerable to QA than any of these three other types. These observed patterns of survival following intrastriatal QA injection suggest that calbindin and parvalbumin content does not by itself determine the vulnerability of striatal neurons to QA-mediated excitotoxicity in mature adult rats. For example, parvalbuminergic striatal interneurons were not impervious to QA, while cholinergic striatal interneurons are highly resistant and SS/NPY+ striatal interneurons are highly vulnerable. Both cholinergic and SS/NPY+ interneurons are devoid of any known calcium buffering protein. Similarly, calbindin does not prevent striatal projection neuron vulnerability to QA excitotoxicity. Nonetheless, our data do suggest that calbindin may offer striatal neurons some protection against moderate excitotoxic insults, and this may explain the reportedly slightly greater vulnerability of striatal neurons that are poor in calbindin to ischemia and Huntington's disease.

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Relative Resistance of Striatal Neurons Containing Calbindin or Parvalbumin to Quinolinic Acid-Mediated Excitotoxicity Compared to Other Striatal Neuron Types

Abstract

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