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Muscarinic M1, M3, Nicotinic,GABAA and GABAB Receptor ...

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al., 2004). GAD expression, a marker of GABAergic activity showed decreased<br />

expression in corpus striatum. GABA receptors decreased in hypoglycemic rats.<br />

Decreased GABA-mediated inhibition in the corpus striatum is attributed to<br />

changes in biosynthetic capacity of the GAD present (Raza et al., 1994). <strong>GABAA</strong>α1<br />

<strong>and</strong> <strong>GABAB</strong> receptor subtype expression showed down regulation in<br />

hypoglycemic rats compared to diabetic <strong>and</strong> control rats. Results were confirmed<br />

by immunohistochemical study. All classes of striatal neurons receive prominent<br />

inhibitory GABAergic inputs. These inhibitory interactions are likely to be<br />

essential for striatal processing (Waldvogel et al., 2004). Hypoglycemia induced<br />

decrease in GABAergic function thus impairs striatal inhibitory function. It is<br />

suggested that GABAergic inhibition in the striatum is one of the mechanisms that<br />

normally prevent excessive movements (Nakamura et al., 1990; Yoshida et al.,<br />

1991). Reduced inhibition in the striatum contributes to movement disorders such<br />

as some forms of dystonia (Kreil & Richter, 2005) or myoclonus (Darbin et al.,<br />

2000).<br />

GABAergic inputs to striatal interneurons also originate from several<br />

sources <strong>and</strong> GABA receptor blockade at these sites, counteracting an ambient<br />

GABAergic tone that contributed to the changes in neuronal spiking. Cholinergic<br />

interneurons receive GABAergic input predominately from Medium Spiny<br />

Neurons collaterals (Martone et al., 1992). GABAergic inhibition in the striatum<br />

also act to inhibit seizure generation (Dematteis et al., 2003) or propagation<br />

(Sasaki et al., 2000; Benedek et al., 2004; Biraben et al., 2004; Bouilleret et al.,<br />

2005;). Short-term <strong>and</strong> long-term regulation of corticostriatal synaptic efficacy is<br />

critical in some pathophysiological conditions <strong>and</strong> an altered corticostriatal<br />

synaptic activity has been implicated in neurodegenerative diseases (Calabresi et<br />

al., 1998). Modulations of striatal GABA levels therefore represent a<br />

pharmacological target of interest in the treatment of movement disorders <strong>and</strong><br />

seizures. Our results showed decreased GABA receptors in the striatum of the<br />

hypoglycemic rats. This decreased GABA receptors facilitate the rapid spread of<br />

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