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

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

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during experimental condition. Various anatomical, electrophysiological <strong>and</strong><br />

pathological observations provide evidence that ACh plays a major role in the<br />

control of striatal function <strong>and</strong> in the regulation of motor control (Jabbari et al.,<br />

1989). The results of confocal studies confirmed the alterations of muscarinic <strong>M1</strong><br />

<strong>and</strong> <strong>M3</strong> receptor at protein level which mediated neuronal damage during<br />

condition of glucose deprivation induced by hypoglycemia. It is widely accepted<br />

that certain brain regions <strong>and</strong> specific neuronal cell types express differential<br />

sensitivity to hypoglycemic insults during glucose deprivation <strong>and</strong> striatal neurons<br />

are particularly prone to develop neuronal damage under energy deprivation<br />

(Haddad & Jiang, 1993). <strong>M1</strong> receptors are responsible for the presynaptic<br />

inhibition of GABA release while <strong>M3</strong> receptors exert an inhibitory control on the<br />

release of glutamate in the striatum (Sugita et al., 1991). These studies shows the<br />

importance of maintaining synaptic neurotransmission mediated though<br />

muscarinic <strong>M1</strong>, <strong>M3</strong> receptor subtypes which were found to be affected by<br />

recurrent hypoglycemia during diabetes.<br />

CNS mAChRs regulate a large number of important central functions<br />

including cognitive, behavioural, sensory, motor <strong>and</strong> autonomic processes (Felder<br />

et al., 2000; Eglen, 2005). The striatum also expresses high sensitivity to<br />

hypoglycemic insults. During these pathological conditions, striatal synaptic<br />

transmission is altered depending on presynaptic inhibition of transmitter release<br />

<strong>and</strong> opposite membrane potential changes occur in neurones <strong>and</strong> in cholinergic<br />

interneurones (Calabresi et al., 2000) . Involvement of muscarinic <strong>M3</strong> receptor in<br />

the presynaptic inhibition of synaptic transmission at excitatory synapses results in<br />

a decrease in neurotransmitter release <strong>and</strong> synaptic activity (Washburn & Moises,<br />

1992). The high sensitivity of striatal spiny neurons to energy deprivation is<br />

expressed as a disruption of intrinsic membrane properties as well as an alteration<br />

of synaptic characteristics of the recorded cells (Xu, 1995). The present study on<br />

total muscarinic, muscarinic <strong>M1</strong>, <strong>M3</strong> receptor expression levels in corpus striatum<br />

113

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