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

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Discussion
modulate the second messenger responses to other neurotransmitters such as
noradrenaline and 5-hydroxytryptamine (Karbon et al.,, 1984).
The cellular basis of motor learning has been mostly attributed to long
term depression (LTD) at excitatory parallel fiber (PF)-Purkinje cell (PC)
synapses. LTD is induced when PFs are activated in conjunction with a climbing
fiber (CF), the other excitatory input to PCs. Recently, by using whole-cell patchclamp
recording from PCs in cerebellar slices, a new form of synaptic plasticity
was discovered. Stimulation of excitatory CFs induced a long-lasting rebound
potentiation (RP) of GABAA receptor mediated inhibitory postsynaptic currents
(IPSCs) (Bibiana et al., 2008; Peer et al., 2009). Purkinje cells express a high
density of GABAB receptor, a Gi/o-protein-coupled receptor for the inhibitory
neurotransmitter GABA (Kuner et al., 1999). As the entire output of the cerebellar
cortex is carried by the firing of Purkinje cells, any mechanism able to modulate
the firing pattern of Purkinje cells will influence cerebellar function. Purkinje cells
fire spontaneously, even in the absence of glutamate input and the pattern of firing
is very strongly influenced by high conductance, high frequency GABAergic
inputs (Hausser & Clark, 1997). Considering the importance of GABA
transmission in influencing Purkinje cell firing (Kanjhan et al., 1999), decreased
GABA receptor expression in cerebellum is suggested to affect GABAergic
transmission. Immunohistochemical studies using specific antibodies of GABAAα1
have proved the decreased expression status of this receptor subtype in the
cerebellum. In the present study, behavioural study using grid walk test showed
impaired motor performance in hypoglycemic rats. Reduction in spontaneous
motor activity follows recurrent hypoglycemia is reported by Duncan et al (2010).
Loss of coordination of motor movement, inability to judge distance and timing,
incapacity to perform rapid alternating movements, and hypotonia have been
reported during cerebellar damage (Blumer et al., 2004) and hypoglycemic
induced cerebellar dysfunction . These studies indicate that during hypoglycemic
stress, the subunits of GABA receptors assemble in different combinations with