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

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Literature Review
nicotinic acetylcholine receptor in the brain, consisting entirely of α7 subunits
(Rang et al., 2003). As with other nicotinic acetylcholine receptors, functional α7
receptors are pentameric i.e., (α7)5 stoichiometry. It is located in the brain, where
activation yields post- and presynaptic excitation (Rang et al., 2003), mainly by
increased Ca 2+ permeability.
Neuronal nicotinic cholinergic receptors are crucial to acetylcholine
neurotransmission in both the CNS and autonomic nervous system. However, in
the CNS, these receptors are more often associated with modulation of release of
several neurotransmitters including dopamine, norepinephrine, GABA and
glutamate (Alkondon et al., 1999; Girod & Role, 2001). In the CNS, nicotinic
acetylcholine receptors mediate the release of glutamate (De Filippi et al., 2001;
Rossi et al., 2003; Reno et al., 2004) and norepinephrine (O Leary & Leslie,
2003). Thus, these receptors significantly influence the activity within the CNS
circuitry and deregulation of this activity could contribute to disorders involving
the CNS. Abnormalities of nicotinic acetylcholine receptor function in the
hippocampus lead to cognitive and memory impairments (Green et al., 2005;
Levin et al., 2002) and sensory gating deficits (Adler et al., 1998). Nicotinic
acetylcholine receptors are involved with neuroplastic responses, such as dendritic
growth in cholinoceptive neurons (Torrao et al., 2003).
GABA regulation of glucose homeostasis
GABA is a major inhibitory neurotransmitter in the mammalian central
nervous system (CNS) and is synthesized from glutamic acid by glutamic acid
decarboxylase (GAD) (Gerber & Hare , 1979). There is significant ongoing work
aimed at understanding the specific roles of synaptic and extrasynaptic GABA in
regulating neural activity in both normal and pathological conditions. Precise
GABAergic synaptic signaling is critical to the accurate transmission of
information within neural circuits and even slight disruptions can produce
hypersynchronous activity (Chagnac-Amitai & Connors, 1989). Moreover,