A New Specific Neuronal Modulatory Effect Of Nicotine: The Functional Cross Talk Between Nicotinic And Glutamate Receptors

1080 words - 5 pages

The nicotinic acetylcholine receptors (nAChRs) are fast ionotropic receptor channels present and widely distributed throughout the central nervous system (CNS) of mammals. This class includes several receptor subtypes with different pharmacological and physiological features which mainly depend on their subunits composition [1,2]. In the CNS, these receptors subtypes are expressed and functionally operating mostly at the membrane level in neurons or glial cells, where - when activated- they modulate the release of many neurotransmitters [3,4]. Their stimulatory effect, which is in turn linked to the permeability to cations [5], may be different according to the specific receptor subtypes ...view middle of the document...

We provided immunocytochemical and neurochemical evidences supporting the co-localization and the functional interaction between nAChRs and NMDA receptors in dopaminergic terminals of the rat nucleus accumbens. We showed that brief pretreatment in vitro with nicotine for few minutes decreased the NMDA-induced dopamine release from nucleus accumbens nerve terminals, indicating that the recruitment of nAChRs dynamically and negatively regulates NMDA receptors through the selective internalization of GluN2B-NMDA receptors.
Inasmuch, in a previous paper, our group had also demonstrated that nicotine caused a decrease of the amount of neuronal α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors present in the same dopaminergic nerve terminals [19]. This effect was found to be selective for AMPA receptors located on noradrenergic nerve endings [20], and did not occur to AMPA receptors present on gamma-aminobutyric acid (GABA) and cholinergic nerve terminals [21]. Likewise, the modulatory action of nicotine has been associated to the internalization of the GluA2 subunit of the AMPA receptors. Interestingly, the nAChR involved in dopamine release in the nucleus accumbens belongs to several nAChR subtypes (likely α6β3β2, α6α4β3β2, α4β2 and/or α4α5β2) [22] but not to the α7 nAChR subtype. These studies have been extended to explore whether the nicotine-glutamate receptors cross-talk concerns also the modulation of other neurotransmitters such as glutamate and GABA, whose release is also stimulated by α7 nAChR subtypes [9,23] and by glutamatergic NMDA and AMPA receptors [21,24]. The results are very striking and show that this modulatory action seems to be selective and involve some receptor systems and not others (unpublished observations).
These events can be summarized with the term “metamodulation” (as proposed by Katz and Edwards in the late 1990) [25]. Metamodulation refers to the possibility that different neurotransmitters can cooperate to modulate neurotransmission in the CNS. Actually, although neurotransmitters are often analyzed individually for their mediated effects, it is largely recognized that they can cooperate to reciprocally interact in controlling neuronal activity. The complexity that originates from that converging action is impressive and might account for the modulation of synaptic plasticity in selected CNS regions. For instance, the pharmacological effect exerted by nicotine described here reduces glutamate-induced release of dopamine by favoring NMDA or AMPA ...

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