J.-J.L. and C.A.M. contributed equally to this work.
Chronic nicotine exposure during adolescence differentially influences calcium-binding proteins in rat anterior cingulate cortex
Article first published online: 23 NOV 2005
European Journal of Neuroscience
Volume 22, Issue 10, pages 2462–2474, November 2005
How to Cite
Liu, J.-J., Mohila, C. A., Gong, Y., Govindarajan, N. and Onn, S.-P. (2005), Chronic nicotine exposure during adolescence differentially influences calcium-binding proteins in rat anterior cingulate cortex. European Journal of Neuroscience, 22: 2462–2474. doi: 10.1111/j.1460-9568.2005.04423.x
- Issue published online: 23 NOV 2005
- Article first published online: 23 NOV 2005
- Received 13 May 2005, revised 22 August 2005, accepted 7 September 2005
- nicotine withdrawal;
- nicotinic acetylcholine receptors;
We have recently shown that chronic amphetamine exposure selectively up-regulates parvalbumin (PV) calcium-binding proteins in the anterior cingulate cortex (ACC). In this study, we evaluated the effects of chronic nicotine (NIC) exposure on PV, calbindin D28k (CB) and calretinin (CR) calcium-binding protein immunostaining in ACC GABAergic interneurons. Chronic NIC exposure for 3 weeks in adolescent rats, either via drinking water (the oral group) or by twice daily subcutaneous injections (the injection group), resulted in the expression of high levels of CR proteins in the ACC but not in the parietal cortex. Larger increases in the density of CR-immunoreactive (ir) neurons were noted in the NIC-injected rats at 0-day withdrawal (45% increase) compared with the oral group (26% increase). The larger increases in CR-ir neuron density in the NIC-injected rats were also reflected by prominent CR-ir processes across cortical layers. The density of PV-ir neurons was also increased (37%) at 0-day withdrawal but only in the oral NIC group and no changes in CB-ir neuron density were observed in either NIC group. Combined dual-immunofluorescence and confocal microscopy revealed that somatodendritic α4 nicotinic acetylcholine receptors colocalized with cortical neurons stained positively for CR, PV or CB. These results suggest that CR- and/or PV-ir-containing GABA interneurons may be involved in channeling the effects of NIC in the ACC, which is closely associated with the ventral basal ganglia circuit that is linked to brain reward function.