Chronic nicotine and smoke treatment modulate dopaminergic activities in ventral tegmental area and nucleus accumbens and the γ-aminobutyric acid type B receptor expression of the rat prefrontal cortex

✍ Scribed by Shu-Peng Li; Moon Seok Park; Jong Hun Kim; Myeong Ok Kim

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 516 KB
• Volume: 78
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.20329

✦ Synopsis

Dopaminergic afferents from the mesencephalic areas, such as ventral tegmental area (VTA), synapse with the ␥-aminobutyric acid (GABA)-ergic interneurons in the prefrontal cortex (PFC). Pharmacological and electrophysiological data show that the reinforcement, the dependenceproducing properties, as well as the psychopharmacologic effects of nicotine depend to a great extent on activation of nicotinic receptors within the mesolimbocortical dopaminergic projection. To explore further the relationship between the mesencephalic dopaminergic neurons and PFC GABAergic neurons, we investigated the effects of nicotine and passive exposure to cigarette smoke on the regulation of tyrosine hydroxylase (TH) in VTA and substantia nigra (SNC) and dopamine (DA) D 1 receptor levels in nucleus accumbens (NAc) and caudate-putamen (CPu). Also, the simultaneous changes in GABA B receptors mRNAs in the PFC were studied. The results showed that chronic nicotine and smoking treatment differentially changed the levels of TH protein in VTA and SNC and DA D 1 receptor levels in Nac and CPu. GABA B1 and GABA B2 receptor mRNA levels also showed different change patterns. Ten and thirty minutes of smoke exposure increased GABA B1 receptor mRNA to a greater extent than that of GABA B2 , whereas GABA B2 was greatly enhanced after 1 hr of smoke exposure. The TH levels in VTA were closely related to DA D 1 receptor levels in NAc and with GABA B receptor mRNA changes in PFC. These results suggest that the mesolimbic pathway and GABA B receptor mRNA in PFC are modulated by nicotine and cigarette smoke, implying an important role in nicotine's psychopharmacological effects.