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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ávila-ruiz, Tania Carranza, Vladimir Gustavo, López-López Limón, Daniel I. Martínez, Isabel Flores, Gonzalo Flores-Hernández, Jorge |
| Description | Author Affiliation: Ávila-Ruiz T ( Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, 14 Sur 6301, CP 72570, Puebla, Puebla, México.) |
| Abstract | Nicotine is an addictive substance of tobacco. It has been suggested that nicotine acts on glutamatergic (N-methyl-d-aspartate, NMDA) neurotransmission affecting dopamine release in the mesocorticolimbic system. This effect is reflected in neuroadaptative changes that can modulate neurotransmission in the prefrontal cortex (PFC) and nucleus accumbens (NAcc) core (cNAcc) and shell (sNAcc) regions. We evaluated the effect of chronic administration of nicotine (4.23 mg/kg/day for 14 days) on NMDA activated currents in dissociated neurons from the PFC, and NAcc (from core and shell regions). We assessed nicotine blood levels by mass spectrophotometry and we confirmed that nicotine increases locomotor activity. An electrophysiological study showed an increase in NMDA currents in neurons from the PFC and core part of the NAcc in animals treated with nicotine compared to those of control rats. No change was observed in neurons from the shell part of the NAcc. The enhanced glutamatergic activity observed in the neurons of rats with chronic administration of nicotine may explain the increased locomotive activity also observed in such rats. To assess one of the possible causes of increased NMDA currents, we used magnesium, to block NMDA receptor that contains the NR2B subunit. If there is a change in percent block of NMDA currents, it means that there is a possible change in expression of NMDA receptor subunits. Our results showed that there is no difference in the blocking effect of magnesium on the NMDA currents. The magnesium lacks of effect after nicotinic treatment suggests that there is no change in expression of NR2B subunit of NMDA receptors, then, the effect of nicotine treatment on amplitude of NMDA currents may be due to an increase in the quantity of receptors or to a change in the unitary conductance, rather than a change in the expression of the subunits that constitute it. |
| File Format | HTM / HTML |
| ISSN | 08874476 |
| Issue Number | 6 |
| Volume Number | 68 |
| e-ISSN | 10982396 |
| Journal | Synapse |
| Language | English |
| Publisher | Wiley |
| Publisher Date | 2014-06-01 |
| Publisher Place | United States |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Neurology Ganglionic Stimulants Administration & Dosage N-methylaspartate Metabolism Neurons Drug Effects Nicotine Nucleus Accumbens Prefrontal Cortex Animals Body Weight Cells, Cultured Blood In Vitro Techniques Magnesium Compounds Pharmacology Male Membrane Potentials Motor Activity Physiology Neurotransmitter Agents Patch-clamp Techniques Pyramidal Cells Rats Rats, Sprague-dawley Receptors, N-methyl-d-aspartate Antagonists & Inhibitors Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cellular and Molecular Neuroscience |
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