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Full-gestational exposure to nicotine and ethanol augments nicotine self-administration by altering ventral tegmental dopaminergic function due to NMDA receptors in adolescent rats.
J Neurochem. 2014 Mar; 128(5):701-12.JN

Abstract

In adult rats, we have shown full-gestational exposure to nicotine and ethanol (Nic + EtOH) augmented nicotine self-administration (SA) (increased nicotine intake) compared to pair-fed (PF) offspring. Therefore, we hypothesized that full-gestational exposure to Nic + EtOH disrupts control of dopaminergic (DA) circuitry by ventral tegmental area (VTA) NMDA receptors, augmenting nicotine SA and DA release in nucleus accumbens (NAcc) of adolescents. Both NAcc DA and VTA glutamate release were hyper-responsive to intra-VTA NMDA in Nic + EtOH offspring versus PF (p = 0.03 and 0.02, respectively). Similarly, DA release was more responsive to i.v. nicotine in Nic + EtOH offspring (p = 0.02). Local DL-2-Amino-5-phosphonopentanoic acid sodium salt (AP5) (NMDA receptor antagonist) infusion into the VTA inhibited nicotine-stimulated DA release in Nic + EtOH and PF offspring. Nicotine SA was augmented in adolescent Nic + EtOH versus PF offspring (p = 0.000001). Daily VTA microinjections of AP5 reduced nicotine SA by Nic + EtOH offspring, without affecting PF (p = 0.000032). Indeed, nicotine SA in Nic + EtOH offspring receiving AP5 was not different from PF offspring. Both VTA mRNA transcripts and NMDA receptor subunit proteins were not altered in Nic + EtOH offspring. In summary, adolescent offspring exposed to gestational Nic + EtOH show markedly increased vulnerability to become dependent on nicotine. This reflects the enhanced function of a subpopulation of VTA NMDA receptors that confer greater nicotine-induced DA release in NAcc. We hypothesized that concurrent gestational exposure to nicotine and ethanol would disrupt the control of VTA dopaminergic circuitry by NMDA receptors. Resulting in the augmented nicotine self-administration (SA) in adolescent offspring.

Authors+Show Affiliations

Department of Pharmacology, University of Tennessee Health Science Center, Memphis, TN, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24147868

Citation

Roguski, Emily E., et al. "Full-gestational Exposure to Nicotine and Ethanol Augments Nicotine Self-administration By Altering Ventral Tegmental Dopaminergic Function Due to NMDA Receptors in Adolescent Rats." Journal of Neurochemistry, vol. 128, no. 5, 2014, pp. 701-12.
Roguski EE, Sharp BM, Chen H, et al. Full-gestational exposure to nicotine and ethanol augments nicotine self-administration by altering ventral tegmental dopaminergic function due to NMDA receptors in adolescent rats. J Neurochem. 2014;128(5):701-12.
Roguski, E. E., Sharp, B. M., Chen, H., & Matta, S. G. (2014). Full-gestational exposure to nicotine and ethanol augments nicotine self-administration by altering ventral tegmental dopaminergic function due to NMDA receptors in adolescent rats. Journal of Neurochemistry, 128(5), 701-12. https://doi.org/10.1111/jnc.12504
Roguski EE, et al. Full-gestational Exposure to Nicotine and Ethanol Augments Nicotine Self-administration By Altering Ventral Tegmental Dopaminergic Function Due to NMDA Receptors in Adolescent Rats. J Neurochem. 2014;128(5):701-12. PubMed PMID: 24147868.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Full-gestational exposure to nicotine and ethanol augments nicotine self-administration by altering ventral tegmental dopaminergic function due to NMDA receptors in adolescent rats. AU - Roguski,Emily E, AU - Sharp,Burt M, AU - Chen,Hao, AU - Matta,Shannon G, Y1 - 2013/11/15/ PY - 2013/06/27/received PY - 2013/10/16/revised PY - 2013/10/17/accepted PY - 2013/10/24/entrez PY - 2013/10/24/pubmed PY - 2014/4/30/medline KW - NMDA receptors KW - drug acquisition KW - ethanol KW - gestational drug exposure KW - nicotine SP - 701 EP - 12 JF - Journal of neurochemistry JO - J. Neurochem. VL - 128 IS - 5 N2 - In adult rats, we have shown full-gestational exposure to nicotine and ethanol (Nic + EtOH) augmented nicotine self-administration (SA) (increased nicotine intake) compared to pair-fed (PF) offspring. Therefore, we hypothesized that full-gestational exposure to Nic + EtOH disrupts control of dopaminergic (DA) circuitry by ventral tegmental area (VTA) NMDA receptors, augmenting nicotine SA and DA release in nucleus accumbens (NAcc) of adolescents. Both NAcc DA and VTA glutamate release were hyper-responsive to intra-VTA NMDA in Nic + EtOH offspring versus PF (p = 0.03 and 0.02, respectively). Similarly, DA release was more responsive to i.v. nicotine in Nic + EtOH offspring (p = 0.02). Local DL-2-Amino-5-phosphonopentanoic acid sodium salt (AP5) (NMDA receptor antagonist) infusion into the VTA inhibited nicotine-stimulated DA release in Nic + EtOH and PF offspring. Nicotine SA was augmented in adolescent Nic + EtOH versus PF offspring (p = 0.000001). Daily VTA microinjections of AP5 reduced nicotine SA by Nic + EtOH offspring, without affecting PF (p = 0.000032). Indeed, nicotine SA in Nic + EtOH offspring receiving AP5 was not different from PF offspring. Both VTA mRNA transcripts and NMDA receptor subunit proteins were not altered in Nic + EtOH offspring. In summary, adolescent offspring exposed to gestational Nic + EtOH show markedly increased vulnerability to become dependent on nicotine. This reflects the enhanced function of a subpopulation of VTA NMDA receptors that confer greater nicotine-induced DA release in NAcc. We hypothesized that concurrent gestational exposure to nicotine and ethanol would disrupt the control of VTA dopaminergic circuitry by NMDA receptors. Resulting in the augmented nicotine self-administration (SA) in adolescent offspring. SN - 1471-4159 UR - https://www.unboundmedicine.com/medline/citation/24147868/Full_gestational_exposure_to_nicotine_and_ethanol_augments_nicotine_self_administration_by_altering_ventral_tegmental_dopaminergic_function_due_to_NMDA_receptors_in_adolescent_rats_ L2 - https://doi.org/10.1111/jnc.12504 DB - PRIME DP - Unbound Medicine ER -