Next Article in Journal
Chromosomal Evolution and Evolutionary Relationships of Lebiasina Species (Characiformes, Lebiasinidae)
Previous Article in Journal
p-Coumaric Acid Has Protective Effects against Mutant Copper–Zinc Superoxide Dismutase 1 via the Activation of Autophagy in N2a Cells
Previous Article in Special Issue
Increased Brain-Derived Neurotrophic Factor in Lumbar Dorsal Root Ganglia Contributes to the Enhanced Exercise Pressor Reflex in Heart Failure
Open AccessReview

Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration

1
Department of Biological Sciences, Pusan National University, 63-2 Busandaehak-ro, Geumjeong-gu, Busan 46241, Korea
2
Research Center for Safety Pharmacology, Korea Institute of Toxicology, 141 Gajeong-ro, Yuseong-gu, Daejeon 34114, Korea
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(12), 2943; https://doi.org/10.3390/ijms20122943
Received: 7 May 2019 / Revised: 8 June 2019 / Accepted: 14 June 2019 / Published: 16 June 2019
(This article belongs to the Special Issue Brain-Derived Neurotrophic Factor 2018)
Nicotine causes tobacco dependence, which may result in fatal respiratory diseases. The striatum is a key structure of forebrain basal nuclei associated with nicotine dependence. In the striatum, glutamate release is increased when α7 nicotinic acetylcholine receptors expressed in the glutamatergic terminals are exposed to nicotine, and over-stimulates glutamate receptors in gamma amino-butyric acid (GABA)ergic neurons. These receptor over-stimulations in turn potentiate GABAergic outputs to forebrain basal nuclei and contribute to the increase in psychomotor behaviors associated with nicotine dependence. In parallel with glutamate increases, nicotine exposure elevates brain-derived neurotrophic factor (BDNF) release through anterograde and retrograde targeting of the synapses of glutamatergic terminals and GABAergic neurons. This article reviews nicotine-exposure induced elevations of glutamatergic neurotransmission, the bidirectional targeting of BDNF in the striatum, and the potential regulatory role played by BDNF in behavioral responses to nicotine exposure. View Full-Text
Keywords: glutamate receptor; neurotrophic factor; nicotine dependence; TrkB; striatum glutamate receptor; neurotrophic factor; nicotine dependence; TrkB; striatum
Show Figures

Figure 1

MDPI and ACS Style

Kim, J.; Yang, J.H.; Ryu, I.S.; Sohn, S.; Kim, S.; Choe, E.S. Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration. Int. J. Mol. Sci. 2019, 20, 2943. https://doi.org/10.3390/ijms20122943

AMA Style

Kim J, Yang JH, Ryu IS, Sohn S, Kim S, Choe ES. Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration. International Journal of Molecular Sciences. 2019; 20(12):2943. https://doi.org/10.3390/ijms20122943

Chicago/Turabian Style

Kim, Jieun; Yang, Ju H.; Ryu, In S.; Sohn, Sumin; Kim, Sunghyun; Choe, Eun S. 2019. "Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration" Int. J. Mol. Sci. 20, no. 12: 2943. https://doi.org/10.3390/ijms20122943

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop