Synaptic mechanisms underlie nicotine-induced excitability of brain reward areas

Autor: Huibert D. Mansvelder, J. Russel Keath, Daniel S. McGehee
Přispěvatelé: Integrative Neurophysiology
Jazyk: angličtina
Rok vydání: 2002
Předmět:
Atropine
Insecticides
Patch-Clamp Techniques
Dopamine
Action Potentials
Receptors
Nicotinic

Synaptic Transmission
Cholinergic Antagonists
Rats
Sprague-Dawley

Nicotine
Mice
0302 clinical medicine
gamma-Aminobutyric Acid
Neurons
0303 health sciences
Chemistry
General Neuroscience
Smoking
Ganglionic Stimulants
Electrophysiology
Nicotinic agonist
medicine.anatomical_structure
Acetylcholinesterase
GABAergic
Brain stimulation reward
medicine.drug
medicine.medical_specialty
Adolescent
Neuroscience(all)
Glutamic Acid
Muscarinic Antagonists
In Vitro Techniques
Neurotransmission
03 medical and health sciences
Glutamatergic
Reward
Quinoxalines
Internal medicine
medicine
Animals
Humans
030304 developmental biology
Ventral Tegmental Area
Organothiophosphorus Compounds
Rats
Endocrinology
nervous system
Cholinesterase Inhibitors
Neuron
Excitatory Amino Acid Antagonists
Neuroscience
030217 neurology & neurosurgery
Zdroj: Neuron, 33(6), 905-919. Cell Press
Mansvelder, H D, Keath, J R & McGehee, D S 2002, ' Synaptic mechanisms underlie nicotine-induced excitability of brain reward areas ', Neuron, vol. 33, no. 6, pp. 905-919 . https://doi.org/10.1016/S0896-6273(02)00625-6
ISSN: 0896-6273
DOI: 10.1016/S0896-6273(02)00625-6
Popis: A single nicotine exposure increases dopamine levels in the mesolimbic reward system for hours, but nicotine concentrations experienced by smokers desensitize nAChRs on dopamine neurons in seconds to minutes. Here, we show that persistent modulation of both GABAergic and glutamatergic synaptic transmission by nicotine can contribute to the sustained increase in dopamine neuron excitability. Nicotine enhances GABAergic transmission transiently, which is followed by a persistent depression of these inhibitory inputs due to nAChR desensitization. Simultaneously, nicotine enhances glutamatergic transmission through nAChRs that desensitize less than those on GABA neurons. The net effect is a shift toward excitation of the dopamine reward system. These results suggest that spatial and temporal differences in nicotinic receptor activity on both excitatory and inhibitory neurons in reward areas coordinate to reinforce nicotine self-administration.
Databáze: OpenAIRE