Dopaminergic Regulation of Synaptic Plasticity of Striatal Cholinergic Interneurons

2002 ◽  
pp. 191-194 ◽  
Author(s):  
Masami Miura ◽  
Takeo Suzuki ◽  
Toshihiko Aosaki
Keyword(s):  
Synaptic Plasticity ◽  
Cholinergic Interneurons ◽  
Dopaminergic Regulation

scholarly journals Dopaminergic Regulation of Striatal Interneurons in Reward and Addiction: Focus on Alcohol

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Rhona Clarke ◽  
Louise Adermark
Keyword(s):  
Physiological Activity ◽  
Dorsal Striatum ◽  
Primary Component ◽  
Medium Spiny Neurons ◽  
Dopaminergic Transmission ◽  
Cholinergic Interneurons ◽  
Guided Learning ◽  
Striatal Interneurons ◽  
Dopaminergic Regulation

Corticobasal ganglia networks coursing through the striatum are key structures for reward-guided behaviors. The ventral striatum (nucleus accumbens (nAc)) and its reciprocal connection with the ventral tegmental area (VTA) represent a primary component of the reward system, but reward-guided learning also involves the dorsal striatum and dopaminergic inputs from the substantia nigra. The majority of neurons in the striatum (>90%) are GABAergic medium spiny neurons (MSNs), but both the input to and the output from these neurons are dynamically controlled by striatal interneurons. Dopamine is a key neurotransmitter in reward and reward-guided learning, and the physiological activity of GABAergic and cholinergic interneurons is regulated by dopaminergic transmission in a complex manner. Here we review the role of striatal interneurons in modulating striatal output during drug reward, with special emphasis on alcohol.

scholarly journals Coincidence of cholinergic pauses, dopaminergic activation and depolarization drives synaptic plasticity in the striatum

2019 ◽  
Author(s):  
Yan-Feng Zhang ◽  
Simon D. Fisher ◽  
Manfred Oswald ◽  
Jeffery R. Wickens ◽  
John N. J. Reynolds
Keyword(s):  
Synaptic Plasticity ◽  
Reinforcement Learning ◽  
Long Term Potentiation ◽  
Dopamine Neurons ◽  
Projection Neurons ◽  
Cholinergic Interneurons ◽  
Term Potentiation ◽  
Phasic Activation

AbstractPauses in the firing of tonically-active cholinergic interneurons (ChIs) in the striatum coincide with phasic activation of dopamine neurons during reinforcement learning. However, how this pause influences cellular substrates of learning is unclear. Using two in vivo paradigms, we report that long-term potentiation (LTP) at corticostriatal synapses with spiny projection neurons (SPNs) is dependent on the temporal coincidence of ChI pause and dopamine phasic activation, critically accompanied by SPN depolarization.

scholarly journals Dopaminergic Regulation of Nucleus Accumbens Cholinergic Interneurons Demarcates Susceptibility to Cocaine Addiction

2020 ◽  
Vol 88 (10) ◽  
pp. 746-757 ◽  
Author(s):  
Joo Han Lee ◽  
Efrain A. Ribeiro ◽  
Jeongseop Kim ◽  
Bumjin Ko ◽  
Hope Kronman ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Cocaine Addiction ◽  
Cholinergic Interneurons ◽  
Dopaminergic Regulation

scholarly journals Dopamine-Dependent Synaptic Plasticity in the Striatal Cholinergic Interneurons

2001 ◽  
Vol 21 (17) ◽  
pp. 6492-6501 ◽  
Author(s):  
Takeo Suzuki ◽  
Masami Miura ◽  
Kin-ya Nishimura ◽  
Toshihiko Aosaki
Keyword(s):  
Synaptic Plasticity ◽  
Cholinergic Interneurons

scholarly journals Accumbens cholinergic interneurons mediate cue-induced nicotine seeking and associated glutamatergic plasticity

2020 ◽  
Author(s):  
Jonna M. Leyrer-Jackson ◽  
Michael Holter ◽  
Paula F. Overby ◽  
Jason M. Newbern ◽  
Michael D. Scofield ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Glutamate Release ◽  
Neuronal Population ◽  
Medium Spiny Neurons ◽  
Self Administration ◽  
Nucleus Accumbens Core ◽  
Cholinergic Interneurons ◽  
Seeking Behavior ◽  
Underlying Mechanisms

AbstractNicotine, the primary addictive substance in tobacco, is widely abused. Relapse to cues associated with nicotine results in increased glutamate release within nucleus accumbens core (NAcore), modifying synaptic plasticity of medium spiny neurons (MSNs) which contributes to reinstatement of nicotine seeking. However, the role of cholinergic interneurons (ChIs) within the NAcore in mediating these neurobehavioral processes in unknown. ChIs represent less than 1% of the accumbens neuronal population yet are activated during drug seeking and reward-predicting events. Thus, we hypothesized that ChIs may play a significant role in mediating glutamatergic plasticity that underlies nicotine seeking behavior. Using chemogenetics transgenic rats that express Cre under the control of the choline acetyltransferase (ChAT) promoter, ChIs were bi-directionally manipulated prior to cue-induced reinstatement. Following nicotine self-administration and extinction training, ChIs were activated or inhibited prior to a cue reinstatement session. Following reinstatement, whole-cell electrophysiology from NAcore MSNs was used to assess changes in plasticity, measured via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) / N-Methyl-D-Aspartate (NMDA) (A/N) ratios. Chemogenetic inhibition of ChIs inhibited cued nicotine seeking and resulted in decreased A/N, whereas activation of ChIs had no effect, demonstrating that ChI inhibition prevents transient synaptic potentiation (t-SP) associated with cue-induced nicotine seeking. To assess potential underlying mechanisms, accumbens α4β2- and α7-containing nicotinic ACh receptors (nAChRs) were pharmacologically inhibited and MSN synaptic morphology was assessed following reinstatement. Inhibition of both nAChR subtypes prevented cue-induced nicotine seeking and t-SP (measured via changes in spine head diameter). Together, these results demonstrate that these neurons mediate cue-induced nicotine reinstatement and underlying synaptic plasticity within the NAcore.

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