PMID- 37659438
OWN - NLM
STAT- MEDLINE
DCOM- 20231026
LR  - 20240210
IS  - 1873-7064 (Electronic)
IS  - 0028-3908 (Print)
IS  - 0028-3908 (Linking)
VI  - 240
DP  - 2023 Dec 1
TI  - A novel inhibitory corticostriatal circuit that expresses mu opioid 
      receptor-mediated synaptic plasticity.
PG  - 109696
LID - S0028-3908(23)00286-1 [pii]
LID - 10.1016/j.neuropharm.2023.109696 [doi]
AB  - Corticostriatal circuits are generally characterized by the release of glutamate 
      neurotransmitter from cortical terminals within the striatum. It is well known 
      that cortical excitatory input to the dorsal striatum regulates addictive 
      drug-related behaviors. We previously reported that anterior insular cortex (AIC) 
      synaptic inputs to the dorsolateral striatum (DLS) control binge alcohol drinking 
      in mice. These AIC-DLS glutamate synapses are also the sole sites of 
      corticostriatal mu opioid receptor-mediated excitatory long-term depression 
      (MOR-LTD) in the DLS. Recent work demonstrates that some regions of cortex send 
      long-range, direct inhibitory inputs into the dorsal striatum. Nothing is known 
      about the existence and regulation of AIC-DLS inhibitory synaptic transmission. 
      Here, using a combination of patch clamp electrophysiology and optogenetics, we 
      characterized a novel AIC-DLS corticostriatal inhibitory circuit and its 
      regulation by MOR-mediated inhibitory LTD (MOR-iLTD). First, we found that the 
      activation of presynaptic MORs produces MOR-iLTD in the DLS and dorsomedial 
      striatum. Then, we showed that medium spiny neurons within the DLS receive direct 
      inhibitory synaptic input from the cortex, specifically from the motor cortex and 
      AIC. Using transgenic mice that express cre-recombinase within 
      parvalbumin-expressing inhibitory neurons, we determined that this specific 
      cortical neuron subtype sends direct GABAergic projections to the DLS. Moreover, 
      these AIC-DLS inhibitory synaptic input subtypes express MOR-iLTD. These data 
      suggest a novel GABAergic corticostriatal circuit that could be involved in the 
      regulation of drug and alcohol consumption-related behaviors.
CI  - Copyright (c) 2023 Elsevier Ltd. All rights reserved.
FAU - Munoz, Braulio
AU  - Munoz B
AD  - Department of Pharmacology & Toxicology, Indiana University School of Medicine, 
      Indianapolis, IN, 46202, USA. Electronic address: bmunozra@iupui.edu.
FAU - Atwood, Brady K
AU  - Atwood BK
AD  - Department of Pharmacology & Toxicology, Indiana University School of Medicine, 
      Indianapolis, IN, 46202, USA; Stark Neurosciences Research Institute, Indiana 
      University School of Medicine, Indianapolis, IN, 46202, USA.
LA  - eng
GR  - R01 AA027214/AA/NIAAA NIH HHS/United States
GR  - UL1 TR002529/TR/NCATS NIH HHS/United States
PT  - Journal Article
DEP - 20230901
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Receptors, Opioid, mu)
RN  - 0 (Glutamates)
SB  - IM
MH  - Mice
MH  - Animals
MH  - *Receptors, Opioid, mu/genetics/metabolism
MH  - *Neuronal Plasticity/physiology
MH  - Synaptic Transmission/physiology
MH  - Corpus Striatum/metabolism
MH  - Mice, Transgenic
MH  - Glutamates
PMC - PMC10591984
MID - NIHMS1930424
OTO - NOTNLM
OT  - Anterior insular cortex
OT  - Dorsal striatum
OT  - GABA transmission
OT  - Long-term depression
OT  - Medium spiny neurons
OT  - Parvalbumin interneurons
COIS- Declaration of competing interest The authors declare no conflict of interest.
EDAT- 2023/09/03 00:41
MHDA- 2023/10/26 06:42
PMCR- 2024/12/01
CRDT- 2023/09/02 19:23
PHST- 2023/05/18 00:00 [received]
PHST- 2023/08/28 00:00 [revised]
PHST- 2023/08/30 00:00 [accepted]
PHST- 2024/12/01 00:00 [pmc-release]
PHST- 2023/10/26 06:42 [medline]
PHST- 2023/09/03 00:41 [pubmed]
PHST- 2023/09/02 19:23 [entrez]
AID - S0028-3908(23)00286-1 [pii]
AID - 10.1016/j.neuropharm.2023.109696 [doi]
PST - ppublish
SO  - Neuropharmacology. 2023 Dec 1;240:109696. doi: 10.1016/j.neuropharm.2023.109696. 
      Epub 2023 Sep 1.