Presynaptic and postsynaptic modulation of glutamatergic synaptic transmission by activation of α1- and β-adrenoceptors in layer V pyramidal neurons of rat cerebral cortex

Synapse ◽  
2009 ◽  
Vol 63 (4) ◽  
pp. 269-281 ◽  
Author(s):  
Masayuki Kobayashi ◽  
Masao Kojima ◽  
Yuko Koyanagi ◽  
Kazunori Adachi ◽  
Kazuyuki Imamura ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Synaptic Transmission ◽  
Pyramidal Neurons ◽  
Rat Cerebral Cortex ◽  
Glutamatergic Synaptic Transmission ◽  
Layer V

scholarly journals Dopamine D2 receptors modulate intrinsic properties and synaptic transmission of parvalbumin interneurons in the mouse primary motor cortex

2019 ◽  
Author(s):  
Jérémy Cousineau ◽  
Léa Lescouzères ◽  
Anne Taupignon ◽  
Lorena Delgado-Zabalza ◽  
Emmanuel Valjent ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Synaptic Transmission ◽  
Motor Skills ◽  
Primary Motor Cortex ◽  
Pyramidal Neurons ◽  
D2 Receptors ◽  
Receptor Subtypes ◽  
Parvalbumin Interneurons ◽  
Layer V ◽  
Gabaergic Synaptic Transmission

AbstractDopamine (DA) plays a crucial role in the control of motor and higher cognitive functions such as learning, working memory and decision making. The primary motor cortex (M1), which is essential for motor control and the acquisition of motor skills, receives dopaminergic inputs in its superficial and deep layers from the midbrain. However, the precise action of DA and DA receptor subtypes on the cortical microcircuits of M1 remains poorly understood. The aim of this work was to investigate how DA, through the activation of D2 receptors (D2R), modulates the cellular and synaptic activity of M1 parvalbumin-expressing interneurons (PVINs) which are crucial to regulate the spike output of pyramidal neurons (PNs). By combining immunofluorescence, ex vivo electrophysiology, pharmacology and optogenetics approaches, we show that D2R activation increases neuronal excitability of PVINs and GABAergic synaptic transmission between PVINs and PNs in layer V of M1. Our data reveal a mechanism through which cortical DA modulates M1 microcircuitry and might participate in the acquisition of motor skills.Significance StatementPrimary motor cortex (M1), which is a region essential for motor control and the acquisition of motor skills, receives dopaminergic inputs from the midbrain. However, precise action of dopamine and its receptor subtypes on specific cell types in M1 remained poorly understood. Here, we demonstrate in M1 that dopamine D2 receptors (D2R) are present in parvalbumin interneurons (PVINs) and their activation increases the excitability of the PVINs, which are crucial to regulate the spike output of pyramidal neurons (PNs). Moreover the activation of the D2R facilitates the GABAergic synaptic transmission of those PVINs on layer V PNs. These results highlight how cortical dopamine modulates the functioning of M1 microcircuit which activity is disturbed in hypo- and hyperdopaminergic states.

scholarly journals Cannabinoids Modulate Synaptic Strength and Plasticity at Glutamatergic Synapses of Rat Prefrontal Cortex Pyramidal Neurons

2000 ◽  
Vol 83 (6) ◽  
pp. 3287-3293 ◽  
Author(s):  
Nathalie Auclair ◽  
Satoru Otani ◽  
Philippe Soubrie ◽  
Francis Crepel
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Transmission ◽  
Cannabinoid Receptors ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Type I ◽  
Glutamatergic Synaptic Transmission ◽  
Layer V ◽  
Stimulation Of

Cannabinoids receptors have been reported to modulate synaptic transmission in many structures of the CNS, but yet little is known about their role in the prefrontal cortex where type I cannabinoid receptor (CB-1) are expressed. In this study, we tested first the acute effects of selective agonists and antagonist of CB-1 on glutamatergic excitatory postsynaptic currents (EPSCs) in slices of rat prefrontal cortex (PFC). EPSCs were evoked in patch-clamped layer V pyramidal cells by stimulation of layer V afferents. Monosynaptic EPSCs were strongly depressed by bath application (1 μM) of the cannabinoid receptors agonists WIN55212-2 (−50.4 ± 8.8%) and CP55940 (−42.4 ± 10.9%). The CB-1 antagonist SR141716A reversed these effects. Unexpectedly, SR141716A alone produced a significant increase of glutamatergic synaptic transmission (+46.9 ± 11.2%), which could be partly reversed by WIN55212-2. In the presence of strontium in the bath, the frequency but not the amplitude of asynchronous synaptic events evoked in layer V pyramidal cells by stimulating layer V afferents, was markedly decreased (−54.2 ± 8%), indicating a presynaptic site of action of cannabinoids at these synapses. Tetanic stimulation (100 pulses at 100 Hz, 4 trains) induced in control condition, no changes ( n = 7/18), long-term depression (LTD; n = 6/18), or long-term potentiation (LTP; n = 5/18) of monosynaptic EPSCs evoked by stimulation of layer V afferents. When tetanus was applied in the presence of WIN 55,212-2 or SR141716-A (1 μM) in the bath, the proportion of “nonplastic” cells were not significantly changed ( n = 7/15 in both cases). For the plastic ones ( n = 8 in both cases), WIN 55,212-2 strongly favored LTD ( n = 7/8) at the apparent expense of LTP ( n = 1/8), whereas the opposite effect was observed with SR141716-A (7/8 LTP; 1/8 LTD). These results demonstrate that cannabinoids influence glutamatergic synaptic transmission and plasticity in the PFC of rodent.

Measurement of the effects of hypothyroidism on the number and distribution of spines along the apical shaft of pyramidal neurons of the rat cerebral cortex

1977 ◽  
Vol 126 (3) ◽  
pp. 547-550 ◽  
Author(s):  
Fernando Sanchez-Toscano ◽  
Francisco Escobar del Rey ◽  
Gabriella Morreale de Escobar ◽  
Antonio Ruiz-Marcos
Keyword(s):  
Cerebral Cortex ◽  
Pyramidal Neurons ◽  
Rat Cerebral Cortex

A novel rat medial prefrontal cortical slice preparation to investigate synaptic transmission from amygdala to layer V prelimbic pyramidal neurons

2006 ◽  
Vol 151 (2) ◽  
pp. 148-158 ◽  
Author(s):  
Luis Orozco-Cabal ◽  
Sebastian Pollandt ◽  
Jie Liu ◽  
Leoncio Vergara ◽  
Patricia Shinnick-Gallagher ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Pyramidal Neurons ◽  
Cortical Slice ◽  
Slice Preparation ◽  
Prefrontal Cortical ◽  
Layer V ◽  
Medial Prefrontal Cortical

scholarly journals Intranasal Administration of Rotenone Reduces GABAergic Inhibition in the Mouse Insular Cortex Leading to Impairment of LTD and Conditioned Taste Aversion Memory

2020 ◽  
Vol 22 (1) ◽  
pp. 259
Author(s):  
Hiroki Toyoda ◽  
Ayano Katagiri ◽  
Takafumi Kato ◽  
Hajime Sato
Keyword(s):  
Synaptic Transmission ◽  
Taste Aversion ◽  
Conditioned Taste Aversion ◽  
Intranasal Administration ◽  
Pyramidal Neurons ◽  
Insular Cortex ◽  
Long Term Potentiation ◽  
Cellular Mechanisms ◽  
Layer V

The pesticide rotenone inhibits mitochondrial complex I and is thought to cause neurological disorders such as Parkinson’s disease and cognitive disorders. However, little is known about the effects of rotenone on conditioned taste aversion memory. In the present study, we investigated whether intranasal administration of rotenone affects conditioned taste aversion memory in mice. We also examined how the intranasal administration of rotenone modulates synaptic transmission and plasticity in layer V pyramidal neurons of the mouse insular cortex that is critical for conditioned taste aversion memory. We found that the intranasal administration of rotenone impaired conditioned taste aversion memory to bitter taste. Regarding its cellular mechanisms, long-term depression (LTD) but not long-term potentiation (LTP) was impaired in rotenone-treated mice. Furthermore, spontaneous inhibitory synaptic currents and tonic GABA currents were decreased in layer V pyramidal neurons of rotenone-treated mice compared to the control mice. The impaired LTD observed in pyramidal neurons of rotenone-treated mice was restored by a GABAA receptor agonist muscimol. These results suggest that intranasal administration of rotenone decreases GABAergic synaptic transmission in layer V pyramidal neurons of the mouse insular cortex, the result of which leads to impairment of LTD and conditioned taste aversion memory.

Sign in / Sign up

Export Citation Format

Share Document