Plasticity in the projection from the anterior thalamic nuclei to the anterior cingulate cortex in the rat in vivo: paired-pulse facilitation, long-term potentiation and short-term depression

Neuroscience ◽  
2002 ◽  
Vol 109 (3) ◽  
pp. 401-406 ◽  
Author(s):  
C. Gemmell ◽  
S.M. O’Mara
Keyword(s):  
Anterior Cingulate Cortex ◽  
Long Term Potentiation ◽  
Anterior Cingulate ◽  
Thalamic Nuclei ◽  
Short Term ◽  
Paired Pulse ◽  
Term Potentiation ◽  
Anterior Thalamic Nuclei

scholarly journals Presynaptic long-term potentiation requires extracellular signal-regulated kinases in the anterior cingulate cortex

2020 ◽  
Vol 16 ◽  
pp. 174480692091724
Author(s):  
Qi-Yu Chen ◽  
Zhi-Ling Zhang ◽  
Qin Liu ◽  
Chao-Jun Chen ◽  
Xiao-Kang Zhang ◽  
...  
Keyword(s):  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Long Term Potentiation ◽  
Anterior Cingulate ◽  
Term Potentiation ◽  
Extracellular Signal

Mouse hippocampo-prefrontal paired-pulse facilitation and long-term potentiation in vivo

Neuroreport ◽  
2001 ◽  
Vol 12 (6) ◽  
pp. 1191-1193 ◽  
Author(s):  
Yoshinori Izaki ◽  
Masatoshi Takita ◽  
Masahiko Nomura
Keyword(s):  
Long Term Potentiation ◽  
Paired Pulse ◽  
Paired Pulse Facilitation ◽  
Term Potentiation

scholarly journals Long-term potentiation in the anterior cingulate cortex and chronic pain

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130146 ◽  
Author(s):  
Min Zhuo
Keyword(s):  
Chronic Pain ◽  
Anterior Cingulate Cortex ◽  
Dorsal Horn ◽  
Glutamate Release ◽  
Cingulate Cortex ◽  
Long Term Potentiation ◽  
Anterior Cingulate ◽  
Spinal Cord Dorsal Horn ◽  
Term Potentiation

Glutamate is the primary excitatory transmitter of sensory transmission and perception in the central nervous system. Painful or noxious stimuli from the periphery ‘teach’ humans and animals to avoid potentially dangerous objects or environments, whereas tissue injury itself causes unnecessary chronic pain that can even last for long periods of time. Conventional pain medicines often fail to control chronic pain. Recent neurobiological studies suggest that synaptic plasticity taking place in sensory pathways, from spinal dorsal horn to cortical areas, contributes to chronic pain. Injuries trigger long-term potentiation of synaptic transmission in the spinal cord dorsal horn and anterior cingulate cortex, and such persistent potentiation does not require continuous neuronal activity from the periphery. At the synaptic level, potentiation of excitatory transmission caused by injuries may be mediated by the enhancement of glutamate release from presynaptic terminals and potentiated postsynaptic responses of AMPA receptors. Preventing, ‘erasing’ or reducing such potentiation may serve as a new mechanism to inhibit chronic pain in patients in the future.

scholarly journals Heterosynaptic long-term potentiation from the anterior cingulate cortex to spinal cord in adult rats

2018 ◽  
Vol 14 ◽  
pp. 174480691879840
Author(s):  
Qi-Yu Chen ◽  
Tao Chen ◽  
Li-Jun Zhou ◽  
Xian-Guo Liu ◽  
Min Zhuo
Keyword(s):  
Spinal Cord ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Long Term Potentiation ◽  
Anterior Cingulate ◽  
Adult Rats ◽  
Term Potentiation

scholarly journals A Single Brief Burst Induces GluR1-dependent Associative Short-term Potentiation: A Potential Mechanism for Short-term Memory

2010 ◽  
Vol 22 (11) ◽  
pp. 2530-2540 ◽  
Author(s):  
Martha A. Erickson ◽  
Lauren A. Maramara ◽  
John Lisman
Keyword(s):  
Knockout Mice ◽  
Short Term Memory ◽  
Long Term Potentiation ◽  
Dual Process ◽  
Short Term ◽  
Model Learning ◽  
Term Memory ◽  
Term Potentiation

Recent work showed that short-term memory (STM) is selectively reduced in GluR1 knockout mice. This raises the possibility that a form of synaptic modification dependent on GluR1 might underlie STM. Studies of synaptic plasticity have shown that stimuli too weak to induce long-term potentiation induce short-term potentiation (STP), a phenomenon that has received little attention. Here we examined several properties of STP and tested the dependence of STP on GluR1. The minimal requirement for inducing STP was examined using a test pathway and a conditioning pathway. Several closely spaced stimuli in the test pathway, forming a single brief burst, were sufficient to induce STP. Thus, STP is likely to be induced by the similar bursts that occur in vivo. STP induction is associative in nature and dependent on the NMDAR. STP decays with two components, a fast component (1.6 ± 0.26 min) and a slower one (19 ± 6.6 min). To test the role of GluR1 in STP, experiments were conducted on GluR1 knockout mice. We found that STP was greatly reduced. These results, taken together with the behavioral work of D. Sanderson et al. [Sanderson, D., Good, M. A., Skelton, K., Sprengel, R., Seeburg, P. H., Nicholas, J., et al. Enhanced long-term and impaired short-term spatial memory in GluA1 AMPA receptor subunit knockout mice: Evidence for a dual-process memory model. Learning and Memory, 2009], provide genetic evidence that STP is a likely mechanism of STM.

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