Short-Term Plasticity Turns Plastic. Focus on “Synaptic Transmission at the Calyx of Held Under In Vivo-Like Activity Levels”

2007 ◽  
Vol 98 (2) ◽  
pp. 577-578 ◽  
Author(s):  
Erwin Neher
2008 ◽  
Vol 174 (2) ◽  
pp. 227-236 ◽  
Author(s):  
Martin D. Haustein ◽  
Thomas Reinert ◽  
Annika Warnatsch ◽  
Bernhard Englitz ◽  
Beatrice Dietz ◽  
...  

2013 ◽  
Vol 109 (4) ◽  
pp. 932-939 ◽  
Author(s):  
Juhyon Kim ◽  
Hitoshi Kita

The cortico-striato (Str)-globus pallidus external segment (GPe) projection plays major roles in the control of neuronal activity in the basal ganglia under both normal and pathological conditions. The present study used rat brain-slice preparations to address our hypothesis that the gain of this disynaptic projection is dynamically controlled by activations of short-term plasticity mechanisms of Str-GPe synapses. The Str-GPe projection neurons fire with very different frequency and firing patterns in vivo depending on the condition of the animal. The results show that the Str-GPe synapses have very strong short-term enhancement mechanisms and that repetitive burst activation of the Str-GPe synapses, which mimic oscillatory burst firing of Str neurons, can sustain enhanced states of synaptic transmission for tens of seconds. The results reveal that the short-term enhancement of Str-GPe synapses contributes to the generation of pauses in the firing of GPe neurons and that signal transfer function in the Str-GPe projection is highly dependent on the firing pattern of Str neurons.


2020 ◽  
Vol 13 (10) ◽  
pp. 297
Author(s):  
Vergine Chavushyan ◽  
Ani Soghomonyan ◽  
Gohar Karapetyan ◽  
Karen Simonyan ◽  
Konstantin Yenkoyan

The search for new therapeutics for the treatment of Alzheimer’s disease (AD) is still in progress. Aberrant pathways of synaptic transmission in basal forebrain cholinergic neural circuits are thought to be associated with the progression of AD. However, the effect of amyloid-beta (Aβ) on short-term plasticity (STP) of cholinergic circuits in the nucleus basalis magnocellularis (NBM) is largely unknown. STP assessment in rat brain cholinergic circuitry may indicate a new target for AD cholinergic therapeutics. Thus, we aimed to study in vivo electrophysiological patterns of synaptic activity in NBM-hippocampus and NBM-basolateral amygdala circuits associated with AD-like neurodegeneration. The extracellular single-unit recordings of responses from the hippocampal and basolateral amygdala neurons to high-frequency stimulation (HFS) of the NBM were performed after intracerebroventricular injection of Aβ 25–35. We found that after Aβ 25–35 exposure the number of hippocampal neurons exhibiting inhibitory responses to HFS of NBM is decreased. The reverse tendency was seen in the basolateral amygdala inhibitory neural populations, whereas the number of amygdala neurons with excitatory responses decreased. The low intensity of inhibitory and excitatory responses during HFS and post-stimulus period is probably due to the anomalous basal synaptic transmission and excitability of hippocampal and amygdala neurons. These functional changes were accompanied by structural alteration of hippocampal, amygdala, and NBM neurons. We have thus demonstrated that Aβ 25–35 induces STP disruption in NBM-hippocampus and NBM-basolateral amygdala circuits as manifested by unbalanced excitatory/inhibitory responses and their frequency. The results of this study may contribute to a better understanding of synaptic integrity. We believe that advancing our understanding of in vivo mechanisms of synaptic plasticity disruption in specific neural circuits could lead to effective drug searches for AD treatment.


2002 ◽  
Vol 3 (1) ◽  
pp. 53-64 ◽  
Author(s):  
Henrique von Gersdorff ◽  
J. Gerard G. Borst

2001 ◽  
Vol 85 (5) ◽  
pp. 2088-2099 ◽  
Author(s):  
John S. Fitzpatrick ◽  
Garnik Akopian ◽  
John P. Walsh

Two forms of short-term plasticity at inhibitory synapses were investigated in adult rat striatal brain slices using intracellular recordings. Intrastriatal stimulation in the presence of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (20 μM) andd,l-2-amino-5-phosphonovaleric acid (50 μM) produced an inhibitory postsynaptic potential (IPSP) that reversed polarity at −76 ± 1 (SE) mV and was sensitive to bicuculline (30 μM). The IPSP rectified at hyperpolarized membrane potentials due in part to activation of K+ channels. The IPSP exhibited two forms of short-term plasticity, paired-pulse depression (PPD) and synaptic augmentation. PPD lasted for several seconds and was greatest at interstimulus intervals (ISIs) of several hundred milliseconds, reducing the IPSP to 80 ± 2% of its control amplitude at an ISI of 200 ms. Augmentation of the IPSP, elicited by a conditioning train of 15 stimuli applied at 20 Hz, was 119 ± 1% of control when sampled 2 s after the conditioning train. Augmentation decayed with a time constant of 10 s. We tested if PPD and augmentation modify the ability of the IPSP to prevent the generation of action potentials. A train of action potentials triggered by a depolarizing current injection of constant amplitude could be interrupted by stimulation of an IPSP. If this IPSP was the second in a pair of IPSPs, it was less effective in blocking spikes due to PPD. By contrast, augmented IPSPs were more effective in blocking spikes. The same results were achieved when action potentials were triggered by a depolarizing current injection of varying amplitude, a manipulation that produces nearly identical spike times from trial to trial and approximates the in vivo behavior of these neurons. These results demonstrate that short-term plasticity of inhibition can modify the output of the striatum and thus may be an important component of information processing during behaviors that involve the striatum.


Neuron ◽  
2009 ◽  
Vol 62 (4) ◽  
pp. 539-554 ◽  
Author(s):  
Bin Pan ◽  
Robert S. Zucker

2008 ◽  
Vol 586 (13) ◽  
pp. 3129-3146 ◽  
Author(s):  
Matthias H. Hennig ◽  
Michael Postlethwaite ◽  
Ian D. Forsythe ◽  
Bruce P. Graham

2005 ◽  
Vol 37 (3) ◽  
pp. 261-272 ◽  
Author(s):  
M. V. Storozhuk ◽  
S. Yu. Ivanova ◽  
P. G. Kostyuk

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