scholarly journals Altered neurotransmission in the lateral amygdala in aged human apoE4 targeted replacement mice

2014 ◽  
Vol 35 (9) ◽  
pp. 2046-2052 ◽  
Author(s):  
Rebecca C. Klein ◽  
Shawn K. Acheson ◽  
Brian E. Mace ◽  
Patrick M. Sullivan ◽  
Scott D. Moore
Keyword(s):  
2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Anwesha Banerjee ◽  
Jonathan A. Luong ◽  
Anthony Ho ◽  
Aeshah O. Saib ◽  
Jonathan E. Ploski

2010 ◽  
Vol 107 (28) ◽  
pp. 12692-12697 ◽  
Author(s):  
Joshua P. Johansen ◽  
Hiroki Hamanaka ◽  
Marie H. Monfils ◽  
Rudy Behnia ◽  
Karl Deisseroth ◽  
...  

2001 ◽  
Vol 85 (2) ◽  
pp. 714-723 ◽  
Author(s):  
E.S.L. Faber ◽  
R. J. Callister ◽  
P. Sah

In this study, we characterize the electrophysiological and morphological properties of spiny principal neurons in the rat lateral amygdala using whole cell recordings in acute brain slices. These neurons exhibited a range of firing properties in response to prolonged current injection. Responses varied from cells that showed full spike frequency adaptation, spiking three to five times, to those that showed no adaptation. The differences in firing patterns were largely explained by the amplitude of the afterhyperpolarization (AHP) that followed spike trains. Cells that showed full spike frequency adaptation had large amplitude slow AHPs, whereas cells that discharged tonically had slow AHPs of much smaller amplitude. During spike trains, all cells showed a similar broadening of their action potentials. Biocytin-filled neurons showed a range of pyramidal-like morphologies, differed in dendritic complexity, had spiny dendrites, and differed in the degree to which they clearly exhibited apical versus basal dendrites. Quantitative analysis revealed no association between cell morphology and firing properties. We conclude that the discharge properties of neurons in the lateral nucleus, in response to somatic current injections, are determined by the differential distribution of ionic conductances rather than through mechanisms that rely on cell morphology.


2009 ◽  
Vol 65 ◽  
pp. S137
Author(s):  
Chieko Tazuke ◽  
Hideki Miwa ◽  
Minoru Matsui ◽  
Ayako M. Watabe ◽  
Toshiya Manabe

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Ke-Xin Li ◽  
Mu He ◽  
Wenlei Ye ◽  
Jeffrey Simms ◽  
Michael Gill ◽  
...  

TMEM16B (ANO2) is the Ca2+-activated chloride channel expressed in multiple brain regions, including the amygdala. Here we report that Ano2 knockout mice exhibit impaired anxiety-related behaviors and context-independent fear memory, thus implicating TMEM16B in anxiety modulation. We found that TMEM16B is expressed in somatostatin-positive (SOM+) GABAergic neurons of the central lateral amygdala (CeL), and its activity modulates action potential duration and inhibitory postsynaptic current (IPSC). We further provide evidence for TMEM16B actions not only in the soma but also in the presynaptic nerve terminals of GABAergic neurons. Our study reveals an intriguing role for TMEM16B in context-independent but not context-dependent fear memory, and supports the notion that dysfunction of the amygdala contributes to anxiety-related behaviors.


2016 ◽  
pp. 165-169 ◽  
Author(s):  
J.-J. ZHANG ◽  
X.-D. LIU ◽  
L.-C. YU

Acute morphine exposure induces antinociceptive activity, but the underlying mechanisms in the central nervous system are unclear. Using whole-cell patch clamp recordings, we explore the role of morphine in the modulation of excitatory synaptic transmission in lateral amygdala neurons of rats. The results demonstrate that perfusion of 10 μM of morphine to the lateral amygdala inhibits the discharge frequency significantly. We further find that there are no significant influences of morphine on the amplitude of spontaneous excitatory postsynaptic currents (sEPSCs). Interestingly, morphine shows no marked influence on the evoked excitatory postsynaptic currents (eEPSCs) in the lateral amygdala neurons. These results indicate that acute morphine treatment plays an important role in the modulation on the excitatory synaptic transmission in lateral amygdala neurons of rats.


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