Journal: Brain research

Article Title: Controlled cortical impact before or after fear conditioning does not affect fear extinction in mice

doi: 10.1016/j.brainres.2015.02.031

Figure Lengend Snippet: Controlled cortical impact (CCI) prior to conditioning does not affect fear conditioning or extinction. (A) Experimental timeline: mice were subjected to CCI or sham injury. After a two-week recovery period, all mice underwent fear conditioning (Cond), extinction training (Ext), and test for extinction memory (Test). (B) Sham controls (n=12) and CCI (n=12) display comparable levels of freezing 30 s immediately prior to the first tone of extinction (Ext; shaded region) and prior to the first tone of test (Test; shaded region), which is an index of context fear. Sham controls and CCI display comparable levels of freezing during Cond, Ext, and Test. (C) Total distance traveled in the open field between sham and CCI was similar, suggesting CCI does not affect locomotor activity.

Article Snippet: Fear conditioning and extinction Delay fear conditioning, which is largely hippocampal independent ( Phillips and LeDoux, 1992 ), was performed in operant chambers (17 ×17 ×25 cm 3 ; Ugo Basile, Model 46003, Varese, Italy) within sound-attenuating cubicles (Ugo Basile, Model 46000-595).

Techniques: Activity Assay

Journal: Brain research

Article Title: Controlled cortical impact before or after fear conditioning does not affect fear extinction in mice

doi: 10.1016/j.brainres.2015.02.031

Figure Lengend Snippet: Controlled cortical impact (CCI) administered post-fear conditioning (p.c.) does not affect fear expression or extinction. (A) Experimental timeline: sham injury and CCI occurred 24 h after conditioning (Cond). Following a two-week recovery period, all mice underwent extinction training (Ext) and test for extinction memory (Test). (B) Sham controls (n=14) and p.c. CCI (n=14) displayed comparable levels of freezing 30 s immediately prior to the first tone of extinction (Ext; shaded region) and prior to the first tone of test (Test; shaded region). Sham controls and CCI had similar levels of freezing during Cond, Ext, and Test. (C) Total distance traveled in the open field between sham (n=10) and CCI (n=10) was also similar, suggesting that CCI does not affect locomotor activity.

Article Snippet: Fear conditioning and extinction Delay fear conditioning, which is largely hippocampal independent ( Phillips and LeDoux, 1992 ), was performed in operant chambers (17 ×17 ×25 cm 3 ; Ugo Basile, Model 46003, Varese, Italy) within sound-attenuating cubicles (Ugo Basile, Model 46000-595).

Techniques: Expressing, Activity Assay

Journal: bioRxiv

Article Title: Dopamine in the basal amygdala signals salient somatosensory events during fear learning

doi: 10.1101/716589

Figure Lengend Snippet: VTA neurons, and amongst them dopamine neurons, respond to footshocks and acquire CS - responsiveness. ( A ) Schematic showing an optrode with 16 recording channels implanted in the VTA of a DAT Cre × ChR2-eYFP mouse. ( B ) Post-hoc histological image showing the placement of an optrode (dashed line) in the VTA in the example mouse of panels B – H (FT7612). The tracks of two tetrodes are visible (arrows). Bottom, scheme of the design of four tetrodes (T1 - T4) around the optical fiber. ( C ) Illustration of optogenetic identification of putative DAT + units. Raster plot for four electrodes (E1-E4) of one tetrode, showing unsorted spikes aligned to the onsets of n = 100, 2 ms – long laser light pulses (blue shading). Spikes at 2-8 ms after the light pulse were collected and subjected to spike clustering (see Materials and Methods). ( D ) Time course of freezing of the example mouse during the three days of the fear learning protocol. ( E ) Spiking activity of a single opto-tagged putative DAT + unit during day 2 (training day). AP frequency (top) and z-score (bottom) are shown in response to the CS (averages over the n = 30 tone presentations for each tone block), as well as in response to footshocks (averages over the n = 6 footshock presentations; right). ( F ) Spiking activity of the same unit as (E), but for responses to CS presentations on day 3 (threat memory retrieval). Right, AP-waveforms for the unit shown in E, F. ( G, H ) Responses of all units in this mouse (FT7612) to tone presentations during day1 - day 3 (G), and to footshocks on day 2 (H). Z-scores were analyzed and plotted as a function of time (number of tone block). Units classified as CS - entrained are shown in pink, and the others in gray. Thick red and black lines show average ± S.E.M. across these groups, respectively. Square symbols connected by lines represent DAT + units identified by optotagging. ( I, J, K ) Venn-type diagrams showing the number of units in the different response classes and their overlap. The data in (I) is from the example mouse shown in panels B-H. Note the overall similar distribution and overlap of response types across n = 3 mice. Two US responsive units in mouse FT6963 showed a reduction in firing upon the footshock (J, dashed areas).

Article Snippet: A classical auditory cued threat memory paradigm was performed in a conditioning chamber of a NIR Video Fear Conditioning Optogenetics Package for Mouse (MED-VFC-OPTO-M, Med Associates Inc., VT, USA).

Techniques: Activity Assay, Blocking Assay

Journal: The Journal of Biological Chemistry

Article Title: An Antibody Biosensor Establishes the Activation of the M 1 Muscarinic Acetylcholine Receptor during Learning and Memory * ^♦

doi: 10.1074/jbc.M115.681726

Figure Lengend Snippet: M 1 mAChR is activated in the hippocampus following drug treatment and memory acquisition. A, C57/BL6/NTAC mice were injected (i.p.) with vehicle or xanomeline (5 mg/kg). After 30 min, tissues were fixed by transcardial perfusion, and sections were obtained and stained with the phospho-specific serine 228 antibody and with DAPI stain to reveal the nuclei. Shown are representative sections through the CA1 region of the hippocampus. B, C57/BL6/NTAC mice ( Wild-Type ) or M 1 mAChR-knock-out mice ( M1-KO ) were injected (intraperitoneally) with BQCA (15 mg/kg) or vehicle, and after 30 min hippocampal membranes were prepared from which the M 1 mAChR was immunoprecipitated. The sample was then processed in Western blots, which were probed with phospho-specific serine 228 antibody or an M 1 mAChR-specific antibody to detect total M 1 mAChR. C, quantification of Western blots from B . The data are presented as means ± S.E. ( n = 3). Statistical analysis uses Student's paired t test. D, C57/BL6/NTAC mice were subjected to a fear conditioning training protocol or to an unpaired immediate foot shock as a control; 30 min later tissue was fixed by transcardial perfusion, and sections obtained and stained with phosphorylated Ser 228 -specific antibody ( upper panel ) or anti-c-FOS antibody ( lower panel ). All the data shown are typical of at least three independent experiments.

Article Snippet: Male C57Bl6/NTAC mice (8–15 weeks old) were placed in the conditioning chamber (Stoelting ANY-maze fear conditioning system), and after a 2-min adaptation period, the mice received three tone/foot shock pairings, where a tone (conditioned stimulus, 2.8 kH, 85 db, 30 s) always co-terminated with the foot shock (unconditioned stimulus, 2 s, 0.4 mA).

Techniques: Injection, Staining, Knock-Out, Immunoprecipitation, Western Blot, Control