Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Abstract

Synaptic tagging and capture (STC) and cross-tagging are two important mechanisms at cellular level that explain how synapse-specificity and associativity is achieved in neurons within a specific time frame. These long-term plasticity-related processes are the leading candidate models to study the basis of memory formation and persistence at the cellular level. Both STC and cross-tagging involve two serial processes:(1) setting of the synaptic tag as triggered by a specific pattern of stimulation, and (2) synaptic capture, whereby the synaptic tag interacts with newly synthesized plasticity-related proteins (PRPs). Much of the understanding about the concepts of STC and cross-tagging arises from the studies done in CA1 region of the hippocampus and because of the technical complexity many of the laboratories are still unable to study these processes. Experimental conditions for the preparation of hippocampal slices and the recording of stable late-LTP/LTD are extremely important to study synaptic tagging/cross-tagging. This video article describes the experimental procedures to study long-term plasticity processes such as STC and cross-tagging in the CA1 pyramidal neurons using stable, long-term field-potential recordings from acute hippocampal slices of rats.

The p75 Neurotrophin Receptor Is an Essential Mediator of Impairments in Hippocampal-Dependent Associative Plasticity and Memory Induced by Sleep Deprivation

“…The mice were decapitated after anesthetization using CO 2 and the brains were quickly removed and placed into cold (4°C) artificial CSF (ACSF). The ACSF contained the following (in mM): 124 NaCl, 3.7 KCl, 1.0 MgSO 4 .7H 2 O, 2.5 CaCl 2 .2H 2 O, 1.2 KH 2 PO 4 , 24.6 NaHCO 3 , and 10 D-glucose, equilibrated with 95% O 2 -5% CO 2 (carbogen; total consumption 16 L/h; Shetty et al, 2015). From each mouse, 6 -8 transverse hippocampal slices (400 m thick) were prepared from the right hippocampus by using a manual tissue chopper.…”

“…For baseline recording and testing at each time point, four 0.2 Hz biphasic constant-current pulses (0.1 ms/polarity) were used. More details about the preparation, incubation and electrophysiological procedures were described by Shetty et al (2015).…”

MicroRNA‐134‐5p inhibition rescues long‐term plasticity and synaptic tagging/capture in an Aβ(1–42)‐induced model of Alzheimer’s disease

“…Slices were treated with 200 nM Aβ (1–42) oligomers (Anaspec Inc) in a similar manner described in our previous reports (Krishna et al, ; Sharma et al, ) and 1 µM miR‐134 inhibitor (miR‐134i) oligonucleotide (AUM‐ANT‐A‐500 FANA miR‐134‐5p‐1 Inhibitor, AUM Biotech, LLC) or 1 µM scrambled miR‐134 inhibitor (FANA scrambled miR‐134 Inhibitor, AUM Biotech, LLC) at a flow rate of 1 ml/min of ACSF and 16 L/hr of carbogen for three hours during the incubation time. The entire process of animal dissection, hippocampal slice preparation and placement of slices on the chamber was done within approximately five minutes to ensure that hippocampal slices were in good condition for electrophysiology studies (Shetty et al, ). Since the number of aged mice were limited, both right and left hippocampus and a total of five interface chambers were used simultaneously to conduct five different experiments from each mouse.…”

Inactive variants of death receptor p75NTRreduce Alzheimer’s neuropathology by interfering with APP internalization

“…Our electrophysiological procedures are described in greater detail in Shetty et al (Shetty et al, 2015). Briefly, mice were decapitated after anesthesia with CO2 and the brains were quickly removed into cold (4°C) artificial cerebrospinal fluid (ACSF: 124mM NaCl, 3.7mM KCl, 1.0mM MgSO4, 2.5mM CaCl2, 1.2mM KH2PO4, 24.6mM NaHCO3, and 10mM D-glucose) equilibrated with 95% O2/5% CO2 (carbogen; total consumption 16L/h).…”