scholarly journals Coactivation of β-Adrenergic and Cholinergic Receptors Enhances the Induction of Long-Term Potentiation and Synergistically Activates Mitogen-Activated Protein Kinase in the Hippocampal CA1 Region

2000 ◽  
Vol 20 (16) ◽  
pp. 5924-5931 ◽  
Author(s):  
Ayako M. Watabe ◽  
Paulette A. Zaki ◽  
Thomas J. O'Dell
Keyword(s):  
Protein Kinase ◽  
Long Term Potentiation ◽  
Mitogen Activated Protein Kinase ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Mitogen Activated Protein ◽  
Adrenergic And Cholinergic Receptors

AMPA Silencing Is a Prerequisite for Developmental Long-Term Potentiation in the Hippocampal CA1 Region

2008 ◽  
Vol 100 (5) ◽  
pp. 2605-2614 ◽  
Author(s):  
Therése Abrahamsson ◽  
Bengt Gustafsson ◽  
Eric Hanse
Keyword(s):  
Developmental Stages ◽  
Long Term Potentiation ◽  
Synaptic Strength ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Silent Synapses ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca3

AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) unsilencing is an often proposed expression mechanism both for developmental long-term potentiation (LTP), involved in circuitry refinement during brain development, and for mature LTP, involved in learning and memory. In the hippocampal CA3–CA1 connection naïve (nonstimulated) synapses are AMPA signaling and AMPA-silent synapses are created from naïve AMPA-signaling (AMPA-labile) synapses by test-pulse synaptic activation (AMPA silencing). To investigate to what extent LTPs at different developmental stages are explained by AMPA unsilencing, the amount of LTP obtained at these different developmental stages was related to the amount of AMPA silencing that preceded the induction of LTP. When examined in the second postnatal week Hebbian induction was found to produce no more stable potentiation than that causing a return to the naïve synaptic strength existing prior to the AMPA silencing. Moreover, in the absence of a preceding AMPA silencing Hebbian induction produced no stable potentiation above the naïve synaptic strength. Thus this early, or developmental, LTP is nothing more than an unsilencing (dedepression) and stabilization of the AMPA signaling that was lost by the prior AMPA silencing. This dedepression and stabilization of AMPA signaling was mimicked by the presence of the protein kinase A activator forskolin. As the relative degree of AMPA silencing decreased with development, LTP manifested itself more and more as a “genuine” potentiation (as opposed to a dedepression) not explained by unsilencing and stabilization of AMPA-labile synapses. This “genuine,” or mature, LTP rose from close to nothing of total LTP prior to postnatal day (P)13, to about 70% of total LTP at P16, and to about 90% of total LTP at P30. Developmental LTP, by stabilization of AMPA-labile synapses, thus seems adapted to select synaptic connections to the growing synaptic network. Mature LTP, by instead strengthening existing stable connections between cells, may then create functionally tightly connected cell assemblies within this network.

Glycosylation of proteins during a critical time window is necessary for the maintenance of long-term potentiation in the hippocampal CA1 region

Neuroscience ◽  
1999 ◽  
Vol 91 (1) ◽  
pp. 175-183 ◽  
Author(s):  
H. Matthies ◽  
J. Kretlow ◽  
H. Matthies ◽  
K.-H. Smalla ◽  
S. Staak ◽  
...  
Keyword(s):  
Time Window ◽  
Critical Time ◽  
Long Term Potentiation ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Term Potentiation ◽  
Hippocampal Ca1

Neural 17β-estradiol facilitates long-term potentiation in the hippocampal CA1 region

Neuroscience ◽  
2011 ◽  
Vol 192 ◽  
pp. 67-73 ◽  
Author(s):  
S. Grassi ◽  
A. Tozzi ◽  
C. Costa ◽  
M. Tantucci ◽  
E. Colcelli ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
17Β Estradiol
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