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The Journal of Neuroscience, March 15, 1998, 18(6):2108-2117
Comparison of Plasticity In Vivo and In
Vitro in the Developing Visual Cortex of Normal and Protein
Kinase A RI -Deficient Mice
Takao K.
Hensch1,
Joshua A.
Gordon1,
Eugene
P.
Brandon2,
G. Stanley
McKnight2,
Rejean L.
Idzerda2, and
Michael P.
Stryker1
1 Neuroscience Graduate Program and W. M. Keck
Center for Integrative Neuroscience, Department of Physiology,
University of California, San Francisco, San Francisco, California
94143-0444, and 2 Department of Pharmacology, University of
Washington School of Medicine, Seattle, Washington 98195
Developing sensory systems are sculpted by an activity-dependent
strengthening and weakening of connections. Long-term potentiation (LTP) and depression (LTD) in vitro have been proposed
to model this experience-dependent circuit refinement. We directly
compared LTP and LTD induction in vitro with plasticity
in vivo in the developing visual cortex of a mouse
mutant of protein kinase A (PKA), a key enzyme implicated in the
plasticity of a diverse array of systems.
In mice lacking the RI regulatory subunit of PKA, we observed three
abnormalities of synaptic plasticity in layer II/III of visual cortex
in vitro. These included an absence of (1)
extracellularly recorded LTP, (2) depotentiation or LTD, and (3)
paired-pulse facilitation. Potentiation was induced, however, by
pairing low-frequency stimulation with direct depolarization of
individual mutant pyramidal cells. Together these findings suggest that
the LTP defect in slices lacking PKA RI lies in the transmission of
sufficient net excitation through the cortical circuit.
Nonetheless, functional development and plasticity of visual cortical
responses in vivo after monocular deprivation did not differ from normal. Moreover, the loss of all responsiveness to stimulation of the originally deprived eye in most cortical cells could
be restored by reverse suture of eyelids during the critical period in
both wild-type and mutant mice. Such an activity-dependent increase in
response would seem to require a mechanism like potentiation in
vivo. Thus, the RI isoform of PKA is not essential for
ocular dominance plasticity, which can proceed despite defects in
several common in vitro models of neural plasticity.
Key words:
visual cortex; plasticity; development; PKA; LTP; LTD; PPF
Copyright © 1998 Society for Neuroscience 0270-6474/98/1862108-10$05.00/0
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