VISUAL DEPRIVATION DECREASES LONG-TERM POTENTIATION IN RAT VISUAL CORTICAL SLICES
cortex; rat; plasticity; depression; period; Neurosciences & Neurology; pathways; induction; long-term potentiation; organization; nmda receptors; evoked-potentials; visual cortex; critical; current source density; dark rearing; monocular deprivation; source density analysis
A major finding in the visual plasticity literature is that visual deprivation is effective only during an early 'sensitive' period, which is lengthened by dark rearing. Unresolved is whether the visual cortex is in a normally plastic state prior to light stimulation. This cannot be addressed using paradigms employing light exposure to assess plasticity. Several developmental studies have investigated a plastic phenomenon termed long-term potentiation (LTP) in slices from cat (J. Neurophysiol., 59 (1988) 124-141) and rat (Brain Res., 439 (1988) 222-229) visual cortex. Susceptibility to the induction of LTP parallels the period of sensitivity to visual deprivation. This suggests that slices can be used to assay visual cortical plasticity, avoiding light exposure. In the present study, field potentials were recorded from slices of the primary visual cortices of dark-reared (DR) and control (CONT) Long Evans hooded rats (17 to 21 days). Field potential profiles recorded before and 90 min following tetanic electrical stimulation were subjected to current source density analysis, yielding extracellular current sink amplitudes. Tetanus resulted in LTP in both CONT and DR slices, but DR slices were significantly less potentiated. These results indicate that the primary visual cortex of DR animals is not fully plastic, indicating a role for light stimulation in inducing visual cortical plasticity.
Berry R L; Perkins A T; Teyler T J
Brain Research
1993
1993-11
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/0006-8993(93)90943-h" target="_blank" rel="noreferrer noopener">10.1016/0006-8993(93)90943-h</a>
Forms of associative synaptic plasticity
2 forms; apical dendrites; area ca1; glutamate; hippocampal ca1; in-vivo; long-term potentiation; ltp; nmda receptors; protein-phosphorylation; receptors
Teyler T J
2001
2001
Book/Monograph
n/a
Aging differentially alters forms of long-term potentiation in rat hippocampal area CA1
aged fischer-344 rats; alzheimers-disease; calcium channels; concentration-dependent manner; cortex; ltp induction; Neurosciences & Neurology; nmda receptors; Physiology; prefrontal; pyramidal neurons; synaptic transmission; visual cortex
Aging differentially alters forms of long-term potentiation in rat hippocampal area CAl. J. Neurophysiol. 79: 334-341, 1998. Long-term potentiation (LTP) of the Schaffer collateral/commissural inputs to CAI in the hippocampus was shown to consist of N-methyl-D-aspartate receptor (NMDAR) and voltage-dependent calcium channel (VDCC) dependent forms. In this study, the relative contributions of these two forms of LTP in in vitro hippocampal slices from young (2 mo) and old (24 mo) Fischer 344 rats were examined. Excitatory postsynaptic potentials (EPSP) were recorded extracellularly from stratum radiat-um before and after II tetanic stimulus consisting of four 200-Hz, 0.5-s trains given 5 s apart. Under control conditions, a compound LTP consisting of both forms was induced and was similar, in both time course and magnitude, in young and old animals. NMDAR-dependent LTP (nmdaLTP), isolated by the application of 10 mu M nifedipine (a voltage-dependent calcium channel blocker), was significantly reduced in magnitude in aged animals. The VDCC dependent form (vdccLTP), isolated by the application of 50 mu M D,L-2-amino-5-phosphonvalerate (APV), was significantly larger in aged animals. Although both LTP forms reached stable values 40-60 min posttetanus in young animals, in aged animals vdccLTP increased and nmdaLTP decreased during this time. In both young and old animals, the sum of the two isolated LTP forms approximated the magnitude of the compound LTP, and application of APV and nifedipine or genestein (a tyrosine kinase inhibitor) together blocked potentiation. These results suggest that aging causes a shift in synaptic plasticity from NMDAR-dependent mechanisms to VDCC-dependent mechanisms. The data are consistent with previous findings of increased L-type calcium current and decreased NMDAR number In aged CAI cells and may help explain age-related deficits in learning and memory.
Shankar S; Teyler T J; Robbins N
Journal of Neurophysiology
1998
1998-01
Journal Article
<a href="http://doi.org/10.1152/jn.1998.79.1.334" target="_blank" rel="noreferrer noopener">10.1152/jn.1998.79.1.334</a>