Biology Reference
In-Depth Information
synthesis of proBDNF can modulate synaptic plasticity in the developing
visual system (
Schwartz, Schohl, & Ruthazer, 2011
).
3. CNS NEURONS LOSE NEURONAL ACTIVITY AFTER
INJURY
After injury or in eyes with neurodegenerative diseases of themammalian
CNS, the CNS neurons cannot regenerate their axons to their targets and die
relatively quickly. They are not replaced from a pool of progenitor or stemcells.
In the visual system, for example, RGC axons injured in the optic nerve (ON)
fail to regenerate back to the brain and often die after injury (
Goldberg&Barres,
2000
). The RGCs lose their trophic responsiveness after axotomy
in vivo
(
Shen,
Wiemelt, McMorris, & Barres, 1999
) and lose their physiological properties af-
terONtransection (
Takao,Miyoshi,Watanabe, &Fukuda, 2002
). Axotomized
RGCs have smaller receptive field centers, weaker visual responses, and lower
spontaneous activity (
Takao et al., 2002
). However, they retain their dendritic
configurations when they survive the axotomy (
Watanabe, Sawai, & Fukuda,
1995
). These results suggest substantial changes in the membrane properties of
the axotomized RGCs and/or possible decrease in the synaptic inputs from bi-
polar and amacrine cells onto the surviving RGCs (
Takao et al., 2002
).
In retinal degenerative diseases, such as retinitis pigmentosa (RP), a rem-
odeling of the inner retina follows the loss of the photoreceptors (
Marc et al.,
2007
), and a subset of inner retinal neurons may also die (
Stone, Barlow,
Humayun, de Juan, & Milam, 1992
). Lose of retinal cells may result in reor-
ganization in target areas such as LGN or V1, similar to how different types of
deafferentation evoke a reorganization of somatosensory maps within the
CNS, and rapid reorganization occurs within minutes after deafferentation
in the mammalian brainstem, thalamus, and cortex (
Moore et al., 2000
). Such
rewiring of neural connections is mediated by plasticitymechanisms which are
strongly modulated by electrical activity (
Brus-Ramer, Carmel, Chakrabarty,
& Martin, 2007
), thus indicating how loss of neuronal electrical activity may
affect reorganization and plasticity locally and/or in the target areas.
4. SURVIVAL-PROMOTING EFFECTS OF ELECTRICAL
ACTIVITY ON NEURONS IN VITRO
In
in vitro
studies of the neuroprotective effects of neuronal activity,
the neurons were activated by depolarizing the neurons by high extracellular
potassium (K
รพ
). In addition, drugs such as forskolin were applied to elevate
the cAMP levels, or electrical stimulation was used to activate the neurons.
