Adult Brains Turn Back Developmental Clock to Repair Damage

A new study by UCLA neuroscientists shows for the first time that a unique pattern of cellular activity found in early brain development also triggers repairs to damaged adult brains. The findings hold implications for treating brain damage caused by stroke and other disorders.

Researchers in the Department of Neurology and Brain Research Institute at UCLA used rat models to show how cells in brains damaged with stroke-like lesions, caused by interruption of blood flow, develop slow synchronous activity. This activity triggers cells to sprout new connections into areas of the brain disconnected by the lesion.

"Our research shows for the first time that this activity works to trigger repairs in adult brains," said Dr. Marie-Francoise Chesselet, professor of neurology at the David Geffen School of Medicine at UCLA and study co-author. "Previously this activity has been identified as a key component of brain development."

Scientists and clinicians had recognized this pattern of activity for many years after brain injury in humans, but its function remained unknown. This new research suggests that these cellular rhythms may be signaling a repair process in the human brain after injury.

"On its own, a damaged brain has a limited ability to repair itself. Recovery is partial," said Dr. S. Thomas Carmichael, assistant professor of neurology at UCLA and study co-author. "A better understanding of how the brain recovers from injury will allow us to manipulate the repair process and to maximize recovery from brain damage caused by stroke and other disorders."

The researchers made their discovery using a model of brain injury that allowed them to isolate signals specific to the sprouting of new connections from other changes that occur because of damage. They then measured the frequency, power and synchroneity of brain activity in a model that induced sprouting and compared to another that did not. The researchers also found that blocking the brain rhythms blocked sprouting as well.

The Journal of Neuroscience, July 15, 2002, 22(14):6062–6070

Synchronous Neuronal Activity Is a Signal for Axonal Sprouting
after Cortical Lesions in the Adult

S. Thomas Carmichael and Marie-Franc¸ oise Chesselet
Department of Neurology, University of California Los Angeles, Los Angeles, California 90095

The ability of the adult brain to form new connections in areas
denervated by a lesion (axonal sprouting) is more widespread
than previously thought, but mechanisms remain unknown. We
have previously demonstrated an unexpected, robust axonal
sprouting of contralateral corticostriatal neurons into the denervated
striatum after ischemic cortical lesions. We now take
advantage of marked differences in the degree of axonal
sprouting from contralateral homotypic cortex after two types
of cortical lesions to define the role of neuronal activity in this
response. Thermal–ischemic lesions (TCL) of sensorimotor cortex,
which induce axonal sprouting, produced two sequential
patterns of low-frequency, synchronized neuronal activity that
are not seen after similarly sized aspiration lesions, which do
not induce axonal sprouting. An early rhythm of synchronous
neuronal activity occurred in perilesion cortex on day 1 after
lesion, with a frequency range of 0.2–2 Hz. A later pattern of
activity occurred on days 2 and 3 after lesion, with a frequency
range of 0.1–0.4 Hz. This second rhythm synchronized neuronal
activity across widespread areas, including the cortical areas
that contain the cell bodies of the sprouting axons. TTX was
used to block this patterned neuronal activity and determine
whether axonal sprouting was prevented. Chronic TTX infusion
into the lesion site blocked the synchronous neuronal activity
after TCL as well as axonal sprouting. Thus, both after different
types of lesions and in the blockade experiments axonal
sprouting was strongly correlated with synchronous neuronal
activity, suggesting a role for this activity in anatomical reorganization
after brain lesion in the adult.

Key words: cerebral ischemia; tetrodotoxin; striatum; repair;
neuroplasticity; regeneration; activity; EEG

Near Boston they took a group of very old people and put them in the surroundigs of their your years. Music and furniture and I presume the full media exxperience. They tested their body processes in detail as this went along. Guess what?