BDNF & Exercise

one post-synaptic effect is to enhance

NMDA neurotransmitter receptor function

IGF-1 and BDNF

act via converging second messenger systems in the neuron

planning and executing movements

advantageous in pursuit of food, survival

could be physical exercise improving energy metabolism

allowing more efficient brain performance

dietary changes that improve memory in the aged animal

also act on BDNF system

ability to perceive food

anticipate animals movements, remember bountiful locations etc. facilitates survival

caloric restriction, or every-other-day-fasting (EODF)

both increase BDNF and enhance cognition

thus, likely the interactions between

cognitive and physical abilities could enhance one another

another strain of mutant mice with low BDNF

eat too much, are overweight and have insulin insensitivity

a pre-synaptic effect BDNF

exerts is to increase synapsis 1 expression, no more transmitter released per action potential

brain uses roughly one quarter of

glucose in blood

people with metabolic disorders also

have low levels of BDNF

the anatomical distribution of BDNF in the brain shows that it is the

highest in hippocampus (learning) and hypothalamus (neuroendocrine: energy regulation)

energy pursuit and consumption, one

important key to efficient brain function

multiple studies in animals and people show exercise

improves cognitive function

blocking BDNF

inhibits learning, restoring it restores learning

IGF-1 also enhances

insulin function

haas been proposed that thought is

internalized movement planning, execution

insulin-like growth factor 1 (IGF-1)

is a hormone made in the brain and in the periphery

IGF-1 enhances hippocampul learning

its hypothesized through interacting with BDNF since IGF-1 stimulates BDNF synthesis

BDNF initiates a number of biochemical changes associated with

learning, both pre and post synaptic

the ventral media hypothalamic nucleus (VMN) plays a role in controlling

lipids (fat) storage in the body

BDNF and pro-BDNF both are found in

low-levels of alzheimers disease

BDNF is also involved with controlling eating behaviors

mice with impaired BDNF levels overeat and become obese

IGF-1 has

neurotropic effects

VMN damage causes

overeating which led to the old theory that VMN is the satiety center in the body

best hunter/gatherers were likely humans who could

perform best cognitive functions (memory) combined with physical functions (speed)

there are limits to improvement

possibly due to individual capabilities

in many non-human animal species, the male that is most successful at

providing resources for offspring often is most successful at reproducing

a recent case study of a person with natural mutation that caused BDNF

receptors to not work showed overeating, obesity and cognitive problems

BDNF administration in these animals also

restores insulin sensitivity

hippocampus, central memory structure fires in

rhythmical patter, ideal for learning while animal is walking

BDNF is important in

synaptogenesis and LTP, both physiological mechanisms of learning in the brain

brain-derived neurotropic factor (BDNF)

synthesis stimulated by physical exercise

exogenous BDNF, either ICV or peripheral will restore mutant mice

that have lower BDNF levels to normal weight range

if males physically compete for territory

the strongest, toughest, most clever reproduce most

advanced human cognitive capabilities may have evolved because

they aid in acquiring food

the high affinity BDNF receptor

trckB is also upregulated by exercise

BDNF stimulates

trckB receptors and is trophic to neurons, pro-BDNF, stimulates p75 receptors and may trigger apoptosis so the balance of BDNF and pro-BDNF is important to determining its net effects

chronic exercise keeps BDNF

upregulated, while other neurotrophins will go back to baseline, so BDNF is the best candidate molecule right now for exercise' effects

hippocampus site BDNF most greatly up-regulated

with exercise also involved with spatial memory

some pro-BDNF is likely cleaved into

BDNF after released, from the neuron while some pro-BDNF is which exerts its own effects is not cleaved into BDNF

pro-BDNF is the precursor protein to

BDNF, it is released from neurons as well as BDNF itself is released