Psyc417 Perinatal Development
Last updated: 1/9/2025
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Brain development is as follows: Neural Tube formation at wee 3, Basic Brain Region Formation Begins at week 10, Neuronal Migration Begins at Week 13, Structural Formation Begins at week 15, Synaptic Pruning Begins at week 25. Myelination Beings between weeks 28 and 40.
All rats are born pre-term (their brain development is not done). Formation of feeding circuit in the hypothalamus occurs before birth in humans, but after birth for rats.
Babies can show suckling and swallowing at week 11 of gestation. But babies born < 30 weeks of gestation can only take small amount in their stomach. If a baby is born < 34 weeks then it cannot coordinate suckling and swallowing.
While in rodents suckling ability occurs within moments after birth and pups can lick and control intake volume as early as postnatal day 3 (P3). Rats use a volumetric satiety signal when they are born. There is no hunger signal for rat pups before 2 weeks, but there are dehydration signals that control its feeding behaviors. They treat water and milk the same. After P15 they have nutritive satiety signal.
Neonatal pups vs. adult decerebrated rats:
- Decerebrated rats can show taste reactivity response but cannot acquire conditioned taste aversion
- Both show direct control of meal intake
- Both show differential responses to stimuli with different palatability levels.
- Decerebrated rats do not initiate meals (indepdentent ingestion) or perform operant behaviors.
- Decerebrated rats are hypohagic are caloric pre-load but not hyperphagic after food deprivation.
Retrograde tracing is used to figure out how the brain is connected.
Dorol vagal complex seems to be complete before the rats are born.
The main input from acurate neurons goes to the paraventricular nucleus.
Direct control uses Dorol Vagal Complex (DVC) and forebrain.
Paraventricular nuculeus of the hypothalamus is dorsal to the third ventricle.
Inputs from most forebrain areas ot the brainstem mature after P8.
Both AgRP/NPY expressing neurons and POMC/CART expressing neurons have leptin receptors (leptin receptors promote anorexigenic signal).
Ghrelin receptors are only on the NPY/AgRP neurons. When this happens NPY/AgRP release GABA which inhibits the POMC/CART expressing neurons.
When humans are born full-term all major hypothalamic cell groups have attained an adult like synaptic conncection. For rat birth, ARC neuron projections are immmiture. During this time leptin acts as a neurotrophic factor to guide giber projection. Giving a leptin or ghrelin injection to a pup during its first three weeks of a pups life do not change feeding intake. Orexigenic and anorexigenic signals do not impact food intake.
It takes until P6 for DMH to develop fibers, P8 for PVN to develop fibers, and P12 for LH.
If a pup's mom consumes a high-fat diet then the pup will grow more and they also have reduced fibers for alpha-MSH and AgRP. One possible reason for this is because the pups develop insulin and leptin resistance. For the other possibility, it could be because of ghrelin. When the pup gets an anti-ghrelin injection it incresases the growth of axons. Leptin is a neurotrophic factor while ghrelin is an anti-neurotrophic factor. Injecting anti-ghrelin causes reduced sensitivity to leptin.
This is relevant because people with Prader-Willis syndrome have a abnormally developed hypothalamus. This causes them to increase food intake and risk for obesity in adulthood.
Mothers who are obese or who are malnourished and have diabetes during gestation and lactation make babies have heavier birth weight, higher plasma leptin and insulin. Reduced desnity of alpha-MSH and AgRP fibers innervating the PVN and DMH and LH. Higher numbers of neurons expressing orexigenic neuropeptides (which make them gain weight). Also have a higher ratio of orexigenic and anorexigenic neuropeptide expression in the hypothalamus.
Not gaining too much weight during pregnancy in the third trimester is associated with lower risk of childhood overweight even in cause of GWG in the first or second trimester. (Third trimester is most important)
When someone people feel full they stop eating even if the food is palatable, but some people keep snacking.
Differences in hypothalamic feeding circuit development likely contribute to apettive traits in early life. Compared with healthy weight children, obese children have high food responsiveness. They also eat more rapidly. They always finish their plates. They also have less sensitive satiety cues.
Babies whose mothers were malnutritioned when they were in the womb have accelerated cognitive again when they are in the middle age.
Beneficial effects when babies drink breastmilk.
Neural tube defectshappen sometimes because of maternal diabetes, maternal obesity, inadequate maternal nutrition, maternal hyperthermia, and drugs.
Folate = Vitamin B9 and it is very important for DNA synthesis, there is an ideal range (too much is not good).
Maternal excess or deficiency of folic acid decreases dendritic branches. This causes an increased rate of apoptosis (measured by labeling TUNEL (DNA fragments)).