Chapter 3A - Prenatal Development Flashcards

1
Q

CONCEPTION

A

CONCEPTION occurs when a single sperm cell from the male unites with an ovum (egg) in the female’s fallopian tube in a process called FERTILISATION.

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2
Q

STAGES of PRENATAL DEVELOPMENT

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Typical prenatal development begins with CONCEPTION and ends with birth, lasting approximately 9 months. It can be divided into three periods:

1) GERMINAL PERIOD (0 to 2 weeks);
2) EMBRYONIC PERIOD (2 to 8 weeks);
3) FETAL PERIOD (8 weeks to birth).

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3
Q

The GERMINAL PERIOD

A

The GERMINAL PERIOD (0 to 2 weeks) is the period of prenatal development that takes place in the first two weeks after conception. It includes:

1) The creation of the fertilised egg, called a ZYGOTE;
2) Rapid cell division of the zygote - through MITOSIS;

3) Cell DIFFERENTIATION, starting from the second week after conception. At this stage the group of cells is referred to as a BLASTOCYST, which consists of:
A) an inner mass that will develop into the EMBRYO;
B) an outer layer of cells - the TROPHOBLAST - which provides nutrition and support for the embryo;

4) IMPLANTATION, or attachment of the blastocyst to the uterine wall, which marks the end of the germinal period and the beginning of the embryonic period.

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4
Q

The EMBRYONIC PERIOD

A

The EMBRYONIC PERIOD (2 to 8 weeks) is the period of prenatal development that occurs from two to eight weeks after conception. It starts with IMPLANTATION - attachment of the blastocyst to the uterine wall - and it includes:

1) Intense differentiation of the EMBRYO into 3 cell layers:
A) The ENDODERM, the inner layer, which will develop into the digestive and respiratory systems.
B) The MESODERM, the middle layer, which will develop into the circulatory system, bones, muscles, excretory system, and reproductive system;
C) The ECTODERM, the outer layer, which will develop into the nervous system, sensory receptors and skin.

2) The formation of life-supporting systems for the embryo, such as:
A) The AMNION, an envelope containing AMNIOTIC FLUID in which the embryo floats - it provides a shockproof environment with controlled temperature.
B) The PLACENTA, a disk-shaped organ in which small blood vessels from the mother and the baby intertwine.
C) The UMBILICAL CORD, which connects the baby to the placenta;

3) Subsequent organ formation within the the first two month of prenatal development, or ORGANOGENESIS.

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5
Q

The FETAL PERIOD

A

The FETAL PERIOD (8 weeks to birth) is the prenatal period between two months after conception and birth during which growth and development continue their dramatic course.

  • 3 months after conception, the fetus becomes active, moving its arms and legs, opening and closing its mouth, and moving its head;
  • 6 months after conception, skin parts have formed, and so have the eyes, eyelids, and a fine layer of hairs covers the head. A grasping reflex is present and irregular breathing movements occur. The fetus is, for the first time, VIABLE - it has a chance of surviving outside of the womb;
  • During the last two months of prenatal development, fatty tissues develop and various organ systems— such as heart and kidneys - function fully;
  • At birth, the average baby weighs 3.5 kg and is about 50 cm long.
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6
Q

DEVELOPMENT of the CORTEX

A

There are 8 stages of CORTICAL DEVELOPMENT:

1) NEUROGENESIS, or the production of neurons and glia cells;
2) MIGRATION of cells to their eventual locations in the nervous system;
3) DIFFERENTIATION of neurons into dis­tinctive types;
4) formation of connections between neurons - growth of AXONS, DENDRITES and SYNAPSES;
5) DEATH of particular neurons;
6) rearrangement of neural connections - PRUNING and MYELINATION.

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7
Q

1 - NEUROGENESIS

A

NEUROGENESIS - the birth of new neurons and glia - occurs in the ventricular zone in the inner face of the neural tube.
At first, cells duplicate by MITOSIS along lines that are PERPENDICULAR to the surface of the ventricular zone producing additional progenitor cells.
Then some daughter cells divide along lines that are PARALLEL to the ventricular zone, forming cells that will migrate away.
At this stage as many as 250000 new cells per minute are produced - until gestational week 7.

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8
Q

2 - CELL MIGRATION

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CELL MIGRATION is guided by RADIAL GLIA, progenitor cells that grow out from the ventricular layer of the outer margins of the nervous system.
2/3 of migrating cells wrap around the radial glia and move along them;
1/3 of new cells migrate horizontally - with no need for radial glia.
Migrating cells form the cerebral cortex in an INSIDE-OUT FASHION - cells destined for the outer cortical layers must travel through the inner layers. Once migration is complete, most - but not all - radial glia pull back their branches.

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9
Q

3 - DIFFERENTIATION OF CELLS

A

Stem cells go through DIFFERENTIATION - the development of more specialized cell types from stem cells.
There are two types of differentiation:
1) along the DORSAL-VENTRAL AXIS, neurons in the ventral half develop into MOTOR neurons, whereas neurons in the dorsal half develop into SENSORY neurons.
2) along the ROSTRAL-CAUDAL AXIS, neurons differentiation results in in the division of the nervous system into the spinal cord, hind­brain, midbrain, and forebrain. The differentiation of the SPINAL CORD and HINDBRAIN is guided by proteins encoded by HOX genes - this does not happen for the forebrain and midbrain.

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10
Q

4A - GROWTH of AXONS and DENDRITES

A

Developing axons and dendrites end in GROWTH CONES, which both sensory and motor abilities and have three structural components:

1) a main BODY containing mitochondria and microtubules;
2) FILOPODIA, spiky extensions;
3) LAMELLIPODIA, fan-shaped extensions located between the filopodia.

Both filopodia and lamellipodia have motor abilities and interact with the extracellular environment, guiding the fiber nerve - they can stick to specific sells pulling the growing axon or dendrite behind them. MICROTUBULES from the main body move forward forming a new segment of the axon/dendrite.

The FILOPODIA respond to both attracting and inhibiting chemicals released by GUIDEPOST CELLS along the way, which attract or repel an approaching growth cone.

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11
Q

4B - FORMATION OF SYNAPSES - SYNAPTOGENESIS

A

SYNAPTOGENESIS takes place as dendrites and axons grow - synaptogenesis rates from birth to about the age of four years are double those seen in adults. This growth rate is maintained until 10 years of age, at which times it declines to reach adult levels at 17 years of age.

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12
Q

5 - PROGRAMMED CELL DEATH - APOPTOSIS

A

As many as 40 to 75 percent of cells die in the process known as APOPTOSIS, or programmed cell death. The number of synapses reaches a maximum at about 2 years of age, after which pruning begins - by 16 years of age, only half of the original synapses remain

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13
Q

6A - SYNAPTIC PRUNING

A

Not only we lose neurons during development, but also synapses, in a process known as SYNAPTIC PRUNING. Only those synapses that participate in functional neural networks are maintained - according to a “use it or lose it” philosophy.
We initially have a burst of synaptic growth which peaks at 8 months, but then there is a reduction of non-functional synapses.

The extended period of synapse elimination has regional variations, with pruning ending by age 12 in the auditory cortex but continuing through mid-adolescence in the prefrontal cortex.

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14
Q

6B - MYELINATION

A

MYELINATION - the formation of myelin sheaths on certain axons - begins at the sixth gestational month and proliferates around the time of birth. It follows two patterns:

1) it occurs in a rostral direction starting with the spinal cord, then hindbrain, midbrain and forebrain;
2) sensory areas of the cortex are myelinated before motor areas.

The prefron­tal cortex - responsible for higher-order cognitive functions - is not completely myelinated until early adulthood.

Myelination shows striking regional variability in timing, with a general posterior-to-anterior trend in the timing of white matter myelination during development. Structural white matter development, in the form of advancing myelination, proceeds in tune with overall cognitive development – with areas involved in lower-order sensory and motor function myelinating earlier than areas involved with higher order executive function.

The FIRST-IN LAST-OUT THEORY of ageing suggests that higher-order cognitive skills - such as problem solving and logical reasoning - are both some of the last to develop and the first to degenerate in old age.

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15
Q

NEURAL PLATE and NEURAL TUBE

A

During gestational week three, cells in the ectoderm begin to differentiate into a new layer known as the NEURAL PLATE. Soon after, a depression forms along the midline of the neural tube and two ridges on each side develop to form the NEURAL TUBE. The neural tube will be retained in the adult brain as the system of ventricles, whereas the surrounding tissue will form the brain and the spinal cord.

At the end of gestational week four, the neural tube features three bulges:

1) the PROSENCEPHALON - future forebrain;
2) the MESENCEPHALON - future midbrain;
3) the RHOMBENCEPHALON - future hindbrain.

Further differentiations take place:

1) the prosencephalon divides in DIENCEPHALON and TELENCEPHALON;
2) the rhombencephalon divides in MYELENCEPHALON and METENCEPHALON.

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16
Q

TERATOLOGY

A

A TERATOGEN is any agent that can potentially cause a birth defect or negatively alter cognitive and behavioural outcomes and the field of study that investigates the causes of birth defects is called TERATOLOGY. Teratogens include:

1) PRESCRIPTION and NONPRESCRIPTION DRUGS;
2) PSYCHOACTIVE DRUGS;
3) INCOMPATIBLE BLOOD TYPES;
4) ENVIRONMENTAL HAZARDS;
5) MATERNAL DISEASES;
6) PARENTAL FACTORS.

Three variables modulate the effect of a teratogen:

1) DOSE: the greater the dose of an agent, the greater the effect;
2) GENETIC SUSCEPTIBILITY: the type or severity of abnormalities caused by a teratogen is linked to the genotype of the pregnant woman and the genotype of the embryo or fetus;
3) TIME of EXPOSURE: teratogen exposure does more damage when it occurs at some crucial points in development than at others - in general the embryonic period is more vulnerable than the fetal period.

17
Q

PRESCRIPTION and NONPRESCRIPTION DRUGS as TERATOGENS

A

PRESCRIPTION drugs that can function as teratogens include antibiotics, whereas harmful NONPRESCRIPTION DRUGS include ASPIRIN.

18
Q

PSYCHOACTIVE DRUGS as TERATOGENS

A

PSYCHOACTIVE DRUGS as TERATOGENS include caffeine, alcohol, and nicotine, as well as illicit drugs such as cocaine, methamphetamine, marijuana, and heroin.

FETAL ALCOHOL SYNDROME DISORDERS (FASD) are a cluster of abnormalities and problems that appear in the offspring of mothers who drink alcohol heavily during pregnancy. The abnormalities include facial deformities and defective limbs, face, and heart. FASD kids also show below average intelligence.

Researchers also have found that maternal NICOTINE SMOKING during pregnancy is a risk factor for the development of attention deficit HYPERACTIVITY disorder in children.

Infants whose mothers are addicted to HEROIN show several behavioural difficulties at birth typical of physiological addiction. The difficulties include withdrawal symptoms, such as tremors, irritability, abnormal crying, disturbed sleep, and impaired motor control. The most common treatment for heroin addiction is methadone.

COCAINE and METHAMPHETAMINE use during pregnancy are associated with low birth weight.

19
Q

INCOMPATIBLE BLOOD TYPES as TERATOGENS

A

Incompatibility between the mother’s and father’s blood types poses a risk to prenatal development - if the mother’s and the fetus’ blood types are incompatible, the mother’s immune system may produce antibodies that will attack the fetus. This can result in any number of problems, including miscarriage or stillbirth, anemia, heart defects and brain damage.

20
Q

ENVIRONMENTAL HAZARDS as TERATOGENS

A

Some specific ENVIRONMENTAL HAZARDS to the embryo or fetus include radiation, toxic wastes, and other chemical pollutants such as carbon monoxide, mercury, and lead, as well as certain fertilisers and pesticides.

21
Q

MATERNAL DISEASES as TERATOGENS

A

MATERNAL DISEASES and infections - such as rubella, syphilis, genital herpes and AIDS - can produce defects in offspring by crossing the placental barrier, or they can cause damage during birth.

22
Q

PARENTAL FACTORS as TERATOGENS

A

Some PARENTAL FACTORS can act as teratogens:

1) MATERNAL DIET: one aspect of maternal nutrition that is important for normal prenatal development is FOLIC ACID - lack of folic acid is related to neural tube defects and premature birth.
2) MATERNAL AGE: two maternal ages are of special interest - adolescence and thirty-five and older. The mortality rate of infants born to adolescent mothers is double that of infants born to mothers in their twenties. The risk that a child will have Down syndrome is directly linked to maternal age, with women older than 50 having a 10% probability of having a child with down syndrome.
3) MATERNAL STRESS negatively affects development.
4) PATERNAL FACTORS, such as exposure to lead, radiation, certain pesticides, and petrochemicals, which may cause abnormalities in sperm that lead to miscarriage or diseases such as childhood cancer.