Bio Bases Flashcards
what are glial cells for
Provide support for information processing neurons
what are the glial cells in the CNS/PNS
Astrocytes, oligodendrocytes, microglial (CNS);
Schwann, satellite, and enteric glia (PNS)
describe glial cells in the CNS
Astro- prun of neurons, form new neurons; Regulate blood flow, but also transfer mitochondria to neurons, and supply the building blocks of neurotransmitters, which fuel neuronal metabolism - synchronize activity of the axon by taking up chemicals released by the axon
oligo- form myelin sheath in brain and spinal cord;
micro- remove debris from injured cells (pain perception)
differences in motor, sensory, and interneurons
Motor: stimulate muscles or glands
sensory: responds to environmental stimul (light, odor, touch)
interneurons: receive input from and send input to other neurons
why is the axon hillock important
Plays important role in neural communication; cone shaped area that gives rise to the axon (site of integration); determines if signals warrant propagation of action potential and transmission of signal
why is myelination important
Helps insulate and speed conduction; it forms around the nerves; the sheath allows electrical impulses to transmit quickly and efficiently along the nerve cells
what are the nodes of ranvier
Gaps between sections of myelin where the axon is exposed
what are the two parts of the autonomic nervous system
Parasympathetic nervous system- controls body’s rest and digest functions; keep body relaxed and maintain daily functions
Sympathetic nervous system- controls the body’s fight or flight response; prepares the body for physical activity
role of the frontal, parietal, occipital, and temporal lobe
Frontal- movement and high level cognition
Parietal- spatial cognition (attention), sensory
Occipital- visual processing
Temporal- auditory processing, aspects of learning, recognition of objects
sagittal, horizontal, coronal planes
saggital: cut down the middle, left and right
horizontal (axial, transverse): cut in half, top and bottom
coronal (frontal): cut in half, front and back
grey matter vs white matter
Grey matter: consists of cell bodies that form the outer layers of the cortex and nuclei within the brain. Unmyelinated neuron cell bodies and short, unmyelinated axons
White matter: light colored interior; packed with fatty myelin that surrounds axons sending information in and out of the cortex
Glutamate is an excitatory neurotransmitter. What does that mean?
It stimulates nerve cells to take action; This action makes it more likely that chemical messages will continue to pass between nerve cells, rather than being stopped.
What are agonists and antagonists?
Agonists: An agonist is a drug that binds to the receptor, producing a similar response to the intended chemical and receptor.
Antagonist: is a drug that binds to the receptor either on the primary site, or on another site, which all together stops the receptor from producing a response.
What are the monoamine?
neurotransmitters that contain an aromatic ring connected to an amino group by a two-carbon chain.
How are the monoamines different from the catecholamines?
Monoamines are a class of neurotransmitters and neuromodulators that are derived from aromatic amino acids and are characterized by their chemical structure. Monoamines are divided into two major classes based on their chemical structure: catecholamines and indolamines:
Catecholamines
Contain a nucleus catechol group, which is a benzene group with two adjacent hydroxyl groups, and an ethylamine side chain with a single amine group. Catecholamines include dopamine, norepinephrine, and epinephrine, and are synthesized from the amino acid L-tyrosine. Catecholamines are associated with both proinflammatory and antiinflammatory effects, and can also have immunosuppressive, vasoconstrictive, and coagulative effect
Indolamines
Contain 5-hydroxytryptophan (5-HT), also known as serotonin, and melatonin, and are synthesized from the amino acid L-tryptophan
What could a monoamine oxidase inhibitor be?
Class of antidepressants that treat depression and other psychiatric illnesses by preventing the breakdown of certain brain chemicals
If a drug blocks the autoreceptors which has an effect of stimulating the release of a neurotransmitter into the synapse, is it an agonist or antagonist?
Agonist
What area of the brain do most addictive drugs have their effect?
Nucleus accumbs (basal ganglia)
What are the models of drug abuse?
Moral Model: abuse is due to failure of moral character or lack of self control.
Disease Model: addiction is considered to be a disease that requires medical treatment.
Physical Dependence Model: abusers continue to use drugs to avoid withdrawal symptoms.
Positive Reward Model: drug abuse and addiction are due to powerful reinforcement.
Which models of drug abuse work or not and why?
Moral- Little evidence that morality-based programs affect abuse rates.
Disease- no evidence of physical or biochemical abnormalities.
Physical dependence- But some people become addicted before physical dependence develops, and some addictive drugs such as cocaine don’t produce withdrawal symptoms.
Positive reward- Self-administration experiments using animals shows that addiction can occur in the absence of physical dependence or withdrawal symptoms.
What are the two original main theories of emotion?
James-Lange theory: the emotions we feel are caused by bodily changes; emotions differ due to different physiological responses.
Cannon-Bard theory: emotions precede physiological responses and help deal with a changing environment.
What are some suggestions for getting off antidepressants?
Take your time
Make a plan
Consider psychotherapy
Stay active
Seek support
Complete the taper
How can antidepressant withdraw look like depression?
Discontinuation symptoms include anxiety and depression; Anxiety and depression symptoms reason on medication in first place
What is the difference between withdrawal and depression?
Emerge within days to weeks of stopping the medication or lowering the dose, whereas relapse symptoms develop later and more gradually. Include physical complaints that aren’t commonly found in depression, such as dizziness, flulike symptoms, and abnormal sensations.
-Discontinuation symptoms disappear quickly if you take a dose of the antidepressant, while drug treatment of depression itself takes weeks to work.
-Discontinuation symptoms resolve as the body readjusts, while recurrent depression continues and may get worse.
Is having discontinuation symptoms the same as being addicted?
No it is not;
A person who is addicted craves the drug and often needs increasingly higher doses. Few people who take antidepressants develop a craving or feel a need to increase the dose
What is the difference between ED50 and LD50?
Why do we want the ED50 and LD50 to be far apart?
LD50, or lethal dose 50 is the lethal dose for 50% of individuals tested. ED50 stands for the effective dose 50, and in this case efficacy is seen as the maximum effect a drug can cause at any given dose. The smaller the ED50, the more potent the drug.
This should make sense to you because a wide or large TI can only occur if the LD50 is very high and the ED50 is much lower. In other words, this means the dose at which a drug is effective is far smaller than the dose at which the drug is lethal, giving us a wide margin of safety between the two doses.
What does the ED50 and LD50 have to do with the therapeutic index?
Both ED50 and LD50 are used to calculate the TI, or therapeutic index: the margin of safety of a drug. It is equal to LD50 divided by ED50. The higher the TI the better, as that means the margin of safety of a drug is wider.
What is the third model of emotion, how does it differ or add to James/Cannon, what research to support it?
Schachter’s cognitive attribution model: emotional labels (e.g., anger, fear, joy) are attributed to relatively nonspecific feelings of physiological arousal.
Which emotion we experience depends on cognitive systems that assess the context.
But there is evidence that patterns of autonomic activity differ between some emotions
Are there universal emotions? What are they? Do researchers agree on core emotions across all cultures?
anger, sadness, happiness, fear, disgust, surprise, contempt, and embarrassment.
But researchers do not yet agree about the number of basic emotions. One clue may come from the number of facial expressions we have.
Facial expressions are not completely universal; researchers have found isolated groups whose identifications of emotions from facial expressions did not fully agree with those of Westerners.
What areas of the brain involved in smiling and does this suggest that smiling makes you feel better?
Cingulate cortex
Facial feedback hypothesis: sensory feedback from our facial expressions can affect our mood, e.g., forcing a smile can make you feel happier.
What role does the amygdala seem to play in fear conditioning? What is the research evidence that supports this?
It is a key structure in the mediation of fear; lesions abolish fear
Forms associations between emotional responses and specific memories of stimuli stored elsewhere in the brain
Research- circuitry of fear (rat), tone with shock
Are cannabinoids involved in fear extinction? How do we know?
Yes; mice missing one type of cannabinoid receptors have a harder time extinguishing fear responses, suggesting cannabinoid signaling is important for fear extinction
Do different emotions activate different areas of the brain?
Yes; brain imaging shows unique network of brain areas is responsible for the emotion of love
Emotions are associated with bilateral changes in insula, amygdala, caudate, putamen, cingulate cortex, and prefrontal cortex activity
What factors affect the stress response in early development for rat pups?
Separated for long periods and received little maternal attention
Is fight or flight the only stress response?
No, there is also freeze
How does generational stress lead to epigenetic changes?
Epigenetic regulation- maternal deprivation exerts negative effect on adult stress responses by causing long-lasting changes in the expression of genes for adrenal steroid receptors in the brain
Define stress and outline the neuroendocrine changes that acute and chronic stress may produce in humans and other animals.
Stress is any circumstance that upsets homeostatic balance
Stimulates adrenal medulla to release epinephrine and noreprinephirne (increase heart rate and breathing)
Discuss possible explanations for what appears to be a marked sex difference in the prevalence of depression.
Women more susceptible to depression than men
May involve reproductive hormones; clinical depression often related to events in female reproductive cycle
Postpartum depression suggests some combo of hormones can precipitate depression
Outline the three stages of memory formation; include the regions of the brain believed to be involved and refer to evidence as appropriate.
Encoding- sensory info passed to short term memory (medial temporal lobe)
Consolidation – short term memory passed to long term memory (hippocampus and other medial temporal structures)
Retrieval- stored information is used (medial temporal)
Describe the symptoms of Broca’s and Wernicke’s aphasias; discuss organization of language in the brain based on studies of patients with neurological damage.
Broca- interfere with speech production
Werncke- interfere with language comprehension
Fluent aphasia- not understand read/hear
Global aphasia- total loss of ability to understand language, speak, read, write
What is selective attention and explain the difference between top-down and bottom-up processes.
Selective attention- select/process information while surpressing irrelevant distractors
Bottom-up processing involves taking in sensory information and processing it to form a coherent understanding of the task at hand. Top-down processing, on the other hand, involves using pre-existing knowledge and context to guide the understanding and execution of the task
What is the importance of studying monozygotic and dizygotic twins in epidemiological studies of disease models? What do they tell us about the genetic influence on disease heritability? What do the monozygotic and dizogotic twin studies tell us about the heritability of schizophrenia?
Mono- share identical genes; dizy- share 50% genes
Identical concordance rate is 50% pointing to genetic factor
More closely related a person is, greater that person’s chances are of also developing it
What are some of the brain differences that have been found in those with and without schizophrenia?
Cerebral ventricals enlarged (lateral ventricals)
Hippocampus and amygdala smaller
Abnormalities in activity of limbic networks
Corpus callosum has altered structure/function
Loss of gray matter
Reduced metabolic activity in frontal lobes
Is excess dopamine the main cause of schizophrenia? What is the evidence for or against this hypothesis?
It is one hypothesis of many
Says excess synaptic dopamine or dopamine receptors
Support came from amphetamine users who develop symptoms similar. Amphetamine promotes release of dopamine and blocks its reuptake
What role might stress play in the development of schizophrenia?
Stressful events increase risk of dev.; appears in adolescents (puberty, college)
Prenatal stress- influenza, low birth weight, lack of oxygen
Caused by interaction of genetic factors and stress
What are the three different generations of antipsychotics? How do they generally work?
1st gen: D2 receptor antagonists (block D2)
2nd gen: affinity for other receptors (block serotonin receptors and D2 receptors); increase dopamine release
3rd: blocking dopamine D2 receptors in areas with high dopamine levels and promoting dopamine in areas with low dopamine levels. They also balance serotonin activity, which affects mood and sleep.
What areas of the brain show increased and decreased activation among individuals with depression? What are the implications of this/ in other words what do these brain areas do?
Increased activity in prefrontal cortex (thinking, problem solving) and amygdala (fear/stress)
Decreased blood flow in parietal (social beh, self consciousness) and posterior temporal cortex (managing emotions) and anterior cingulate (motivation, emotion regulation, pain perception)
What is the McGill Pain Scale?
Describes three aspects of pain:
Sensory-discriminative quality (e.g. throbbing, gnawing, shooting)
Motivational-affective (emotional) quality (e.g. tiring, sickening, fearful)
Cognitive eval. Quality (e.g. no pain, mild, excruc)
What is Gate Control Theory?
Gate control theory of pain is a theory that explains how non-painful sensations can reduce or override painful sensations
Stimuli that compete with nociceptive stimuli and reach the brain faster will reduce the perception of the painful stimulus
What is the difference between pain and nociception?
Nociception is the sensation of pain
Pain is the perception
What is synesthesia? What are some examples of synesthesia that you have either heard of or looked up that are unique?
Condition in which stimuli in one modality evoke the involuntary experience of an additional sensation in another modality
What causes pain?
Sensory nerve endings nociceptors (pain receptors) come into contact with a painful or noxious stimulus
How is social rejection related to pain?
SJ activates the anterior cingulate cortex, upset level corelates with activation of region (pos. correlation)
Ppl who took Tylenol reported fewer hurt feelings than those taking placebo; less activation of the anterior cingulate
What is an analgesic? What are other medicines to treat pain?
A drug that reduces pain
Acupuncture- only some ppl achieve continued relief from chronic pain
—-acts by releasing endogenous opiates (Nal. Blocks or reduces its analgesic effects)
What is the main brain area associated with the pain pathway?
The anterolateral (spinothalamic) system transmits sensations of pain and temperature
Sensation of pain travels from its origin to the brain via spin crossing midline in spinal cord before ascending to the thalamus
What are ways that we or other animals can thermoregulate?
Responses to cold: shivering of muscles, constriction of blood vessels, metabolism of brown fat, increased thyroid activity
Responses to heat: accelerated respiration, perspiration, dilation of vessels
What does redundancy mean in reference to thermoregulation?
The body has multiple systems for regulating the internal environment; allows for compensation if one monitoring system fails
Neurons of the preoptic area integrate sensory inputs and drive physiological thermoregulatory responses
How does the size and myelination of an axon influence sensation transmission?
Large axons conduct action potentials faster than small axons do; myelination speeds conduction even more
Light tough receptors use moderately large, myelinated fibers and send information to the CNS rapidly
What is the purpose of fevers?
Helps fight infections
What are the two different kinds of thirst and how are they triggered?
Osmotic thirst- stimulated by high extracellular solute concentration. Water is pulled out of the cells when extracellular salt concentration is too high.
Hypovolemic thirst- stimulated by low extracellular fluid volume
What is the relationship between glucose and glucogen?
Glucose is a form of glucogen that can be stored
Glucose- principal sugar used for energy, especially in the brain
Glucogen- complex cab made of glucose molecules; stored for short term in the liver and muscles
Can a person or animal simply cut significant calories to reduce weight? What happens to their metabolism?
Ppl and animals adjust their metabolism in response to under or overnutrition, thus tend to resist losing or gaining weight
Start of diet, the basal metabolic rate will fall to prevent losing weight
What are the roles of the ventral medial and lateral hypothalamus in hunger signals?
VMH lesions cause animals to eat to excess and become obese; suggests that VMH is a satiety center
LH lesions cause cessation of eating; suggests LH is a hunger center
Is there a brain region for attention? What is it?
Yes
Posterior parietal lobe
Cingulate cortex
What is the role of the thalamus in processing most sensory information?
The thalamus transmits the information to the cerebral cortex
Most sensory pathways pass through regions of the thalamus
Why is adaptation important from an evolutionary perspective?
important from an evolutionary perspective because it allows the evolutionary process to occur piecemeal. Adaptations are inheritable characteristics that increase an organism’s ability to: find food and water, protect itself, and manage in extreme environments
What are the different kinds of sensory information transmitted on the skin cells?
Vibrations
Touch (fast adapting)
Touch (slow adapting)
Stretch (slow adapting)
How does outside energy get converted to information in the nervous system for different sensory systems?
Utilize receptor organs to convert outside information (light, sound) into neural activity
All senses use same type of energy to communicate with brain- action potentials
What is the treatment for Tourette’s Syndrome? What mechanism is it working on?
Haloperidol, a dopamine antagonist, is a primary treatment
Dopamin D2 receptors are denser in caudate nucleus of person with disorder
Is there a brain based treatment for OCD? Is that the most recommended treatment?
Cingulatomy (surgical disruption of circuits in the cingulate cortex) benefits some severly disabled OCD patients
OCD responds to SSRIs in most cases; suggests serotonin dysfunction plays a major role
What are used to treat anxiety disorders and what mechanisms are they working on? In other words, what are they doing in the brain?
Benzos are an anxiolytic (anxiety reducing)
They bind to GABA receptors and enhance GABA’s inhibitory actions by increasing the flow of Cl- ions into cells
Serotonin 5-HTIA receptor agonists and SSRIs are also used
What is bipolar disorder, how is it generally treated pharmacologically and how does that work?
Periods of depression alternating with expansive mood
Lithium treats it; mechanism is unknown
Widespread actions in the brain; interacts with circadian clock, boosts BDNF activity
What are the gender differences in depression and why?
Women have greater susceptibility to depression
May involve reproductive hormones
GABA and glutamate are inhibitory neurotransmitters. What does this mean?
prevent chemical messages from being passed along, which decreases the likelihood of a neuron firing an action potential. This prevents neurons from becoming overexcited, and can also make neurons less sensitive to incoming stimuli. In some cases, inhibitory neurotransmitters can have a relaxing effect
Why would the nervous system need inhibition?
to function properly. It helps shape and organize the flow of information through neuronal networks to create a precise neural code.
stabilizing and tuning the responses of networks of excitatory neurons.
generations of anti-depressants
1st-Monoamine oxidase inhibitors (MAOIs)
1st- Tricyclic antidepressants (TCAs)
2nd- Dopamine re-uptake inhibitors
2nd- 5-HT2 receptor antagonists
2nd- Selective Norephinephrine Re-uptake inhibitors
2nd- Selective Serotonin Re-uptake inhibitors(SSRIs)
how MAOIs and TCAs work
by blocking the monoamine oxidase (MAO) enzyme, which breaks down neurotransmitters in the brain.
blocking the reabsorption of serotonin and norepinephrine, neurotransmitters that regulate mood and behavior, in the brain.
How Dopamine re-uptake inhibitors
and
5-HT2 receptor antagonists work
increase dopamine levels in the brain by blocking the dopamine transporter (DAT).
by binding to serotonin 5-HT2 receptors without activating them, which blocks the actions of serotonin or serotonin 5-HT2 receptor agonists
How does Selective Norephinephrine Re-uptake inhibitors
AND
Selective Serotonin Re-uptake inhibitors
increase norepinephrine levels in the brain by blocking its reabsorption into nerve cells.
by preventing nerve cells from reabsorbing serotonin, a chemical messenger that carries signals between brain cells
Is there a role for cortisol/ stress in depression?
*Suggests that dysfunction of the hypothalamic-pituitary-adrenal axis may be involved in depression.
*Dexamethasone suppression test: reveals tendency to release excess cortisol.
Cortisol and depression information continued
Circulating cortisol levels are usually higher in people with depression than in psychiatric or healthy controls. In this plot, each dot represents an individual case. (C) People with depression may display increased levels of cortisol across the circadian rhythm of release.
Evidence that cortisol and stress impact depression
Evidence shows that the hypothalamic-pituitary-adrenal system is involved in depression.
Dexamethasone suppression test: reveals tendency to release excess cortisol.
The same dose of dexamethasone is far less effective at suppressing the next day’s cortisol release in people with depression.
Why not to quit antidepressants cold turkey
What is the reason the author gives for why not to quit cold turkey?
Coming off your medication can cause antidepressant withdrawal – and could set you up for a relapse of depression.
Neurons eventually adapt to the current level of neurotransmitters, and symptoms that range from mild to distressing may arise if the level changes too much too fast-for example, because you’ve suddenly stopped taking your antidepressant.
neurons
how many are there
do they stay consistent or change
grey matter or white matter?
Neuron: responsible for the communication between neuron via electrochemical impulses (neurotransmission)
-Human brain contains 100 billion
-They are modified by experience (they learn, remember, forget)
-make up grey matter in the brain
three kinds of neurons
Can either be excitatory, inhibitory, or a combination of both
apoptosis
During early development many more neurons are created than will survive due to neuronal pruning called apoptosis (refinery process)
-Helps with growth, immune surveillance, and neuroplastic development
-Neurons can malfunction causing changes in cognition, emotions, and behavior
-If too many cells get a chance to grow cancer tumors can develop
cell body (soma)
“control center,” contains RNA and DNA
The bulbous, non-process portion of a neuron or other brain cell type, containing the cell nucleus.
axon
long projection fiber from the cell body that transmits nerve impulses away from the cell body to the terminal buttons where neurotransmitters are stored and released into the synapse
-Axons begin to sprout from neuron’s cell body as they migrate to their targets
-Begin to grow during the prenatal period with the anterior commissure visible at 3 months gestation
myelin sheath
white matter or gray matter?
what myelinates first?
cover the axons and insulates it to facilitate neurotransmission (white in appearance)
-Make up most of the brain’s white matter
-White matter can be destroyed or damaged as a result of traumatic brain injury and neurologic disease such as Multiple Sclerosis (a disease in which the immune system eats away at the myelin sheaths of nerve cells)
-Spinal cord and sensory-motor tracts are first to myelinate
-Prefrontal cortex probably not fully myelinated until young adulthood🡪 this is why teenagers make stupid/risky decisions
-Appears to be correlated with acquisition and development of visual, motor, cognitive, and social skills
corpus callosum
connections between cortical and subcortical structures
myelination
process by which axons are “sheathed” in a protective layer of lipids and proteins
-Similar to function to the rubber coating of an electrical cord
-Myelin facilitates efficient neurotransmission (i.e., sending and receiving of impulses from the presynaptic neuron to the postsynaptic neuron)
-Increases brain weight from 400 grams at birth to 1410 grams at age 15
dendrite
(tree) structure that radiates out from the cell body and receives impulses from other neurons
-Growth visible at about 7 months gestation
-Growth and formation of synapses is heavily dependent on environmental stimulation following birth
node of ranvier
part of axon that has no sheath so that potassium and sodium can enter into the axon
dopamine neurotransmission
For example, Dopamine🡪 produces two types of behavior, please and motor functions
-Dopamine antagonist (blockers) decrease psychotic symptoms such as hallucinations
explain the process of neurotransmission
Neuron is just sitting there with a negative charge, -.70 millivolt
Ratio of ions inside favor the negative (chloride)
Outside the neuron is more positive ions (potassium and sodium)
Creates electrical gradient attraction
Concentration gradient: too much crowing of similar ions, so they want to get inside where there is more room
Dendrites pick up stimulation, opens nodes, positive ions go rushing in
The charge changes to about +.40 millivolt and pops open all the nodes down to the terminal buttons which then open as well
Channels close and become more negative than originally started
Slowly creeps back to original resting state
seizure and neurotransmission
Too many neurons firing at once can cause a seizure
action potential
the change in electrical potential associated with the passage of an impulse along the membrane of a muscle or nerve cell
absolute refractory period
when an action potential will not occur no matter how much stimulation is received by the neuron
Need this period so that the neuron doesn’t burn out, it is a measure of control
relative refractory period
when stronger than normal stimulation is needed to cause an action potential
propogation
The spread of the action potential down an axon, caused by successive changes in electrical charge along the length of the axon’s membrane
when nodes open to allow chemicals in to charge the neuron
nuclei
aggregated community of neurons that are related in function
are neurons directly connected
Neurons are not directly connected, rather they send chemicals (neurotransmitters) across a microscopic gap called the synaptic gap
-Each neuron may have thousands of synapses
aggregation
process by which neurons mass to form major nuclei including the corpus callosum and basal ganglia
neuroplasticity
learning, stronger connections, making room for what is important (adaptation)
-Plasticity after a brain injury neurons will borrow from each other or assume new positions
-Adults recover better than children because they already learned skills
-Brain damage occurring prior to 1 year of age tends to result in disproportionality greater impairments than those occurring later
-The brain may benefit considerably from plasticity is damage occurs between 1 and 5 years
-Benefits of plasticity are likely to dimmish substantially for injured brain following 5 years of age, although functions may recover by another process
crowding and neuroplasticity
▪ Crowding happens when too much borrowing is taking place🡪 verbal functioning may go from 50% to 85% but visual functioning may drop from 100% to 85%
neuroglia or glial cells (Nerve glue)
-Makes up 50% of the total volume of the Central Nervous System
-Is the structural support for neurons
-Will fill cavities with scar tissues caused by brain damage/lesions
-Insulates synapses
-Produces Cerebral Spinal fluid
-Repairs damaged neurons
-Facilitates transmission of signals across neurons
astrocytes
are a type of glial cell that helps synchronize activity of the axon by wrapping around the presynaptic terminal and taking up chemicals release by the axon
astrocytoma
giant tumor of astrocytes that overproduced because of a lack of apoptosis
microglia
removes waste material and other microorganisms that could prove harmful to the neuron
oligodendrocytes (brain) and schwann cells (spinal)
build the myelin sheath, in the brain and spinal cord respectively, that surrounds the axon of some neurons
radial glia
guides the migration of neurons and the growth of their axons and dendrites during embryonic development
-If the radical glia do not work🡪 abnormality in neural migration (ex. Dyslexia)
brain development from 25 days to 33 years
25 days gestation: neural tube forms
-When it does not close, spina bifida occurs
40 weeks gestation: the spinal cord, brain stem, and a substantial amount of forebrain (cerebral cortex and some subcortical structures like the thalamus) develop
Birth-First Year: cerebellum’s maximum growth rate
3-33 years old: everything is the same except myelination, which finishes at 23-24 years of age
proliferation and cell migration
-Nerve cells form via mitosis in the ventricular lining of the brain
-form axons and dendrites
-Fastest rate of brain growth occurs prenatally when 250,000 brain cells are formed each minute of mitosis
neuronal migration
consists of neurons being guided by the radial fibers of glial cells to the proper neuroanatomical destination, likely to be governed by a number of variables including genetic, physiological, chemical, and environmental factors
5th month of fetal development and migration
migration process is rapid as several layers of the cerebral cortex are visible
nerve growth factor and most severe abnormality in neural migration
chemical that helps neurons figure out where to go
-Abnormalities in neural migration
▪ Most severe: Lissencephaly- “smooth brain” when brain fails to form sulci and gyri, the brain is equivalent to a 12-week embryo
heterotopia
a neurodevelopmental disorder that is characterized by displaced pocket of grey matter (neurons) that appear in the ventricular walls or white matter due to aborted neural migration (seizures may result)
