EXAM 4 STUDY GUIDE

Neurulation

Neurulation

Process where the neural tube develops from the ectoderm.

Neurogenesis

Mitosis producing neurons from non-neuronal cells.

Cell migration

Movement of cells to establish distinct neural cell populations.

Differentiation

Cells becoming distinct types of neurons or glial cells.

Synaptogenesis

Establishment of synaptic connections.

Apoptosis

Selective death of many neurons through programmed cell death.

Synapse rearrangement

Loss and fine-tuning of synapses.

Myelination

Glial cells wrapping axons in myelin sheaths.

Neural plate

Thickening of the ectoderm that becomes the central nervous system.

Ectoderm

Outer layer of cells.

Neural crest

Ridges of the ectoderm.

Neural groove

Thickening cell layers of the neural plate forming the neural groove.

Neural tube

Structure formed from the fusion of the ridges of the neural crest.

Spina bifida

Failure of neural tube closure in the lower back.

Anencephaly

Failure of neural tube closure at the top of the neural tube.

Neurogenesis

Progenitor cells divide through mitosis in the ventricular zone.

Mitosis

Cell division process resulting in two identical daughter cells.

Ventricular zone

Region where neurogenesis occurs in the developing brain.

Progenitor cells

Cells that give rise to neurons and glial cells.

Neuroblasts

Immature neurons that will differentiate into neurons or glial cells.

Dentate gyrus and olfactory bulb

Regions of adult neurogenesis in the brain.

Cell migration

Process during corticogenesis where cells move from inner to outer layers.

Radial glial cells

Guide cells to migrate along during corticogenesis.

Cell adhesion molecules (CAMs)

Promote adhesion to radial glia during migration.

Differentiation

Process where cells acquire specific appearance and function.

Spinal motor neuron differentiation

Example of differentiation where cells express specific genes.

Neural stem cells

Undifferentiated cells that can become various cell types.

Growth cones

Structures guiding axons and dendrites to target cells.

Lamellipodia

Thin layers of cytoplasm in growth cones.

Filopodia

Finger-like outgrowths aiding in growth cone direction.

CAMs

Molecules promoting adhesion to the environment.

Chemoattractants

Chemical signals attracting growth cones.

Chemorepellants

Chemical signals repelling growth cones.

Synaptogenesis

Rapid formation of synapses on dendrites.

Apoptosis

Selective cell death during development.

Neurotrophic factors

Promote cell survival and inhibit apoptosis.

Diablo pathway

Mitochondrial release of protein leading to apoptosis.

Synapse rearrangement

Refinement of synaptic connections.

Synaptic pruning

Process of removing and refining synapses.

Neural activity

Influences synaptic growth and survival.

Neurotrophic factors

Contribute to synaptic growth and survival.

Sensory memory

Holds sensory impressions briefly before further processing.

Short-term memories (STMs)

Last seconds to 30 seconds, unless encoded into long-term memory.

Working memory (WM)

Contains short-term memories for active processing.

Long-term memory

Stores memories for days to years, retrieved when needed.

Associationism

William James' idea that experiences link ideas in the mind.

Equipotentiality

All cortex parts contribute equally to behaviors, not accurate for memory.

Mass action

Cortex works as a whole, more cortex is better, not fully accurate.

H.M

Had profound anterograde amnesia and graded retrograde amnesia.

Serial position curves

Show primacy effect (LTM) and recency effect (STM/WM).

Declarative memory

Knowledge to tell others, MTL dependent, tested through talking.

Nondeclarative memory

Skills shown by doing, independent of MTL.

Medial temporal lobe (MTL)

Includes hippocampus, entorhinal, perirhinal, and parahippocampal cortices.

Neuroplasticity

Nervous system's ability to change in response to experience.

Long-term potentiation (LTP)

Stable increase in synaptic effectiveness.

Hebbian synapses

Neurons that fire together strengthen their connections.

LTP induction

NMDA receptors act as coincidence-detectors for synaptic changes.

Synaptic consolidation

Hours to days, stabilizes engram through synaptic changes.

Systems consolidation

Days to years, strengthens corticocortical connections.

Neural replay

Reactivation of memory traces during sleep promotes memory consolidation.

Reconsolidation

Protein synthesis-dependent return of memory trace to stable storage.

Amnesia

Memory impairment resulting from brain damage (MTL or diencephalon) or psychogenic causes.

Phobias

Crippling emotional reactions associated with a particular class of stimuli.

PTSD

Repeated reexperiencing of a traumatic event, often triggered by otherwise innocuous stimuli.

Addiction

Reinforcement learning gone awry.

Alzheimer's disease

Dementia resulting from progressive degeneration of MTL and other cortical areas.

Amygdala

Brain region involved in the stress response and memory encoding.

Drug dependence (addiction)

Overwhelming desire to self-administer a drug of abuse.

Substance abuse

A less severe pattern of drug use that does not fully meet the criteria for dependence.

Reinforcement learning

Process where addictive drugs increase dopamine release in the brain's reward pathway.

Memory decline during normal cognitive aging

Impairments in encoding and retrieval accompanied by neural changes.

Alzheimer's disease symptoms

Memory and emotional disorders, cognitive decline, disorientation, and personality changes.

Amyloid plaques

Buildup of b-amyloid protein in the brain, a hallmark of Alzheimer's disease.

Neurofibrillary (tau) tangles

Clustering of the tau protein in the brain, seen in Alzheimer's disease.

Cholinergic deterioration

Decrease in acetylcholine levels in the brain, observed in Alzheimer's disease.

Early-onset AD

Rare form with significant genetic component, linked to mutations in APP and presenilin genes.

Late-onset AD

More common form influenced by environmental factors, associated with ApoE4 gene mutation.

Amyloid cascade hypothesis

Hypothesis suggesting b-amyloid buildup contributes to Alzheimer's disease, influenced by APP, presenilin, and ApoE mutations.

Treatments for AD

Cholinergic agonists, methods to decrease b-amyloid accumulation, and preventive measures like cognitive and physical activity.