Bio Midterms PDF

CHAPTER 4: I. Genetics and Behavior 1. Heredity vs. Environment: ○ Heredity: Refers to the genetic factors inherited from parents. ○ Environment: External influences affecting behavior and development. ○ Both genetic and environmental factors contribute to behavior an...

CHAPTER 4: I. Genetics and Behavior 1. Heredity vs. Environment: ○ Heredity: Refers to the genetic factors inherited from parents. ○ Environment: External influences affecting behavior and development. ○ Both genetic and environmental factors contribute to behavior and physical traits. ○ Example: People born blind exhibit facial expressions similar to those of sighted relatives, implying a genetic contribution to these expressions (Peleg et al., 2006). 2. Mendelian Genetics: ○ Inheritance through dominant and recessive genes, with complex interactions influencing traits. ○ Genes: Units of heredity maintaining their structure across generations. ○ Chromosomes: Strands of genes that come in pairs. ○ DNA (Deoxyribonucleic Acid): The molecule that carries genetic information, composed of four bases (adenine, guanine, cytosine, and thymine). ○ RNA (Ribonucleic Acid): Synthesized from DNA and used to create proteins. Messenger RNA (mRNA): Copies genetic information from DNA for protein synthesis. ○ Proteins: Chains of amino acids formed based on RNA sequences. They can be structural or act as enzymes (biological catalysts regulating chemical reactions). ○ Dominant and Recessive Genes: Dominant Gene: Expressed in both homozygous and heterozygous conditions. Recessive Gene: Expressed only in the homozygous condition (e.g., the gene for blue eyes). Example: Eye color—brown eyes are dominant, blue eyes are recessive. 3. Gene Expression: ○ Homozygous: Having two identical genes on a chromosome pair. ○ Heterozygous: Having two different genes on a chromosome pair. ○ Gene Variability: Some genes can overlap or interact with other chromosomes, influencing traits like height (which is controlled by multiple genes). ○ Epigenetics: Study of how gene expression can change without altering the DNA sequence itself, often influenced by environmental factors. Example: Acetyl groups added to histone proteins loosen their grip on DNA, allowing certain genes to be expressed, while methyl groups can suppress gene expression. II. Evolution and Behavior 1. Sex-Linked and Sex-Limited Genes: ○ Differentiated by location and activation, impacting traits specific to one sex. ○ Sex-Linked Genes: Found on sex chromosomes (X or Y). Example: Red-green color vision deficiency, controlled by an X-linked gene.  ○ Sex-Limited Genes: Present in both sexes but expressed more in one sex due to hormonal influences (e.g., chest hair in men, breast size in women). 2. Mutations and Genetic Changes: ○ Mutations: Changes in DNA that affect gene expression, such as point mutations where one DNA base changes. ○ Microduplications and Microdeletions: Alterations in chromosome segments, sometimes associated with disorders like schizophrenia. ○ Example: The FOXP2 gene differs between humans and chimpanzees, contributing to differences in language ability (Konopka et al., 2009). 3. Epigenetics: ○ Epigenetic changes can be inherited for a generation or two. Experiences such as maternal malnutrition can affect gene expression, predisposing offspring to traits like obesity. ○ Environmental influences can modify gene expression without altering the underlying DNA sequence. ○ Methylation: The addition of methyl groups to DNA, often silencing genes. ○ Acetylation: The addition of acetyl groups to histones, making genes more accessible for expression. ○ Drug Addiction: Alters gene expression in the brain via epigenetic changes. ○ Trauma: Severe early childhood trauma can affect gene methylation, increasing the risk of disorders like depression and PTSD. 4. Heredity vs. Environment Heredity: Refers to genetic contributions to traits. Heritability ranges from 0 (no genetic contribution) to 1 (complete genetic control). Environment: Includes external factors and experiences that influence traits. 5. Estimating Heritability Twin Studies: ○ Monozygotic Twins: Identical twins sharing 100% of their genes. ○ Dizygotic Twins: Fraternal twins sharing about 50% of their genes. ○ Higher similarity between monozygotic twins compared to dizygotic twins suggests a genetic influence. Adoption Studies: ○ Similarities between adopted children and their biological parents suggest genetic influence. Virtual Twins: Children adopted into the same family at the same age can indicate environmental influences if they show similarities. Genetic Studies: ○ Candidate Gene Approach: Tests specific genes for their association with traits. ○ Genome-Wide Association Studies (GWAS): Examines all genes across individuals to find associations with traits, though results can be complex and sometimes misleading.  6. Examples of Heritability High Heritability Traits: Loneliness, neuroticism, cognitive performance, educational attainment, etc. Low Heritability Traits: Religious affiliation. 7. Effect of Environment on Heritability Environmental Modification: Even traits with high heritability can be influenced by environmental interventions. PKU (Phenylketonuria): A genetic disorder that can be managed with a special diet, illustrating how environment can modify genetic traits. III. Evolutionary Psychology Overview Definition: Evolutionary psychology studies how behaviors evolved through natural selection and the functional advantages provided by these behaviors. Evolutionary Theory Descent with Modification: The idea that species evolve through changes over generations. Natural Selection: ○ Variation: Offspring generally resemble their parents but can have genetic variations. ○ Selection: Genes associated with successful reproduction become more common over generations. ○ Artificial Selection: Breeders select individuals with desired traits to produce the next generation. Common Misconceptions: ○ Lamarckian Evolution: The false idea that traits acquired during an individual’s life are inherited by offspring. ○ Human Evolution: Evolution continues based on reproductive success, not just survival. ○ Evolution and Improvement: Evolution improves fitness relative to current environments but does not necessarily imply progress or improvement. ○ Evolutionary Benefit: Evolution benefits genes, not individuals or species. Genes use individuals to propagate themselves. How Genes Influence Behavior Gene-Behavior Interaction: Genes influence behavior through complex interactions with the environment and body chemistry. Roundabout Effects: Genes can influence behavior indirectly through various pathways, such as increased success in certain activities leading to more focus on those activities. Key Concepts 1. Evolutionary Explanations:  ○ Behavioral Evolution: Behaviors characteristic of a species are believed to have evolved to provide advantages to ancestors. ○ Functional Explanations: Focuses on how genes reflecting those of ancestors favor certain behaviors. 2. Examples: ○ Vision: Species develop vision types (e.g., color vs. peripheral) suited to their lifestyle needs. ○ Sleep Patterns: Species that face more threats sleep less compared to those with fewer threats. ○ Eating Habits: Eating patterns adapt to survival needs (e.g., bears store fat, small birds eat minimally). 3. Human Behaviors: ○ Goose Bumps: Erection of hairs as a vestigial trait for insulation and intimidation in ancestors. ○ Infant Grasp Reflex: Grasp reflex in infants as an evolutionary trait aiding survival in ancestors. 4. Controversial Explanations: ○ Sexual Behavior: Differences in casual sex preferences between men and women, possibly linked to reproductive strategies. ○ Aging and Longevity: Variation in aging linked to genetic factors; aging might be an evolved adaptation to reduce competition with descendants. 5. Altruistic Behavior: ○ Definition: Actions that benefit others at a potential cost to oneself. ○ Human Altruism: Examples include charitable donations and life-saving acts. ○ Nonhuman Altruism: Less common and often motivated by self-interest (e.g., crows attracting others to share food for protection). 6. Theoretical Explanations for Altruism: ○ Kin Selection: Altruism directed toward relatives to promote the survival of shared genes. ○ Reciprocal Altruism: Helping others with the expectation of reciprocation or based on observed helpfulness. ○ Group Selection: Cooperative groups thrive better, but uncooperative individuals can benefit. Effective in humans due to ability to enforce cooperation. Criticisms and Challenges Testing Explanations: Criticized for proposing explanations without adequate empirical testing. Development of the Brain 1. Introduction Concept: Brain development involves changes in neurons, their connections, and how experiences shape development. 2. Maturation of the Vertebrate Brain Homeobox Genes:  ○ Definition: Genes that regulate anatomical development, including the organization of the body and brain. ○ Impact: Mutations can lead to brain disorders and physical deformities. Neural Tube Formation: ○ Process: Begins around 2 weeks of embryonic development. The neural tube forms from the dorsal surface and develops into the central nervous system. ○ Components: The neural tube becomes the spinal cord and brain ventricles. Early Brain Growth: ○ Weight: At birth, the human brain weighs about 350 grams; by one year, it reaches approximately 1,000 grams, nearing adult weight. ○ Development: Primary sensory areas mature early, while areas responsible for higher cognitive functions, such as the prefrontal cortex, develop later. 3. Growth and Development of Neurons Proliferation: ○ Definition: Production of new cells, primarily occurring before birth. ○ Differences: Human neurons proliferate longer compared to chimpanzees. Migration: ○ Definition: The movement of neurons to their final locations guided by chemicals like immunoglobulins and chemokines. ○ Impact: Deficits in these chemicals can impair brain development and lead to mental retardation. Synaptogenesis: ○ Definition: Formation of synapses, which begins before birth and continues throughout life. ○ Variation: The process slows with age. Myelination: ○ Definition: Formation of myelin sheaths by glial cells, which speeds up neuronal transmission. ○ Process: Begins in the spinal cord and progresses to the brain; continues for decades and is influenced by learning. 4. New Neurons Later in Life 1. Traditional Belief: ○ Past View: Neurons were thought to be formed only during early development. 2. Exceptions: ○ Olfactory Receptors: Continuously regenerate due to stem cells in the nose. ○ Songbirds: Demonstrate seasonal neuronal loss and regeneration. ○ Hippocampus: New neurons form in the adult hippocampus, which is crucial for memory. 3. Research Methods: ○ 14C Method: Uses radioactive carbon to trace the age of cells and determine new neuron formation in humans. The Vulnerable Developing Brain 1. Importance of Early Development  Gastrulation: ○ Definition: An early stage in embryological development that sets the foundation for future development. ○ Significance: Errors during this stage can lead to severe developmental issues. 2. Vulnerability to External Factors Impact of Malnutrition and Toxic Chemicals: ○ Malnutrition: Can severely impact brain development, leading to problems like impaired mental function. ○ Toxic Chemicals: Exposure to harmful substances can disrupt development. Examples: ○ Thyroid Deficiency: Causes mental retardation in infants; less severe effects in adults. ○ Fever: Impairs neuron proliferation in fetuses. ○ Low Blood Glucose: Affects brain development before birth. 3. Fetal Alcohol Syndrome (FAS) Definition: A condition resulting from heavy alcohol consumption during pregnancy. Characteristics: ○ Physical: Facial abnormalities, heart defects. ○ Behavioral: Hyperactivity, impulsiveness, difficulty with attention. ○ Cognitive: Varying degrees of mental retardation. Long-term Effects: ○ Cerebral Cortex: Thinning of the cortex that persists into adulthood. ○ Mechanisms: Neuron Proliferation: Alcohol interferes with early neuron development. Neuron Migration and Differentiation: Later stages affected by alcohol. Synaptic Transmission: Impaired by alcohol, leading to neuron death. 4. Alcohol’s Mechanisms of Damage Apoptosis: ○ Definition: Programmed cell death that can be induced by alcohol. ○ Effect: Alcohol inhibits glutamate receptors (excitatory) and enhances GABA receptors (inhibitory), causing an imbalance that leads to neuron death. Excitotoxicity: ○ Definition: Damage due to excessive stimulation of neurons. ○ Cause: Alcohol initially reduces excitation but later causes excessive excitation as it leaves the system. 5. Influence of Maternal Stress Stress in Animals: ○ Example: Stress in mother rats leads to increased fearfulness and behavioral changes in offspring. Human Analogies: ○ Effects: Children from stressed or impoverished mothers may have increased academic and social difficulties. 6. Sensory Input and Brain Development Ferret Study: ○ Experiment: Redirected visual input to auditory brain areas. ○ Result: The auditory cortex reorganized to process visual information, indicating that sensory input influences cortical development. Mice Study: ○ Experiment: Redirected pain input to touch areas in the cortex. ○ Result: The cortex adapted to process pain in touch areas, demonstrating the role of sensory input in cortical differentiation. 7. Risks of Anesthetic and Anxiety-Reducing Drugs GABA Activity: ○ Definition: GABA is the brain’s main inhibitory neurotransmitter. ○ Effect: Increased GABA activity can reduce brain excitation, potentially leading to increased apoptosis in developing neurons. Risk: Prolonged exposure to these drugs during development might be harmful due to their impact on neuronal survival. Fine-Tuning by Experience I. Introduction Concept: The nervous system can remodel itself based on experiences, similar to how construction workers improvise during house building due to unpredictable details. II. Dendritic Branching and Neuronal Changes Dendrites: Central structures stabilize by adolescence, but peripheral branches remain flexible throughout life. Research Findings: ○ Purves & Hadley (1985): Observed that dendritic branches in mice extend or retract over time. ○ Xu et al. (2007): 6% of dendritic spines change within a month, indicating synaptic turnover related to learning. III. Effects of Environment Enriched vs. Deprived Environments: ○ Greenough (1975), Rosenzweig & Bennett (1996): Enriched environments (e.g., larger cages with objects) lead to a thicker cortex, more dendritic branching, and improved learning. ○ Campi et al. (2011): Wild rats have more neurons in visual areas compared to lab rats in deprived environments. Physical Activity: ○ Running Wheels: Enhance axon and dendrite growth and learning, even in isolation (Marlatt et al., 2012). IV. Far vs. Near Transfer in Training Near Transfer: Improvement in a similar task due to training. Far Transfer: General improvement in intellect due to training. Generally weak and less effective (Melby-Lervåg et al., 2016; Simons et al., 2016). V. Special Experiences and Sensory Adaptation Blindness and Deafness: ○ Blind People: Greater touch sensitivity, especially in fingers. Occipital cortex (usually visual) activates for touch (Burton et al., 2002). ○ Deaf People: Enhanced vision and touch responses in auditory cortex areas (Karns et al., 2012). VI. Music Training Effects on the Brain: ○ Enhanced Auditory Responses: Musicians show stronger responses to sounds, and increased gray matter in the auditory cortex (Schneider et al., 2002). ○ Brain Changes: Musicians have thicker gray matter in areas related to hearing and hand control (Gaser & Schlaug, 2003). Early Training: Starting music training early results in more significant brain changes (Steele et al., 2013). VII. Brain Changes from Brief Practice Examples: ○ Juggling: Changes in brain areas related to movement and coordination (Draganski et al., 2004). ○ Video Games: Short-term playing leads to measurable brain changes (Colom et al., 2012). VIII. Potential Downsides of Reorganization Musician’s Cramp: Extensive practice can lead to overlapping cortical representations, causing difficulties in precise hand movements (Furuya & Hanakawa, 2016). Treatment: Proprioceptive training can help improve control and sensation (Aman et al., 2015) Brain Development and Behavioral Changes 1. Adolescence Impulsiveness: Adolescents are more impulsive compared to adults, which can lead to risky behaviors such as dangerous driving, substance abuse, and spending sprees. Discounting the Future: Adolescents tend to prefer immediate rewards over larger, delayed ones more than adults. For example, they might choose $100 now rather than waiting for a higher amount later (Steinberg et al., 2009). This tendency is not limited to financial decisions but also applies to other types of rewards. Prefrontal Cortex Development: Adolescents show weaker responses in the prefrontal cortex, which is responsible for inhibiting behaviors (Geier et al., 2010). This area’s maturity correlates  with impulse control (Gilaie-Dotan et al., 2014; van den Bos et al., 2014). Despite this, the immaturity of the prefrontal cortex is only a small part of the explanation for impulsive behavior. Most risky behaviors are more common among those with a history of troublesome behaviors (Bjork & Pardini, 2015). The increase in risky behavior during the teenage years may be linked to heightened responses to rewards and the desire for excitement, especially to impress peers (Braams et al., 2015; Casey & Caudle, 2013). 2. Old Age Cognitive Decline: Memory and reasoning abilities generally decline with age. This is due to loss of synapses, slower synaptic changes, and thinning of the temporal and frontal cortices. The hippocampus, crucial for memory, also decreases in volume with age (Fjell et al., 2009; Erickson et al., 2010). Variability in Aging: Cognitive decline varies among individuals. While some experience significant loss, others retain cognitive abilities, often aided by physical fitness and accumulated knowledge (Barzilai et al., 2006; Fletcher et al., 2016). Older individuals may use compensatory strategies, such as activating different brain areas to maintain function (Park & McDonough, 2013). Interventions: Daily exercise has been shown to improve cortical activity, attention, and memory in older adults (Hayes et al., 2013; Hötting & Röder, 2013). Research on blood transfusions between young and old mice suggests potential benefits for cognitive function, though results in humans are still inconclusive (Villeda et al., 2011; Villeda et al., 2014). Key Definitions: Impulsiveness: A tendency to act without thinking, leading to risky behaviors. Prefrontal Cortex: A brain region involved in planning, impulse control, and decision-making. Synaptic Plasticity: The ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Dendritic Spines: Small protrusions on neurons where synapses are located, crucial for learning and memory. Plasticity After Brain Damage 1. Behavioral Recovery from Brain Damage Case Example: A soldier injured in the Korean War initially lost his ability to speak but showed gradual improvement over time. After eight years, he could correctly read and understand complex phrases, demonstrating significant recovery (Eidelberg & Stein, 1974). Recovery Mechanisms: Survivors of brain damage often exhibit behavioral recovery. This involves mechanisms similar to those in brain development, including the growth of new axon and dendrite branches. 2. Causes and Effects of Brain Damage Common Causes: Brain damage can result from tumors, infections, radiation, toxic substances, and degenerative diseases like Parkinson's and Alzheimer’s. In younger people, closed head injuries are a frequent cause, often from falls or accidents (Babikian et al., 2015).  Closed Head Injury: Severity varies, with mild injuries often resulting in brief headaches and severe cases needing hospitalization. The presence of confusion and memory loss following the injury predicts long-term problems (Briggs et al., 2015). Mechanisms of Damage: Rotational forces and blood clots can cause further brain damage. Woodpeckers avoid concussions by using rigid necks and shock-absorbing skulls, a strategy suggesting improvements for helmets (May et al., 1979; Yoon & Park, 2011). 3. Stroke and Its Impact Types of Stroke: ○ Ischemia: Caused by blood clots obstructing arteries, leading to oxygen and glucose deprivation. ○ Hemorrhage: Results from a ruptured artery, flooding the brain with excess blood and chemicals (Unterberg et al., 2004). Effects: Both types cause similar problems, including edema (fluid accumulation) and disruption of the sodium-potassium pump. This leads to excessive glutamate release, overstimulating and damaging neurons (Rossi et al., 2000). 4. Immediate Treatments for Stroke Tissue Plasminogen Activator (tPA): Effective for ischemia, breaking up blood clots if administered within 4.5 hours of the stroke. The challenge is distinguishing between ischemic and hemorrhagic strokes quickly (Moretti et al., 2015). Other Treatments: Researchers are exploring methods to reduce neuron overstimulation, including blocking glutamate and calcium entry, cooling the brain, and using antioxidants. Cannabinoids have shown promise in animal studies for minimizing stroke damage by reducing glutamate release and inflammation (Schomacher et al., 2008; Fernández-Ruiz et al., 2015). 5. Challenges and Research Effectiveness of Cannabinoids: While cannabinoids may reduce stroke damage in rats, their effectiveness in humans is not well-established. Differences in age and health status between animal models and human patients complicate research outcomes (Di Napoli et al., 2016). Key Definitions: Plasticity: The brain’s ability to adapt and reorganize itself after injury or damage. Ischemia: A type of stroke caused by obstruction of blood flow in an artery. Hemorrhage: A type of stroke caused by a ruptured artery leading to bleeding in the brain. Edema: Accumulation of fluid in the brain, increasing pressure and potentially leading to further damage. Glutamate: A neurotransmitter that, when released excessively, can overstimulate and damage neurons. Review of Mechanisms of Recovery After Brain Damage 1. Increased Brain Stimulation ○ Diaschisis: Reduced activity of surviving neurons due to damage to other neurons (van Meer et al., 2010). Increased stimulation can help mitigate this effect.  ○ Experimental Findings: Amphetamine Use: Improved behavior and long-lasting benefits in rats and cats with cortical damage (Feeney & Sutton, 1988). Dopamine: Drugs increasing dopamine release show promise in recovery (Sami & Faruqui, 2015). 2. Regrowth of Axons ○ Peripheral Nervous System: Axons grow back at a rate of about 1 mm per day, following their myelin sheath to the target (Mokalled et al., 2016). ○ Spinal Cord in Fish: Axon regrowth is possible with the help of glial cells (Zhang et al., 2014). ○ Mammalian Brain/Spinal Cord: Regrowth is limited; scar tissue from astrocytes might inhibit regrowth, though recent studies suggest scar tissue might also protect neurons (Anderson et al., 2016). 3. Axon Sprouting ○ Collateral Sprouting: When a neuron loses input, it secretes neurotrophins that induce nearby axons to form new branches to occupy vacant synapses (Ramirez, 2001). ○ Behavioral Recovery: Depends on whether sprouting axons convey similar information to those they replace. For example, entorhinal cortex damage in one hemisphere may lead to axons from the other hemisphere sprouting and restoring behavior (Ramirez et al., 1999). 4. Denervation Supersensitivity ○ Definition: Increased responsiveness of remaining synapses after a certain set becomes inactive (Kostrzewa et al., 2008). ○ Effects: Helps compensate for decreased input but can also increase unwanted sensations like chronic pain (Brown & Weaver, 2012). 5. Reorganized Sensory Representations ○ Phantom Limbs: When an arm is amputated, the corresponding cortical area may become responsive to other body parts, such as the face, leading to sensations in the phantom limb (Florence & Kaas, 1995). ○ Recovery: Phantom sensations can sometimes be reduced by using artificial limbs, which helps displace abnormal sensory connections (Lotze et al., 1999). 6. Learned Adjustments in Behavior ○ Behavioral Recovery: Involves adapting to lost abilities. For instance, individuals may learn to use other senses or strategies to compensate for deficits (Marshall, 1985). ○ Forced Use Therapy: Forcing use of a damaged limb can improve its function, as seen in treatments for stroke recovery (Sens et al., 2012). Summary of Key Concepts: Diaschisis: Decreased neuron activity following damage. Axon Regrowth: Limited in mammals; possible in peripheral nerves and fish. Collateral Sprouting: Formation of new axon branches to fill vacant synapses. Denervation Supersensitivity: Increased synaptic responsiveness due to inactivity. Phantom Limbs: Reorganization of sensory cortices leading to sensations in amputated limbs. Learned Adjustments: Behavioral changes to compensate for brain damage Visual Perception I. Introduction to Visual Perception  Ant Seeing Example: ○ Trick question about an ant seeing 93 million miles (distance to the sun). ○ Demonstrates that sight depends on light entering the eyes, not on "sight rays." II. Historical Perspectives on Vision Ibn al-Haytham (965–1040): ○ Observed that sight occurs when light enters the eyes, not through emission of sight rays. ○ Reasoned that if vision worked by sight rays, they couldn't reach stars instantly. III. Perception and the Brain Light Interaction: ○ You perceive objects when light from them stimulates your eyes, and this information is processed by your brain. ○ Important principle: Perception occurs in the brain, not in the object being observed. Misconceptions about Sight Rays: ○ Many students wrongly believe they send out sight rays from their eyes. IV. General Principles of Perception Descartes' Theory: ○ Incorrect belief that nerves from the eye send a picture-like representation to the brain. ○ In reality, the brain encodes visual information in a non-pictorial form (neuronal activity). Johannes Müller (1838): ○ Described the Law of Specific Nerve Energies: Each nerve carries specific energy unique to its sensory modality (e.g., vision, sound). V. Retinal Structure and Processing Retina Components: ○ Light passes through ganglion, amacrine, and bipolar cells before reaching photoreceptors. ○ Photoreceptors send signals back to ganglion cells, forming the optic nerve. Blind Spot: ○ Location where the optic nerve exits the eye; has no receptors. ○ Brain compensates for the blind spot by filling in missing information. VI. Fovea vs. Peripheral Vision Foveal Vision: ○ Specialized for acute, detailed vision. ○ Direct connection between cones and midget ganglion cells. Peripheral Vision: ○ Better sensitivity to dim light but lower detail resolution due to convergence of input from multiple rods. VII. Visual Receptors: Rods and Cones  Rods: ○ Abundant in peripheral retina. ○ Sensitive to faint light, useful in dim conditions. Cones: ○ Concentrated in the fovea. ○ Essential for color vision and detailed visual processing. VIII. Important Demonstrations Blind Spot Demonstration: ○ Use figures to locate and observe your own blind spot. Mechanical Stimulation of Visual Receptors: ○ Rubbing your eyes can cause you to see light spots due to pressure on visual receptors. Visual Receptors: Rods and Cones - Exam Reviewer Outline 1. Types of Visual Receptors ○ Rods: Abundant in the periphery of the retina. Respond to faint light. Not useful in daylight (bright light bleaches them). ○ Cones: Abundant in and near the fovea. Less active in dim light, more useful in bright light. Essential for color vision. 2. Foveal vs. Peripheral Vision ○ Fovea: High concentration of cones; responsible for sharp, detailed vision. ○ Periphery: Contains mostly rods; sensitive to dim light but lacks detail and color accuracy. 3. Convergence of Receptors ○ Fovea: Each cone connects to a single ganglion cell, providing sharp detail. ○ Periphery: Multiple receptors converge onto single ganglion cells, reducing detail but enhancing light sensitivity. 4. Photopigments ○ Present in both rods and cones. ○ Composed of 11-cis-retinal (derivative of vitamin A) and opsins. ○ Light converts 11-cis-retinal to all-trans-retinal, releasing energy. 5. Ratio of Rods to Cones ○ Rods outnumber cones by 20:1 in humans. ○ Cones provide 90% of the brain's visual input despite being fewer in number. 6. Color Vision ○ Trichromatic Theory: Color vision depends on the relative response rates of three types of cones (short, medium, and long-wavelength sensitive). Different wavelengths produce different perceptions of color. ○ Opponent-Process Theory: Color is perceived through opposing color pairs (red-green, yellow-blue, black-white). Explains phenomena like afterimages. 7. Variations in Vision Among Species ○ Species active at night (e.g., oilbirds) have a much higher ratio of rods to cones (up to 15,000 rods per cone). ○ Adaptations in animals like birds allow them to see ultraviolet light.  8. Genetic Variability in Visual System ○ People vary in the number of optic nerve axons and visual cortex size, affecting their ability to detect faint or rapidly changing stimuli. 9. Afterimage and Illusion Effects ○ Staring at certain colors for a prolonged period can result in negative color afterimages due to the fatigue of color receptors. I. Retinex Theory and Color Vision A. Retinex Theory 1. Proposed by Edwin Land (Land et al., 1983). 2. Combines "retina" and "cortex" – the brain compares information from various retinal areas. 3. Accounts for color and brightness constancy. ○ Example: Identifying objects as the same color under different lighting conditions (e.g., bananas remain yellow). B. Context and Perception 1. Perception depends on comparison and context, not just light wavelengths. ○ Example: A square appearing blue in one context may appear gray without background context. 2. Brightness constancy is based on comparisons. ○ Example: A gray object can appear to have different brightness in different image areas. C. Inference in Visual Perception 1. Visual perception involves reasoning and inferences (Purves & Lotto, 2003). ○ We ask, "What have I seen before that looks like this?" II. Color Vision Theories A. Trichromatic Theory 1. Based on three types of cones (short, medium, and long wavelengths). 2. Explains perception of various colors through combinations of cone signals. B. Opponent-Process Theory 1. Visual system interprets color through opposing pairs (red-green, blue-yellow, black-white). 2. Explains afterimages and certain color combinations. C. Limitations of Both Theories 1. Neither theory explains color constancy adequately. ○ Example: Wearing green-tinted glasses but still seeing paper as white. III. Color Vision Deficiency A. Genetic Basis of Color Vision Deficiency  1. Caused by missing or abnormal cones (Nathans et al., 1989). ○ Most common: Red-green color deficiency. ○ Involves long- and medium-wavelength cones with the same photopigment. 2. Genetics: ○ X-linked condition. ○ More common in men (8% in northern European men,