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Psych 3313: Behavioral Neuroscience (All Lectures, Class Notes, Study Guides, some Flashcards)

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Psych 3313: Behavioral Neuroscience (All Lectures, Class Notes, Study Guides, some Flashcards) PSYCH 3313

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Everything you will need to do well in this class. I received an A, and we had an accumulative final over the 16 chapters.
Behavioral Neuroscience
Laurence Coutellier
Behavioral Neuroscience, neuroscience, axons, neuron, gene, OSU, Soma, neurotransmitter, Astrocyte
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This 1367 page Bundle was uploaded by prows.3 Notetaker on Wednesday February 17, 2016. The Bundle belongs to PSYCH 3313 at Ohio State University taught by Laurence Coutellier in Spring 2013. Since its upload, it has received 31 views. For similar materials see Behavioral Neuroscience in Psychlogy at Ohio State University.


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Date Created: 02/17/16
Period of Life Nervous System Development  Starting at about 2-3 weeks following conception, billions of neurons are formed Prenatal period  Neurons migrate to their appropriate locations  Synapses begin forming and are influenced by fetal activity  Myelination begins at about the 6 month following conception Birth  The brain weighs 300-350 grams (about . 75 pounds)  A period of rapid brain growth begins, extending into adolescence, primarily due to myelination  Myelination of the auditory and visual system is completed soon after birth  Myelination of the corticospinal motor tract is completed by the age of about 18 months Childhood  Experience plays a significant role in the refinement and reorganization of synapses  Adult brain weight of 1,300-1,500 grams (2.9-3.3 pounds) is achieved  At puberty, a second burst of gray matter growth is followed by a period of synaptic pruning Adolescence  Synaptic pruning takes place, largely based on experience  Synapses continue to develop and reorganize  Some limited number of new neurons might be formed  Synapse reorganization continues in some parts of the brain, wheras others experience critical periods of development Adulthood  Myelination of the frontal lobes is completed  Brain weight decreases after age 45, but cognition in healthy adults appears relatively unaffected Chapter 5  Genetics is the science of genes, heredity, and variation in living organisms.  46 chromosomes in humans. (XY) in males, (XX) in females o 23 pairs, 22 pairs are the same in typical humans. The 23 is the sex chromosome, (either XX or XY)  Genes = DNA sequence. It provides instructions for producing proteins (A=adenosine, T=thymine, G=guanine, C=cytosine)  Genome = complete set of instructions for constructing a human being. It is encoded in the DNA. It includes both the genes and the non-coding sequences of the DNA  Phenotype = a person observable characteristics, representing a combination of his/her genes and environmental influences  DNA (base( ATGC))  RNA (Codon triplet (UACG))  Protein (Amino acid)  From DNA sequence (nucleotides) to proteins: 1- Transcription: the first step of gene expression, in which a particular segment of DNA is copied into RNA by the enzyme RNA polymerase. It happens in the nucleus. 2- Translation: the second step of gene expression, in which RNA produced by transcription is decoded by a ribosome complex to produce a specific amino acid chain that will later fold into an active protein. It happens in the cytoplasm.  I 1 codon = 1 Amino acid, - proteins are large molecules consisting of one or more chains of AA  1 gene = 2 alleles; each parents pass 1 allele to their offspring (Think punnet squares)  Meiosis: 23 pairs of chromosomes = over 8 millions combinations  Crossing over: chromosomes exchange segments of DNA  Mutations: spontaneously or in response to exposure to radiations, chemicals, or other mutagens  Gene mutations: Replacement of one nucleotide by another Addition or deletion of a nucleotide  Chromosome mutations: Change in number of chromosomes (polyploidy Change in the structure of a chromosome  Sex-linked characteristics: recessive genes on the X chromosome that are not duplicated on the Y chromosome will be expressed in male offspring o X chromosome inactivation: the random inactivation of half the genes on the X chromosome in each cell of a female organism prevents the production of excess amounts of protein  X-linked diseases usually occur in males. Males have only one X chromosome. A single recessive gene on that X chromosome will cause the disease. The Y chromosome doesn't contain most of the genes of the X chromosome. It therefore doesn't protect the male. o Females can get an X-linked recessive disorder, but this is very rare. An abnormal gene on the X chromosome from each parent would be required, since a female has two X chromosomes. A Single Nucleotide Polymorphism (SNP) occurs when variations in a single base are responsible for the difference between two alleles  The most common cause of variation (3 millions SNPs between 2 peoples)  Most SNPs have no effect on health or development. Some of these genetic differences, however, have proven to be very important in the study of human health.  There are a couple of DNA markers (SNP) that can tell us a lot about our future risk for late onset Alzheimer’s. o These markers deal with the APOE gene.  Apo E 4 is 15 times more likely to develop Alzheimer’s  The proportion of observable differences in a trait between individuals within a population that is due to genetic differences.  23andMe offers genetic testing Genes don’t explain everything… heritability is affected by the environment Human Development Within the 1 week: zygote has divided into 3 germ layers  Endoderm: internal organs  Mesoderm: connective tissue, muscles, bone, blood vessels  Ectoderm: skin, hair, nervous system During the 3 week, the ectoderm is differentiated into skin and neural plate Neural tube: ventricles and central canal of spinal cord Surrounding ectoderm: brain and spinal cord Spina bifida is a developmental congenital disorder caused by the incomplete closing of the embryonic neural tube  Dietary supplementation with folic acid during pregnancy has been shown to be helpful in reducing the incidence of spina bifida th After 10 week, the developing human is called a fetus Overview in 6 steps: • cell proliferation (neurogenesis and gliogenesis) • migration • differentiation • circuit formation • neuron death • refinement of connection Cell proliferations:  Unipotent or oligopotent: ability to develop into one or a few types of mature nervous system cells  Pluripotent: ability to develop into many types of mature nervous system cells  New neural cells are produced from the mitosis of progenitor cells in the ventricular zone lining the neural tube. o 1) Some daughter cells remain in the ventricular zone and keep dividing. o 2) Other daughter cells migrate away from the ventricular zone. Migration:  Neuronal migration is the method by which neurons travel from their origin or birthplace to their final position in the brain.  The cortex is said to be assembled inside-out (new neuroblasts migrate right past those in the existing cortical plate) Differentiation:  Dorso-ventral specialization of the neural tube under control of the protein Sonic hedgehog (shh)  Rostral-caudal specialization of the neural tube under control of the protein encoded by Hox genes. Circuit Formation:  Neurons need to communicate one to each other to transmit information to effector cells o They will grow axons and dendrites and form synapses  Developing axons and dendrites end in growth cones o Filopodia and lamellopodia are capable of movement and pull the growing branches along behind them o The dynamic nature of growth cones allows them to respond to the surrounding environment by rapidly changing direction and branching in response to various stimuli.  To move, growth cones can:  stick to the surface of cells  stick to other axons traveling in the same direction (fasciculation)  grow toward chemical attractants  be repulsed by chemicals o Axon extension is a 3 step process  Protrusion: a rapid extension of filopodia and lamellar extensions along the leading edge of the growth cone  Engorgement: filopodia move to the lateral edges of the growth cone, and microtubules invade further into the growth cone  Consolidation: actin at the neck of the growth cone depolymerizes and the filopodia retract  Synapse formation: synaptogenesis  Development of neuromuscular junction o Growth cone of axon approaches muscle fiber. Prepattern on muscle fiber. o Growth cone forms contact with muscle fiber. Postsynaptic induction. o Pre-synaptic terminal differentiates as a result of signals from muscle cell. Cell death:  Apoptosis: programmed cell death. o Significant numbers of new neurons die during development o Axons in formation advance toward target cells, Target cells produce limited quantities of NGF, competition for NGF, those neurons who get it survive, those who do not go through apoptosis and die. o Apoptosis is a natural part of development of the immature central nervous system. Synaptic Pruning:  It refers to neurological regulatory processes, which facilitate changes in neural structure by reducing the overall number of neurons and synapses Myelination  Starts 24 weeks after fertilization of the egg and goes on until adulthood  Spinal cord hindbrain  midbrain forebrain  Sensory system before motor system  Here is a test used to check for incomplete myelination in babies.. Softly rub the sole of a baby’s foot from the heel towards the large toe. The baby’s toes will fan out, with the large toe pointing up. In contrast, when you do the same to an older child or an adult, his toes will curve inwards. (for myelination)  Leukodystrophy are caused by imperfect growth or development of the myelin. o mostly inherited disorders o gradual decline in an infant or child who previously appeared well (loss body tone, slowdown in mental and physical development) The Role of Experience in Neurodevelopment Plasticity = ability of the nervous system to change in response to experience or to the environment Visual system: In the normal development input from both eyes competes for the control of target cells in the LGN  In the normal development input from both eyes competes for the control of target cells in the LGN  The effect of experience on development must occur during critical periods Imprinting: any kind of phase-sensitive learning (learning occurring at a particular age or a particular life stage) that is rapid and apparently independent of the consequences of behavior. It typically involves an animal or person learning the characteristics of some stimulus, which is therefore said to be "imprinted" onto the subject.  The best known form of imprinting is filial imprinting, in which a young animal learns the characteristics of its parent. Neglect during early childhood shows major temporal lobe brain damage on PET scans Environment can affect development by (1) inducing mutations in DNA sequence (2) changing gene expression without changing in DNA sequence Epigenetics and methylation  Epigenetics is the study of heritable changes in gene activity that are not caused by changes in the DNA sequence  Chromatin is the complex of DNA and the histone proteins with which it associates.  Histone proteins are little spheres that DNA wraps around.  If the way that DNA is wrapped around the histones changes, gene expression can change as well.  Chromatin remodeling is accomplished through addition of methyl groups to the DNA  some areas of the genome are methylated more heavily than others, and highly methylated areas tend to be less transcriptionally active  Environment can affect DNA methylation; these methylations will be transferred to offsprings Disorders of Brain Development Down syndrome (trisomy 21)  A failure of the chromosomes to separate during egg or sperm development. As a result, a sperm or egg cell is produced with an extra copy of chromosome 21  A failure of the chromosomes to separate during egg or sperm development. As a result, a sperm or egg cell is produced with an extra copy of chromosome 21  Extra chromosome 21 DNA leads to an over-expression of certain genes: amyloid, superoxide dismutase.  Over-expression of amyloid gene: The dementia which occurs in Down syndrome is due to too much amyloid beta peptides being produced in the brain. Senile plaques and neurofibrillary tangles are present in nearly all by 35 years of age even though dementia may not be present.  More than 75 percent of those with Down syndrome aged 65 and older have Alzheimer's disease, nearly 6 times the percentage of people in this age group who do not have Down syndrome. Fragile X syndrome  >200 codon repeats = breaking of the X chromosome  Mutations in the FMR1 gene cause fragile X syndrome. The FMR1 gene provides instructions for making a protein called fragile X mental retardation 1 protein, or FMRP. This protein helps regulate the production of other proteins and plays a role in the development of synapses. Phenylketonuria  An autosomal recessive metabolic genetic disorder characterized by a mutation in the gene for the hepatic enzyme phenylalanine hydroxylase (PAH)  Inherited error in metabolism  Can cause mental retardation, convulsions, behavior problems, skin rash, musty body odor  No meat, dairy, nuts, eggs, beans (cereals, fruits, and veggies in moderation)  Babies are tested with both formula and breast milk, and tested no later than 24 hours after being fed. Tested again 7 days later to prevent false negatives. Fetal Alcohol Syndrome  a pattern of mental and physical defects that can develop in a fetus in association with high levels of alcohol consumption during pregnancy  During the first trimester of pregnancy, alcohol interferes with the migration and organization of brain cells  During the third trimester, damage can be caused to the hippocampus, which plays a role in memory, learning, emotion, and encoding visual and auditory information Neuroplasticity Ability of the nervous system to change in response to experience or the environment • Redevelopment and regeneration in response to damage • Reorganization of sensory and cortical maps Axonal degredation  Deterioration of the entire neuron because it affects the cell body + postsynaptic cell atrophy  Possibility of regrowth to the postsynaptic cell  Axonal damage can lead to transneuronal degeneration: neurons that synapse on the damaged neuron degenerate too Transneuronal degredation  The technical cause of transneuronal degeneration is the death of neurons resulting from the disruption of input from or output to other nearby neurons. o There are several different mechanisms by which transneuronal degeneration can occur:  Lesions  Disconnection syndromes (neurologic disorder caused by an interruption in impulse transmission along cerebral fiber pathways)  Lobectomy o Diseases associated with transneuronal degeneration:  Alzheimer’s diseases  Cockayne syndrome (defect in DNA repair mechanism)  Amyotorphic lateral sclerosis (causes anterograde degeneration of corticomotoneurons) In the peripheral nervous system, axon degeneration can be repaired by Schwann cells  Fragmentation of axon and myelin occur in distal stump  Schwann cells from cord, grow into cut, and stumps. Macrophages engulf degenerated axon and myelin.  Axon sends buds into network of Schwann cells and then starts growing along cord of Schwann cells  Axon continues to grow into distal stump and is enfolded by Schwann cells Damage to neuron and redevelopment  Damage to the axon results in the deposition of myelin debris; no macrophages in the CNS to clear the debris, impeding neuronal repair.  CNS damage attracts astrocytes, which form a glial scar that prevents regeneration. No astrocytes are present in the PNS to induce scarring.  CNS neuron regeneration is also hindered by inhibitory components in the myelin such as Nogo, which inhibit neuronal sprouting. The PNS has no such inhibitory molecules Reorganization of sensory and cortical maps  One of the fundamental principles of how neuroplasticity functions is linked to the concept of synaptic pruning, the idea that individual connections within the brain are constantly being removed or recreated, largely dependent upon how they are used.  Training leads to 3% increase in gray matter o Visual cortex increased in size in subjects trained for 3 months to juggle 3 balls  A surprising consequence of neuroplasticity is that the brain activity associated with a given function can move to a different location  Dendrites, spines and synapses can change according to experience The Adult Nervous System Neurogenisis in adulthood  Most active during pre-natal development, neurogenesis is responsible for populating the growing brain with neurons.  Recently neurogenesis was shown to continue in several small parts of the brain of mammals: the hippocampus and the subventricular zone.  There is a trade-off between stability and adaptability (plasticity). Our brains must be stable enough to maintain our identities while staying flexible enough to learn new things and accommodate growth. Historically, we believed the human brain must be very stable to support our complexity.  Factors influencing adult neurogenesis:  Increase:  Exercise, enrichment, learning, antidepressants  Decrease:  Aging, sleep deprivation, stress  Learning and memory  Learning enhances neurogenesis  Factors that increase neurogenesis also enhance learning,  Factors that decrease neurogenesis impair learning  Blocking neurogenesis impairs learning  Mood disorders  Hippocampal volume is smaller in depressed patients  Stress inhibits neurogenesis  Antidepressants enhance neurogenesis The aging nervous system • The human brain is considered mature at 25 years. • Brain weight begins to decrease at age 45 years. • Neurogenesis occurs in the aged brain but at much lower levels • Age-related changes in learning speed and problem solving are mild and occur rather late in life • Lifestyle, genetics and intelligence influence an individual’s aging process Alzheimer’s Disease  Alzheimer's is a type of dementia that causes problems with memory, thinking and behavior. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks.  Alzheimer's is not a normal part of aging, although the greatest known risk factor is increasing age, and the majority of people with Alzheimer's are 65 and older. But Alzheimer's is not just a disease of old age.  Alzheimer’s is a neurodegenerative disease  1 in 10 people over the age of 65  1 in 2 people over the age of 85  Neurofibrillary tangles result from the breakdown of the tau protein, which supports the cytoskeleton  Abnormal amyloid forms plaques  Neuron Loss  Currently, there is no cure for Alzheimer's. But drug and non-drug treatments may help with both cognitive and behavioral symptoms.  NMDA receptor antagonist :Memantine is believed to block the NMDA receptor and reduce glutamate excitotoxicity  Excitotoxicity is the pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotransmitters such as glutamate  Currently, there is no cure for Alzheimer's. But drug and non-drug treatments may help with both cognitive and behavioral symptoms.  Cholinesterase inhibitor: AD = degeneration of the cholinergic projections, loss of cholinergic cell bodies; memory and cognitive disturbances result from reduced cholinergic transmission. Chapter 4 Psychopharmacology is the scientific study of the effects chemical messengers have on mood, sensation, thinking, and behavior. 3 categories of chemical messengers: • Neurotransmitters: communicate locally across the synapse • Neuromodulators : chemical that communicates with target cells more distant than the synapse by diffusing away from the point of release. • Neurohormones: chemical that communicates with target cells at great distance by traveling through the bloodstream. Characteristics of neurotransmitters: • Synthesized by the neuron • Released in response to an action potential • Has a measurable effect on postsynaptic cell • Can duplicate its action experimentally • Some mechanism exists to terminate the effect Small molecules  ACh is a small-molecule neurotransmitter used at the neuromuscular junction (synapse between neuron and muscle fiber), in the autonomic nervous system, and in the CNS Small-molecule Neuropeptides transmission Synthesis In axon terminal In cell body – needs transportation Recycling of vesicles? Yes No Activation Moderate AP frequency High AP frequency Deactivation Reuptake/enzymatic Diffusion away from synapse degradation Function Fast neurotransmission neuromodulation When Ach is destroyed by Acetylocholinesterase (AChE), choline gets reuptaken, Ach is degredated. Postsynaptic neurons that use Ach carry 2 types of receptors: ­ Nicotinic receptor (ionotropic) – responds to nicotine and ACh; mostly excitatory. ­ Smokers Demonstrate Excess Nicotinic Receptors During First Month of Abstinence. The brain develops extra receptors to accommodate the large doses of nicotine from tobacco. The expanded receptor pool contributes to craving and other discomforts of smoking withdrawal. ­ Muscarinic (metabotropic) – responds to muscarine and ACh; excitatory and inhibitory; isolated from mushroom CNS and autonomic nervous system – both receptors Neuromuscular – nicotinic Monoamines - Monoamines are neurotransmitters that contain one amino group that is connected to an aromatic ring by a two-carbon chain (-CH2-CH2-)  Don’t cross blood brain barrier  To increase the level of monoamines in the CNS you must provide amino acid precursors that cross the BBB and that are then synthesized into new neurotransmitters in the CNS. Catecholamine Synthesis Monoamines Catecholamines Indolamines • Dopamine • Serotonin • Norepinephrin • Melatonin e • Epinephrine Dopamine is widely distributed throughout the brain – hippocampus, Amygdala, accumbens, basal ganglia, frontal lobe  Dopamine receptors (D1-D5) are metabotropic  Reward-motivated behavior. Every type of reward that has been studied increases the level of dopamine in the brain, and a variety of addictive drugs, including stimulants such as cocaine, amphetamine, and methamphetamine, act by amplifying the effects of dopamine.  Role in motor control o Substantia nigra is affected in Parkinson’s disease  Role in cognition (planning, problem solving) – frontal cortex  Schizophrenia and ADHD o Antipsychotic drugs like chlorpromazine block DA receptors o Amphetamine psychosis resembles schizophrenia because it blocks DA receptors, raising DA levels – exacerbates schizophrenia. Norepinephrine and epinephrine  Adrenergic receptors:  Metabotropic  In the brain and other organs (heart, muscles, blood vessels) o Role in: vigilance, arousal, fight/flight, learning and memory Serotonin (indolamine) – metabotropic  Role in: sleep, arousal, appetite ●involved in: depression, anxiety  SSRIs (selective serotonin reuptake inhibitor) block the reabsorption (reuptake) of the neurotransmitter serotonin in the brain. Changing the balance of serotonin seems to help brain cells send and receive chemical messages, which in turn boosts mood. (treat depression, anxiety, and some personality disorders) Amino Acids  Glutamate o Principle excitatory transmitter in the CNS o Synthesized from α-ketoglutarate o 4 major types of receptors: AMPA, NMDA, Kainate (all ionotropic) and the fourth is Metabotropic  AMPA and NMDA receptors: Glutamate bind to NMDA and AMPA receptors; AMPA receptors get activated: entrance of Na+; Moderate local depolarization; Dislodge Mg2+ from the NMDA receptor; Ca2+ enters from NMDA receptor (both ligand AND voltage gated)  NMDA receptors plays a critical role in learning and memory functions  GABA (Gamma-AminoButyric Acid) - Principle inhibitory transmitter in the CNS o Synthesized from glutamate through action of Glutamic acid decarboxylase (GAD) o 2 major types of receptors: GABA and GABA A B − o Upon activation, the GABA reAeptor selectively conducts Cl through its pore, resulting in hyperpolarization of the neuron o The GABA reAeptor is also the molecular target of the benzodiazepine class of tranquilizer drugs resulting in sedative, hypnotic, anxiolytic, anticonvulsant, and muscle relaxant properties o Too much inhibition/not enough = BAD Neuropeptides are small protein-like molecules (peptides) used by neurons to communicate with each other. They co-exist in the same neuron with a small molecule neurotransmitter. They are synthesized in the cell body of the neuron.  involved in a wide range of brain functions:  Analgesia (substance P)  Food intake (neuropeptide Y, cholecystokin), metabolism (insulin)  Reproduction, social behaviors (oxytocin, vasopressin)  Learning and memory. Neuropeptide Y and food intake  The binding of NPY to receptors within the periventricular nucleus stimulates food intake in animal models.  The repeated injection of NPY into the hypothalamus summarily results in obesity.  Increased levels of the neuropeptide are also observed in a mutant mouse model of obesity (ob/ob) Gas as a neuropeptide (example – NO, nitric oxide.) This is very rare. Drug actions at the synapse  Receptors can be activated by: endogenous chemicals (hormones or neurotransmitter): compound naturally produced by the body that binds and acts on a receptor (the endogenous agonist for serotonin receptors is serotonin) exogenous chemicals (drugs): compound produced artificially, administered to the body through various routes and that binds and acts on a receptor (isoproterenol acts on β- adrenergic receptors) 2 main classes of drugs: agonist and antagonist  An agonist is a chemical that binds to a receptor and activates the receptor to produce a biological response o Full inverse agonist – -100% efficient relative to endogenous agonist; binds to the same receptor binding-site as an agonist for that receptor but exerts the opposite pharmacological effect of a receptor agonist o Partial agonist – about 50% efficient relative to endogenous agonist; bind and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist, even at maximal receptor occupancy o Super agonist – about 100% efficient relative to endogenous agonist; produce a greater maximal response than the endogenous agonist  Antagonist is a type of receptor ligand or drug that does not provoke a biological response itself upon binding to a receptor, but blocks or dampens agonist-mediated responses o The endogenous ligand binds to receptor and produces an effect o An antagonist drug is close enough in shape to bind to the receptor but not close enough to produce an effect. It also takes up space and so prevents the endogenous ligand from binding Routes of drug administration - systemic injection (iv, ip, im, sc) - central injection (intracerebral) - oral - topical (skin, nasal mucosa) - inhalation Concentration of a drug in the blood (plasma) depends on the method of administration. Nasal: drug absorbs directly into veins Venous system: transports blood from nose directly to heart – no liver metabolism Heart: pumps blood to entire body – no delay Oral meds: sit in stomach for 30-45 mins Portal circulation: all blood from intestines is taken to liver for detoxification Liver: 90% of oral medication is metabolized and destroyed by the liver before it gets to the heart The blood-brain barrier protects the brain from unwanted chemicals in the blood, but presents a huge challenge for getting drugs into the brain  Strategies to pass the BBB: o Pro-drugs: disguising medically active molecules with lipophilic molecules that allow it to better sneak through the BBB o Receptor Mediated Permabilitizers: compounds that increase the permeability of the BBB o Nanoparticles delivery system: the drug is bound to a nanoparticle capable of traversing the BBB (human serum albumin) Individual differences when taking drugs: body weight, gender, genetics, user’s expectations (placebo effect) Drug tolerance and withdrawal: Tolerance is encountered when a subject's reaction to a specific drug is progressively reduced, requiring an increase in concentration to achieve the desired effect. Withdrawal is the group of symptoms that occur upon the abrupt discontinuation or decrease in intake of medications or recreational drugs. Addiction: Drug addiction is a dependence on an illegal drug or a medication. When you're addicted, you may not be able to control your drug use and you may continue using the drug despite the harm it causes. Drug addiction can cause an intense craving for the drug. You may want to quit, but most people find they can't do it on their own. *All drugs of abuse target the brain’s pleasure center and increase dopamine* Psychoactive drug: A chemical substance that crosses the blood–brain barrier and acts primarily upon the central nervous system where it affects brain function, resulting in alterations in perception, mood, consciousness, cognition, and behavior. • Depressants: o alcohol, barbiturates and benzodiazepines (xanex, valium) • Stimulants: o caffeine, nicotine, cocaine, amphetamines • Psychedelics: o marijuana, LSD, psilocybin (derived from a type of mushroom), PCP, ecstasy • Opiates: o morphine, codeine, endorphins Alcohol – GABA rAceptor agonist; neural inhibition  NMDA receptor antagonist – memory loss Caffeine – stimulant  Effects: arousal, increased alertness, decreased sleepiness  Action: counteracts adenosine that naturally circulates at high levels in the nervous system. Adenosine plays a generally protective role, part of which is to reduce neural activity levels  Overdose is about 500mg o 19 year old man dies after taking 25 to 30 No Doz pills in 2007. (at least 2.5 grams of caffeine) o 2011 Fourteen-year-old girl, died after she consumed two 24 ounce Monsters (480mg of caffeine) in a 24 hour period. Cause of death was a heart arrhythmia due to caffeine toxicity. o 2013 A mother is suing Monster Energy for the death of her 19 year old son after he died of cardiac arrest. He drank two 16 ounce Monsters the day before his death and at least two a day for the 3 years proceeding his death. o We experience nausea/vomiting well before death LSD, ecstasy, mushrooms  hallucinogen (cause perceptual distortions)  Serotonin receptor agonists o Short term effects of ecstasy: block reuptake of 5-HT; Increase the levels of 5-HT; Euphoria, mental relaxation o Long-term effects of ecstasy: depression, anxiety, memory loss Opiates  Derived from Opium poppy flower  The major psychoactive opiates are morphine, codeine, and thebaine. o Analgesic (pain relieving) o Hypnotic (sleep inducing) o Euphoric (intense happiness) o Anxiolytic (relieves anxiety) o Highly Addictive  Heroin = opioid analgesic derived from morphine  Endorphins are opiod peptides that function as neurotransmitters Opiates act through the pain pathway (thalamus, brain stem, spinal cord) and the reward pathway (VTA, nucleus accumbens, cortex) How opiates work: 1. Opiates bind to opiate receptors on GABA neuron 2. Slows release of GABA 3. Disinhibition causes nearby neuron to release more dopamine Chapter 10 A sex-determination system is a biological system that determines the development of sexual characteristics in an organism. Most sexual organisms have two sexes.  In some cases, sex is determined by environmental variables (such as temperature) or social variables (e.g. the size of an organism relative to other members of its population)  In other cases (most species), sex determination is genetic: males and females have different alleles or even different genes that specify their sexual morphology.  In mammals, the sex is determined at the time of fertilization o Depends on whether the sperm that fertilizes the egg carries an X or Y sex chromosome  XX: Females  XY: Males Sex chromosome abnormalities:  Turner Syndrome: XO o Fertility problems – normal external genitalia, but abnormal ovaries. Some women with only a partially missing X chromosome may still be fertile. o Growth problems – relatively short, skin folds at the neck o Higher risk of diabetes, osteoporosis, cardiovascular disease o Human growth hormone, female hormone replacement therapy, and assistive reproductive technologies are used to help assist the issues of height, hormone production, and fertility.  Klinefelter syndrome: XXY - male o Reduced production of testosterone o Less muscular body, less facial and body hair, and broader hips than other boys – need hormone treatment at puberty to promote male secondary sex characteristics (deeper voice, broad shoulders, facial hair) and to inhibit female secondary sex characteristics such as breast development.  XYY syndrome o Reduced fertility – (fertile, but slightly more likely to produce sperm with sex chromosome abnormalities) o Acne o Taller and leaner than normal, but for the most part, they are usually within typical limits o Aggression and antisocial behavior??? o IQ slightly below average, higher risk for minor physical abnormalities of the eye, elbow, and chest  Androgen insensitivity syndrome (AIS) o XY genotype, has normal testis that release androgens and anti-mullerain, but there is a lack of functional androgen receptors, and this prevents the development of the wolffian system o Anti-mullerain hormone still works properly, so the female system fails to develop o Mullerain system is responsible for upper 2/3 of the vagina, the result is a very shallow vagina and no ovaries, fallopian tubes, or uterus. (infertile)  Advantages in female sports (XY chromosome, appearance/form/shape of female)  Estimated 1/500 women competing in international levels have AIS  Congenital adrenal hyperplasia (CAH) o Recessive heretible in which fetus’s adrenal glands release elevated amounts of androgens  Females exposed to this are born with ambiguous looking external genitalia. Prenatal development 3 stages: 1- Development of gonads 2- Differentiation of internal organs 3- Development of external genitalia 1- Development of gonads 6 weeks old fetus: Indifferent gonads will evolve into testis if the genotype is XY and ovaries if it is XX. The name “indifferent gonads” is given because at this developmental stage, regardless of the genetic make up of the fetus, the gonads have the potential to be either ovaries or testis. (until 6 weeks after conception)  Role of the sex-determining region of the Y chromosome (SRY) 2- Differentiation of internal organs  Wolffian system develops into seminal vesicles, vas deferent, prostate o After 3 months, testis start to secrete testosterone and anti-mullerain hormone.  Testosterone promotes the development of the wolffian system, and anti- mullerain hormone initiates the degeneration of the mullerain system.  Mullerian system develops into uterus, vagina and fallopian tubes o The mullerain system needs no hormones for development. *Until about the third month, both male and female fetuses have both systems. 3- Development of external genitalia  Hormonal stimulation is necessary for the development of male external genitalia o 5-alpha-dihydrotestosterone (DHT)  Can be abnormalities due to mutation in the gene coding for the 5 -reductase  Will grow “female” external genitals due to lack of prostate growth  No hormone is necessary for the development of female external genitalia Prenatal (primary) sex characteristics – organs  Female – ovaries, vagina, uterus, fallopian tubes.  Male – testes, penis, scrotum, prostate gland, seminal vesicles Puberty (secondary) sex characteristics – after maturation  Female – breasts, pubic hair, armpit hair, changes in voice and skin, increased widening and depth in pelvis  Male – pubic hair, armpit hair, facial hair, changes in voice and skin, broadening of shoulders GnRH: gonadotropin releasing hormone  LH: luteinizing hormone  FSH: follicle-stimulating hormone Malnurishment/being undernourished causes a decrease in progesterone, oestradiol, and testosterone levels.  This causes delayed puberty and amorrhea(no period) Being overweight causes a decrease in progesterone and an increase in testosterone.  This causes amplified ovarian androgen production, anovulation, and hirsutism Adolescent brain There is relatively limited knowledge of how these hormones influence adolescent brain development and specific behavioral, cognitive and affective changes during adolescence. “When reading emotion…adults rely more on the frontal cortex while teens rely more on the amgydala”  Activity in the amygdala during this task likely reflects more of a gut reaction than a reasoned one. In contrast, the prefrontal cortex, involved in reasoning and reflection is activated in the adult brain The adolescent brain and risk taking: higher testosterone levels led to more risk-taking These hormones influence the brain development and behaviors Testis release testosterone Androgens (testosterone) play a direct role in the masculinization of the human brain. Aromatization hypothesis, circulating testosterone from the testes is converted locally in the brain by aromatase to estrogens, which then activate ERs to masculinize the brain Low androgen during the development = female sexual behavior as an adult High androgen during the development = defiminization and masculinization Defiminization: female-specific structure, function, or behavior is prevented from developing Masculinization: production of male typical morphology and behavioral predispositions Androgen insensitivity syndrome is a condition that results in the partial or complete inability of the cell to respond to androgens • Individuals with complete androgen insensitivity syndrome are born phenotypically female, without any signs of genital masculinization, despite having a 46,XY karyotype. • Partial androgen insensitivity syndrome is diagnosed when an individual (46,XY) genitalia is partially, but not completely masculinized. • Mild androgen insensitivity syndrome occurs when a male has fully masculinized genitalia but impaired virilization or spermatogenesis. Congenital adrenal hyperplasia (CAH) (autosomal recessive disease) Due to excess androgens: • ambiguous genitalia, in some females, such that it can be initially difficult to determine sex • early pubic hair and rapid growth in childhood • precocious puberty or failure of puberty to occur (sexual infantilism: absent or delayed puberty) • excessive facial hair, virilization, and/or menstrual irregularity in adolescence • infertility due to anovulation The brain's sexual dimorphism is determined by genes on the sex chromosomes. Genes in cells in the gonads cause the gonads to produce sex hormones that travel to the brain which affect brain cells.  Males have better motor and spatial abilities.  Females have superior memory and social cognition skills. o Mental rotation test: male advantage in mental rotation and assessing horizontality and verticality o Testosterone as a cause of sex differences: adult women who were exposed to unusually high levels of androgens in the womb due to CAH score significantly higher on tests of spatial ability. o Turner’s syndrome patients (some or all of an X chromosome is deleted) scored poorer on social cognition skills tests which females generally do better on  Too much estrogen can have negative effects by weakening performance of learned tasks as well as hindering performance of memory tasks; this can result in females exhibiting poorer performance of such tasks when compared to males Males and females use their brain differently.  Difference in brain connectivity (from a helicopter view of a brain, most neural connections in a male brain run long ways (front to back). In a female brain, most connections run from side to side (as if running from parietal lobe to parietal lobe. (or parallel to the face)) o Explanation for why males tend to be better at motor functions and spatial tests, and why females tend to be better at memory functions and social cognition skills. Erection and ejaculation are controlled by circuits of neurons of the spinal cord (lumbar region) and in the brain (medial preoptic area MPOA). MPOA and sexual dimorphic nucleus (SDN): SDN in males in 2.2 larger than in females SDN contains 2.1 times as many cells Large lesions of SDN-POA severely disrupt copulatory behavior in rats  SDN-POA in male rams who mated with males were the same size as the ewe (female) SDN- POA’s (6-8% male-male pref.)  In ferrets, normal SDN ferrets usually choose female partners. Male ferrets with lesions of SDN choose male partners. Ventromedial nucleus of the hypothalamus (VMH) regulates female sexual behavior (e.g. lordosis) Mating partners:  To understand the neural basis of adult partnerships, researchers study prairie voles, a rare example of a species that mates for life.  Interaction between oxytocin and dopamine in the brain’s reward region in female voles likely increases the desire to spend more time with her partner.  In male prairie voles, the hormone arginine vasopressin (and the V1 receptor), which is involved in aggression and territorial behavior, plays an important role in pair-bonding o Males raise young  Vasopressin increases paternal behaviors for males, and oxytocin increases maternal behaviors in females  Oxytocin, vasopressin, and dopamine play a role in pair-bonding in animals  In humans ??? Recent genetic studies show men who have a specific form of the gene that codes for vasopressin receptors are less likely to be married and report more relationship problems than other men.  D2-R in mesolimbic pathway (reward pathway) Maternal bond and oxytocin • Women with higher levels of oxytocin during their first trimester of pregnancy are primed to the formation of an exclusive bond with their infants. • High level of oxytocin postpartum are associated with affectionate parenting. Maternal bond and dopamine  Pup suckling activates the mesocorticolimbic system. This dopaminergic pathway from the ventral tegmental area to the accumbens and prefrontal cortex system is involved in reward seeking and may help to strengthen the pup- dam bond Maternal bond, oxytocin, and post-partum  Lower oxytocin levels before birth and during breastfeeding were associated with a greater risk of postpartum depression.  Maternal neuroendocrine response to feeding 8 weeks among women with depression symptoms (dashed line) or without mood symptoms (solid line). Maternal behavior: Importance of the Medial amygdala, MPOA and VTA  Implanting estrogen into the MPOA facilitates rapid onset of maternal behavior In only 6% of mammalian species, including humans, the father plays a significant role in caring for his young. Being exposed to crying babies activates the prefrontal cortex and the amygdala in both fathers and mothers, but not in non-parents. The level of testosterone in the paternal brain correlates with the effectiveness of the dad's response to the baby's cry Importance of vasopressin and prolactin: Vasopressin is responsible for transforming a naive young male into an affectionate and aggressively protective partner and father Neural control of romantic love:  Romantic love produces a set of complex emotions that are distinctly different from other types of love, such as maternal love, or compassionate love  Increased BOLD response in VTA (region rich in DA activity – mesolimbic reward pathway) evoked by association of a romantic partner suggests that the DA reward and motivation system mediates goal-directed reward seeking behaviour in romantic love. This may explain obsessiveness and impulsiveness found in early stage romantic love.  Changes over time: with time, feelings of romantic love seem to become accompanied by feelings of deep attachment to a partner (activation of the ventral pallidum) Abnormal sexual behavior: Sexual behavior initiates the activation of the mesolimbic dopaminergic pathway (reward pathway) • Reward circuitry consists of dopaminergic projections from VTA to PFC/Acb. • Androgens can influence the circuit via androgen receptors in BST and MPOA projecting to the VTA. Sexual addiction: • A progressive intimacy disorder characterized by compulsive sexual thoughts and acts. Like all addictions, its negative impact on the addict and on family members increases as the disorder progresses. • When sexual addicts are shown porn, their brain's reward centers (Nucleus accumbens) light up just like it would for an alcoholic when seeing a drink ad Erection dysfunction: • Sexual dysfunction characterized by the inability to develop or maintain an erection. Impotence may develop due to disorders of the neural system (dopaminergic system in the hypothalamus). • Dopamine's effects on hypothalamic oxytocin cells are necessary for penile erection • Drugs for erectile dysfunction can target DA receptors or interact with Nitric Oxyde (NO) Chapter 11 Circadian rhythm: Any biological process that displays an endogenous oscillation of about 24 hours  A repeating cycle of about 24 hours Many aspects of mammalian behavior and physiology show circadian rhythmicity: • sleep • physical activity • alertness • hormone levels • body temperature • immune function • digestive activity • menstral cycles • mating seasons The circadian clock affects the daily rhythm of these physiological processes. Circadian: daily rhythm (24 hours) Sleep/wake cycle Vs. Ultradian: less than 24 hours (90–120 minute cycling of the sleep stages during human sleep) Infradian: greater than 24 hours (seasonal rhythm) Circannual: yearly (migration) Multiple rhythms can be expressed within a single system— e.g., LH serum levels Characteristics of a circadian rhythm: • INDEPENDENT of external cues • cues (e.g. light/dark) • The rhythm has an endogenous free-running period that lasts approximately 24 hours. The rhythm persists in constant conditions, (i.e., constant darkness) with a period of about 24 hours. • Light is the most important zeitgeber for human beings. (External cue for setting biological rhythms.) • In the absence of light, human free-running circadian rhythms last approximately 24.2 hours to 24.9 hours. Exposure to sunlight helps reset, or entrain the internal biological clock to the 24-hour cycle of the earth’s rotation. • Totally blind people have free-running cycles longer than 24 hours – sleep disruptions • Entrainable • The rhythm can be reset by exposure to external stimuli (such as light and heat) and will maintain that rhythm when placed in constant conditions. Sleep-wake and other daily patterns of our circadian rhythms are governed by the body's internal clock.  Suprachiasmatic nuclei (SCN) is a region located in the hypothalamus, situated directly above the optic chiasm. It is responsible for controlling circadian rhythms. The neuronal and hormonal activities it generates regulate many different body functions in a 24-hour cycle, using around 20,000 neurons. o the pacemaker of circadian rhythms. It coordinates the activities of other internal clocks that exist in most body cells. o Non-image forming cells (NIF) that contain melanopsin (photopigment) connect to the SCN by the retinohypothalamic pathway o The circadian rhythm in the SCN is generated by a gene expression cycle in individual SCN neurons. This cycle has been well conserved through evolution and in essence is similar in cells from many widely different organisms that show circadian rhythms.  In the fruit fly Drosophila, the cellular circadian rhythm in neurons is controlled by 3 genes which expression oscillates during the day:  Per – per and tim proteins inhibit clock proteins  tim  clock – promotes production of per and tim proteins o as levels of per and tim increase, inhibition of the clock protein ensures that no further per and tim proteins will be produced. As per and tim levels drop over time, the reduced inhibition od clock results in increased production of per and tim.  Light participates in triggering some of these protein fluctuations o SCN is activated only during the day. – regardless of whether the animal is diurnal (monkeys) or nocturnal (raccoons).  helps animals distinguish between day and night by inhibiting melatonin production by the pineal gland.  Melatonin = “sleep hormone” o Peak at about 4am – blind people’s peak at different times, leading to sleep deficiencies and difficulties. Pineal gland tumors also make sleeping difficult because of melatonin malfunctions. o Release is suppressed by light o Autism – low levels  Not dependent on other structures for input to maintain its rhythms. o SCN adjusts to new time after only a few cycles of light and dark, but other peripheral clocks in the lungs, liver, and muscular tissue take many more cycles. Cortisol: hormone released by the adrenal glands that promotes arousal.  High in the morning, lower at night  Higher levels are associated with higher blood pressure, higher heart rate, and the mobilization of the body’s energy stores  Released during times of stress  The release may consequently contribute to poor sleep quality  Contribute to the experience of jetlag Seasonal Affective Disorder: depression that results from insufficient amounts of light during the winter months.  Serotonin levels typically drop in the fall and winter – people vulnerable to SAD may experience a greater than normal decrease, leading to symptoms of depression Disorders of circadian rhythm: Causes by many factors, including: • Shift work • Pregnancy • Time zone changes • Medications • Changes in routine Common disorders:  Jet Lag or Rapid Time Zone Change Syndrome: This syndrome consists of symptoms that include excessive sleepiness and a lack of daytime alertness in people who travel across time zones.  Conflict between internal clock and external cue that set biological rhythm (zeitgebers)  Reduced reaction times, 9% more mistakes on memory tasks  Easier to adjust to a phase delay of our cycle than a phase advance. (setting the clock back and staying up later and waking up later, rather than setting them forward, going to bed earlier, and waking up earlier.) (fall back is easier than spring forward) o 7% decrease in accidents on fall back vs. 7% more accidents on spring forward  Shift Work Sleep Disorder: (shift maladaptation syndrome) This sleep disorder affects people who frequently rotate shifts or work at night. – mostly 11 p.m -7:30 a.m  The primary symptoms are insomnia and excessive sleepiness.  The symptoms coincide with the duration of shift work and usually remit with the adoption of a conventional sleep-wake Schedule. o Experience disturbed sleep, health, personal problems such as personality and mood and interpersonal problems. o More likely to develop breast cancer and make significant errors on the job Sleep Sleep timing is controlled by the circadian clock, sleep-wake homeostasis, and in humans, within certain bounds, willed behavior. The ABCC9 of sleep: a genetic factor regulates how long we sleep Measuring Sleep Patterns Electroencephalogram (EEG) provides a gross record of the brain’s electrical activity Desynchronous activity: independent action of many neurons Synchronous activity: many neurons firing in unison Sleep: characterized by rapid eye movement (REM) sleep and non-REM (nREM) sleep (Phase 1- 4) Beta rhythms: awake and alert; 15 to 20 Hz Alpha rhythms: awake and relaxed; 8 to 12 Hz. Stage 1: Similar to awake EEG Heart rate and muscle tension decrease Theta rhythm of 4-7 Hz Stage 2: • Sleep spindles occur in 0.5 sec bursts of 12 to 14 Hz made by interactions in the thalamus and cortex • K-complexes are sharp negative EEG potentials (burst of brain activity) Both reflect brain’s attempts to monitor external environment while maintaining sleep Stage 3 and 4: Delta waves: large-amplitude, very slow waves of about 1 Hz REM sleep: Rapid eye movement Active EEG with small-amplitude, high-frequency waves, like an awake person Muscles are relaxed–called paradoxical sleep Phases of Sleep Sleep time ranges from 7–8 hours 45–50% is stage 2 sleep, 20% is REM sleep Cycles last 90–110 minutes, but cycles early in the night have more stage 3 and 4, and later cycles have more REM sleep Dreams  Dreams are successions of images, ideas, emotions, and sensations that occur involuntarily in the mind during certain stages of sleep  Dreams mainly occur in the REM stage. REM sleep is revealed by continuous movements of the eyes during sleep. At times, dreams may occur during other stages of sleep. However, these dreams tend to be much less vivid or memorable  During a typical lifespan, a person spends a total of about six years dreaming  Brain regions active during dreaming: limbic system and visual cortex Theories of dream: • Dreams as excitations of long-term memory: Tarnow suggests that dreams are ever- present excitations of long-term memory. • Dreams for strengthening of semantic memories: illogical locations, characters, and dream flow may help the brain strengthen the linking and consolidation of semantic memories • Dreams for removing excess sensory information: dreams are a need and have the function to erase (a) sensory impressions that were not fully worked up, and (b) ideas that were not fully developed during the day Nightmares: a REM dream with frightening Night Terror: NREM episode in which the content individual is partially aroused, disoriented, frightened, and inconsolable  Late in sleep cycle  Within four hours of bedtime  You wake up scared or upset  Wake up disoriented and confused  You feel comforted in response to a  You feel unconsoled or unaware of a


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