BioPsychology EXAM #2

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Last updated 3:45 PM on 10/26/23
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166 Terms

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Drugs

1.Molecular level

2. Behavioral level

nt in the same class share the same chemical structures

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Drugs definition

substances that are taken in small amounts, effects experiences, mood, &/or health.

What is bad about this definition is is very broad and we have to be very specific.

1. Low doses drugs, usually act on particular classes of nt receptor

2. Studied at multiple levels of analysis b/c the act at the molecular level, but also affect behavior.

drugs can be devastating

Change at one level and affect another level

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Dopamine

can bind to D1 and D2 receptors. Nt can bind to different receptors that are specific to that receptor. nt and receptor lock each like lock and key

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EX: Nt and receptor subtypes

nt= Acetylcholine (ACh)

Receptor= 1. Muscarinic and Nicotinic.

These receptors are where ACh can bind.

Agonist such as nicotine mimic ACh and binds to nicotinic.

When nicotine binds to Muscarinic or Nicotinic, it tricks the brain into thinking that it is ACh that binded to the receptors

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Ligand

substance that binds receptor

Type of ligand:

1. Endogenous (Ach)= occur naturally in the body ( the body makes it) (Agonist)---is produced inside the body.

2. Exogenous(nicotine) =agonist= Introduced into the body and compete with the nt binding site.---arising from outside of the body.

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Endogenous

occurring naturally in the body. The body makes it by itself.

ex: ACh

3. Antagonist ligand= block nt

4. Noncompetitive ligand= the bind somewhere and do not block or compete with the nt.

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Exogenous

is introduced into the body. The body does not make it.

EX: Nicotine

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Drug Binding

Drugs with multiple effects typically

1. bind more than one receptor.

2. bind receptors for a long time and

3. have higher affinity for that receptor= low concentration

Higher affinity drugs stay in the receptor binding site for a long time.

Low affinity drugs= high concentration (Need more of the drug)

1. do not stay in the receptor for a long time.

2. do not bind to more than one receptor

3. Do not have multiple affects

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Affinity ( how sticky is the drug)

1. Need higher concentration of low affinity drug. We need a lot so that they can stay in the receptor for a long time.

2. Need low concentration of high affinity drug. We need little bit because we already have too much.

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Agonist ligand

1. Unbound receptor is normally closed.

2. Exogenous ligand= is a drug or toxin that resembles the endogenous ligand and is capable of binding to the receptor nd activating it also. Is classed as Agonist

EX:

Nicotine binds to nicotinic receptor in place of ACh and the brain will not notice. Nicotine competed with Ach

Agonist act as the nt.

Endogenous ligand: Is naturally occurring in our body and activates it own receptor.

EX: ACh binds and activate muscarinic and nicotinic

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Antagonists

Some substances bind to receptors but do not activate them. Instead, they simply block agonists from binding to the receptors.

When nt anatagonists bind to receptor sites, it will prevent the nt from going to post-synaptic neuron and nothing happens in the post-synaptic

EX: Cocain blocks nt so the nt will stay in synaptic gap and it will impact the post-syntactic nt even more

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Noncompetitive Ligand

Drug does not compete with nt for binding site. The drug finds another site on the receptor and modulate effect of the nt.

modulate: exert a modifying or controlling influence on.

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Pre-synaptic Affect

1. Action potential arrive at the axon terminal

2. Causing vesicles to rupture and release transmitter into the synaptic cleft

3. Molecules of neurotransmitter bind to postsynaptic receptors and alter functioning of the postsynaptic cell. In this example, postsynaptic potentials (EPSPs or IPSPs) are created

4a. The action of the released transmitter is rapidly reversed. In a process called, reuptake, transporters on the presynaptic transmitter for eventual recycling

4b. Furthermore, enzymes within axon terminals, such as monoamine axidase (MAO), and other enzymes located within or near synaptic cleft, rapidly inactive neurotransmitters by breaking them down.

Drugs affect neural conduction and synaptic events

See figure 4.9a in your book

Drugs Affect:

neural conduction and syntactic events

See figure 4.9b in your book

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Routes of Administration= How the drug enter the body

1. Rate of parental

2. inhalation ( Gas)

3.Slow route (Oral)

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Routes of Administration= ways the drug enter the body

Rate of parental (Needle)

Absorption:

1. Intravenous-- into vein (1 faster)

2. Intraperitoneal Abdominal-- body cavity

3. Intramuscular- muscle

4. Sub-cutaneous-- under skin ( more dense and the drug enter slower)

Absorption of drug depends on density of capillaries flow.

1--4 are in the order of how fast the drug enter into the blood vessels. 1 goes very fast than 2 ...

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Routes: Inhalation

1. Gases-lungs: A lot of surface area exposed to air & capillaries

2. Smokes different from gas b/c includes vapor & ash particles, but absorbed similarly

3. Solids- inhaled through nose. Not as efficient as lungs as gas.

Damage respiratory system. & lead to lung disease. Also other forms of drugs with unknown toxicity may be formed.

Leads to lung diseases

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Slow Routes

Oral- absorbed mostly through intestines, then through capillaries. They have to make it through the stomach first.

Transdermal--not readily absorbed through epidermis (skin).

EX: Nicotine patch

It will take a long time for the drug to go across the skin. The best thing about it is Nicotine patch works for a long time.

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Types of drugs

1. Opiates

2. Marijuana

3.Alcohol

4. Hallucinogenic Drugs Alter Sensory Perception

5. Stimulants (6. Nicotine, Amphetamine, Ecstasy, Cocaine)

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Opiates

Helps relieve pain

Types of Opiates: Morphine and Heroin = are highly addictive

1. Morphine is the major active substance

analgesic properties (pena queductal gray) Queductal gray=channel in the brain

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Endogenous agonist: opioid Peptides

Two types:

1. Enkephalins

2. endorphins

Both of these opioid make us feel better when we cause pain to ourselves.

There are things we make ourselves that help us when we cause pain to ourselves. The brain release opioids to relieve us from pain naturally.

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Aqueductal

channels in the brain

All brain make their version of morphine. After someone had surgery. doctors used do not give them pain killers. However, doctors give their patients pain killers after surgery because if they do not give them pain killers they will suffer from chronic pain all of their lives. The patients are given pain killers at low dose so that they do not get addicted by it.

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Marijuana

Has a wide array of effects/ multiple effects

1. Is the most widely used illegal drug

2. The active gradient for marijuana is THC

Fake or synthetic THC has been created so that it has less consequence on the patient than the real marijuana. There are THC receptors in hippocampus, this shows that marijuana affects learning and memory.

3. The receptors for marijuana connects in the substantia Nigra,( Parkinston disease). hippocampus, cerebella, cortex, & cerebral cortex

4. Marijuana binds to metabotropic receptors

(Metabotropic= nt binds to G-protein. G-protein actives this membrane, which opens ion channel indirectly or does a cascade of signals)

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Endogenous equivalent is anandimide

our brain version of marijuana receptor .

All of our brain have marijuana receptors because we make our own version.

Once people take marijuana, they can take other drugs very easily.

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Alcohol

Most widely used legal drug

1. Abuse indirectly leads to neuronal damage in the frontal lobe, cbllm, hippocampus

2. Acts predominantly on GABA receptors

3. Alcoholism shows a strong hereditary component (if someone grandparents or parents were alcoholic, that person will have a higher genetic tolerance to alcohol. To avoid also being an alcoholic, the person should avoid taking alcohol).

4. When someone drinks their frontal lobe does not work very well, Cbllm=movement is affected, hippocampus= learning and memory is affected. That why if someone is drunk, they do not remember what they did while being drunk.

If you learn something under water, you will remember it better if you go under water. If you learn something by drinking coffee, drink coffee when you take the exam

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Some Effects of Alcohol Are

Some Effects of Alcohol are reversible with abstinence

Figure 4.11 in the book

abstinence=the fact or practice of restraining oneself from indulging in something, typically alcohol

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Hallucinogenic drugs alter

sensory perception

1. Alters or distort perceptions

hallucinogenic drugs act on:

1. Amine transmitter system

2. LSD= which acts on serotonin (5-HT) receptors

4. Stimulates dopamine release

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Stimulants Increase

stimulates activity in the nervous system and does not stimulate behavior

Types of stimulants

1. Nicotine

2. Amphetamine

3. Ecstasy

4. Cocaine

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Nicotine

1. Activates nicotinic receptors, ACh receptor subtype

2. Nicotinic receptors found at neuromuscular junction, autonomic ganglia (parasympathetic and sympathetic ganglia) and CNS

3. Increases heart rate, blood pressure, secretion of stomach acids

Nicotine has a lot of affects because it receptor is everywhere and it affects young brains

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Amphetamine

Why is it interesting in a bad way

Are bad

1. because more is released but is not recycled.

2. Blocks re-uptake and degradation of nt.

3. This causes a lot of nt to be in synaptic gap---keep on affecting post-syntactic neuron gap

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Stimulant: Amphetamine

have synaptic effect and psychological effect

synaptic effects:

1. Causes the release of catecholamines from pre-synaptic terminal

2. Blocks the re-uptakes of catecholamines

4. Compete with nt for the inactivated enzyme (agonist)

psychological effect:

Increases motivation, but not cognitive ability.

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Stimulants: Ecstasy

Effects on brain structure

Is not whether or not neurons are working. Is just to see if they are there or not.

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Normal Brain Versus exposure to Ecstasy

Affects the brain structure.

14 days after the normal brain is exposed to ecstasy, a lot of brain neurons were not there.

After 7 years of not taking ecstasy, the brain recovered.

If you stop taking ecstasy your brain structure can recover.

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Stimulants:cocaine

1. Affects on brain Function= is the brain working and what is working.

2. Initially used as an anesthetic (benefit)

EX: dentists use it to put on the teeth and it name come from coca cola.

3. Cocaine blocks re-uptake of amines, especially Dopamine. This means that there will be more dopamine in the synapse that will continue to affect post-synaptic neuron .

4. Can cause vascular damage

Risk= addictive

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Cocaine Abuse and Brain Activity

1. Normal brain

2. Only temporal and occipital lobes were there after 10 days of using cocaine.(this means this person can see and can hear but cannot reason well)

3. After 100 days of using cocaine, the person can still hear and have vision. Things did not return to normal.

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Drugs Used to Treat Psychological Disorders

1, Antipsychotic Drugs

2. Antidepressants Drugs

3. Anxiolytics combat Anxiety

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Antipsychotic Drug

Used to treat schizophrenia

When the drug was first created, the first kind was

1. Typical neuroleptics

1st generation were selective D2=dopamine antagonists

2. Atypical neuroleptics (2nd generation)--less side effects. Also impacted dopamine receptors

Dopamine receptors are D1 and D2

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Antidepressants Drugs

Used to treat affective (mood) disorders

1. Monoamine oxidase Inhibitors (MOAIs)

MOA breaks down manoamine nt .

We do not want MOA to break monoamine neurotransmitters. So MOAI is used to prevent MOA from breaking monoamine nt.

2. Tricyclic-block reuptakes of norepinephrine= less side effect 5-HT

3. Selective serotonin reuptake Inhibitors (SSRI)= have less side effects, but take longer to act. Have less side effect because it works on 1 and 2 nt instead of 5 nt.

If the drug work very quickly, they will ware off very quickly.

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Why do we need MAO

Because it needs to break down serotonin in a Non-depressed person because they have too much of it.

However, when someone is depressed, they do not have a lot of serotonin. For this reason we do not want MAO to break down serotonin in depressed people because they do not have a lot of it. MAOI is used to inhibit MAO from breaking down manoamine in depressed person.

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Downregulation

When someone is depressed they are experiencing a down regulation/ decrease serotonin. So MAOI is used to inhibit MAO

When reuptake is blocked, there will be more serotonin in the synapse

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Anxiolytics Combat Anxiety

Benzodiazepines= class of anxiolytics includes diazepam (Valium)

1. Acts on GABA receptors but not nt site

2. Endogenous activator for benzodiazepine site?

3. Allopregnanolore= acts on GABA receptors which inhibits stress hormones

GABA is our main Inhibitory nt. There are 3 types of GABA= GABA a b and c

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Neuromagilator

benzodiazepine and does not compete with GABA it binds somewhere.

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Drug Abuse is Pervasive & Costly/

consequence of drug abuse

1. Medical expenses due to health effects.

2. Crimes committed

3. Costs of addiction treatment & controlling drug trafficking

4. Drug babies born W/brain impairments

If mom takes cocaine when she is pregnant it has less impact on the baby than alcohol.

Legal drugs cause more death in US than Illegal drug

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Different Models of Approaching Drug Abuse

1. Moral model= drugs are bad= Drugs are bad and the person who is taking them is a bad person

2. Disease Model= Addiction is a disease= How can we treat persons medically.

3. Physical dependence model= Addiction occurs b/c people develop a physical dependence on the drug which results in withdrawal symptoms.

Not all drugs cause physical dependence. Some drugs are taken for psychological purposes instead of physical

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Different Models of Approaching Drug Abuse continue

Positive Model= Addiction b/c the drug acts as a positive reinforce= the drug gets ride of the disease or pain.

Physical dependence not necessary= Physical competent is not necessary

Reinforcement Pathway:

Ventral tegmental area releases DA onto nucleus accumbens.

Medolimbocardical pathway ( SEE YOUR NOTES).

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Medolimbocardical pathway

...

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The rat story

Every time a rat presses the level, they get reward. The animal will keep pressing the level to get the drug. The exposure is so rewarding that you can food deprive the animal. The animal will prefer to press the bar so that they can get the drug

The rat presses the bar so that they can get the drug under all situations

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See figure 4.19b

The rat was looking for Acl but they got dopamine instead. Level oof Dopamine arise to 700

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Treatment and Presentation

1. Agonist are drugs that produce common addiction states

2. Antagonists to addictive drug= prevent you from getting pleasure from the drug and will not let the drug bind

3. Antiuraving medications= fell anxious

4. Medications that block drug metabolism

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Tobacco

A highly addictive North American plant whose leaves (usually dried and smoked) are a major source of nicotine.

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fetal alcohol syndrome

a disorder, including intellectual disability and characteristic facial abnormalities, that affects children exposed to too much alcohol (through maternal ingestion) during fetal development

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caffeine

a stimulant compound found in caffeine, cacao, and other

dysphoria= unpleasant feeling; opposite of euphoria

s

Nucleus accubens: receives DA from ventral tegmental area

Insula= A region of cortex lying below the surface, within the lateral sulcus, of the frontal, temporal, and parietal lobes.

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enocannabinoid

An endogenous ligand of cannabinoid receptors; thus, an analog of marijuana that is produced by the brain.

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Chapter 5

...

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Hormones

Chemicals secreted by cells

1. Travels through bloodstream

2. Target cells are involved in producing physiological effects.

EX: Hormone is growth hormone

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Examples of Hormone

1. Endocrine= release hormones within the body

2. Homocostasis= maintenance of a constant internal environment

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What is the difference between hormone and nt

1. Nt travels short distances

2. Hormones travel long distances in the body

The same chemical with the same structure can act as both hormone and nt depending on how far it travels.

EX: Norepinephrine can act as both nt and hormone

You do not want to be too hot because your body will sweet and you do not want to be too cold because your body will shiver. You just want to be right. ( EX: of homeostasis)

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Endocrine Glands

release hormone within the body

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EX: Hormone Travel Through the Bloodstream

Figure 5.2

Group 1. Left undisturbed, young roosters grow up to have normal male characteristics

Group2: It testes are removed during development, roosters do not grow up to have normal male characteristics

Group3: If one of the testes is implanted cavity, young roosters grow up to have normal male characteristics

Conclusion: Because reimplanted testis in an abnormal body site still affected development, Berthold reacted that the testes release a hormal signal that has widespread effects (The location of the testes does not matter because it releases hormones signals that are widespread)

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Types of Chemical Communicatio

Neurocrine= neuronal communication= communication bwt neurons and is short distance

Autocrine= acts on itself

paracrine= regulation of neighboring cells ( parasympathetic and sympathetic )

Figure 5.3

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Types of Chemical Communication continued

Endocrine-secretion into bloodstream

1. Pheromore= signals to conspecies=members of the same species

2. Allomore-signals to other species

Armpit study: Participants were asked to smell the Armpit of each person to see what movie they were watching.

Figure 5.3

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Difference in Neuronal Vs. Hormonal Communication

1. Neuronal comm. goes to a Precise destination

2. Neuronal comm. is faster= they are faster because they travel long distance

3. Neuronal impulse Is all-or-none= If threshold is not met, the A.P will not be fired.

Hormonal message is graded= different amount of hormone being released

4. Some neuronal messages can be controlled ( You can have one neuron synapse on another one)

Hormonal commutation:

1. Can be local or widespread

hormonal message is graded= different amount of hormone being released. If a lot of hormone is release.. it will be big. If little bit of hormone is release it will be small.

4. Some Hormonal messages cannot be controlled.

You can have one neuron synapse on another one.

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Similarities in Neuronal Verus Hormonal Communication

1. Both produce & store chemicals for later release

2. Both stimulate target cells w/chemicals

3. Many different types of nts. hormones

4. Chemical needs to bind to specific receptors

EX: growth hormone will bind to growth hormone receptors. This will bind to metabotropic receptor

5. Sometimes 2nd messenger is activated w/in target cell

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Neuronal versus Hormonal Commutation

Figure 5.3

...

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Hormones Stimulate

Figure 5.4

Several Types of Cells/ Targets cell Receive Several Hormones

One hormone can stimulates can stimulate several types of cells in it class. such as hormone A can stimulate A 1, A 2, A3

You can have one hormone affect 3 different types of hormones.

Hormone A can affect A1, A2, A3.

One brain area can be affected by different hormones as long as here are receptors for them. One brain area can be affected by hormone A, B, C

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Hormone can be classified by

Chemical structure

figure 5.6

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Types of hormone based on their chemical structure

1. Protein hormones= strings of amino acids= different amino acids

2. Amine hormones-strings of a single type of amino acid= same amino acids over and over again

3. steroid hormones-composed of four internnected carbon rings= same amino acids over and over again

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Hormone Binding can exert Different Effects

1. Protein hormones & most amine hormones bind receptors on target cell's membrane, & activate 2nd messengers. ( They are faster because the receptors are sitting on the cell membrane)

2. Steroid hormones pass through the membrane bind receptors inside the cell & affect gene expression (Is slower because the hormone have to go inside the membrane to bind to the receptor)

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Protein & Amine Hormones Act quickly

1. When the extracellular site is bound, shape of the receptor changes, iniating a 2nd messenger

2. Specificity is determined by the selectivity of the receptor (only some cells produce the receptor)

EX: When receptors do not work, the body thinks the hormone does not exist because there will never be a receptor for them to bind. This is not good for the people who have a bad receptor

3. Act relatively quickly & W/ prolonged effects

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Steroid Hormones Act Slowly

Pass in and out of many cells

2. Hours to take effect

3. Alters protein production for slow, but long-lasting effects

4. Steroid receptor cofactors-needed for a cell to respond to steroid

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Feedback Control Mechanisms

The Hormone system & Evaluates effects.

Output of the hormones feedback to inhibit the drive for more hormones.

When too much hormone are made, the body stops it.

Too little are made, the body makes it.

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What happens when there is not to much hormone?

If this is not there, it will keep making hormone. When it is there, it tells the body to stop making hormones

Figure 5.8 a and b

Figure 5.8 c, d

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Hormone Chain of command

Hypothalamus=Brain areas send signals to other brain areas.

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Hypothalamus is divided into

1. Posterior pituitary

2. Anterior pituitary

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Posterior Pituitary is divided into

Vasopressin and oxytocin

which both target organs

The target organs produce Bio response

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Anterior pituitary

hormone release

Is made up of 6 tropic hormones :

1. Adrenal

2. Gonads

3. Milk Production

Multiple target organs

More hormones

multiple target organs

bio response

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Relationship between hypothalamus and posterior pituitary gland

1. Hypothalamus makes vasopressin and oxytocin and then transport them along axons to posterior pituitary.

2. Posterior pituitary- receives axons and hormones (vasopressin and oxytocin) from hypothalamus

3. Posterior pituitary releases the hormones into circulation

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Posterior Pituitary Hormones

1. vasopressin= increases blood pressure.

It main effect is : antidiuretic conserves water

2. Oxytocin- stimulates contraction of uterine muscles

Uterine muscles Triggers Milk letdown reflex and mediates sexual arousal and affectionate response

EX: Bonds with a new born baby ( people who have autism have it). They have genes that can make oxytocin. If oxytocin is given to them, they make more eye contact

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Milk Letdown Reflex

1. infant suckling produces brain activity in the mother

2. Increased brain activity results in inputs to the hypothalamus

3. Oxytocin produced and released

4. Oxytocin causes cells of mammary glands to contract; milk released

5. Baby continues sucking until sated

back to 1 again

The mom hear the baby cry, the milk come out. This is good because the baby is fed really early and fast. Milk come just when the baby being to cry

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Anterior pituitary and Posterior pituitary

See book

figure 5.13

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Anterior Pituitary

Figure 5.13 and figure 5.10

...

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Hypothalamus and Releasing Hormones

1. Hypothalamus axons converge above pituitary stalk (as oppose to going through it)

The pituitary stalk (This region contains a bed of capillaries (hypothalamus pituitary portal system)

2. Hypothalamus secrets hormones into capillaries where blood carries it to

3. Anterior pituitary, which releases (or inhibits the release of tropic hormones ( There are 6 types of tropic hormones)

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Tropic Hormones released by Anterior Pituitary are

1. Adrenocorticotropic hormones (ACTH)

2. Thyroid stimulating hormone (TSH)

3. Luteinizing hormone (LH)

4. Follicle-stimulating hormone (FSH)

5. Prolactin promoter hormone

6. Growth Hormone (GH)

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Adrebicirticotropic hormones (ACTH)

Anterior pituitary control of the Adrenal cortex and Thyroid

1. Adrebicirticotropic hormones (ACTH)---controls production and release of adrenal ctx hormones (which control release of steroid hormones)

2. Thyroid stimulating hormone (TSH)--controls release of Thyroid hormones

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Anterior pituitary control of Gonads

3. Luteinizing hormone (LH)--females--stimulates release of eggs from ovaries

Males--testosterone production

4. Follicle-stimulating hormone (FSH)--females--secretions of estrogen

male--sperm production

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Anterior pituitary control of Milk Production and Body Growth

5. Prolactin-promotes mammary development for lactation (females) = breast develop= 12 and 13 years old

6. Growth Hormone (GH)--influences growth of cells and tissues

produced and released during early stages of sleep

Giving someone growth hormone for the sake of it is unethical

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Organs Affected by Anterior Pituitary Hormones

1. Adrenal Gland

2. Thyroid Gland

3. Gonads

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The Adrenal gland: Two Parts

1. Adrenal Cortex-outer bark of the adrenal glands releases Adrenocorticoids

There are 3 classes of Adrenocorticoids:

Glucortioids. EX: cortisol ( hormone that is released when people get stressed)

Mineralocorticoids. EX. Aldosterone (function is water conservation)

Sex steroids. EX: Androstenedione ( function is responsible for hair is private places) ( does not respond to ACTH. Why? because is part of peripheral nervous system)

2. Adrenal Medulla releases epinephrine and norepinephrine in response to sympathetic n.s activation

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Cortex means

bark= outer layer. Andrenal cortex has two layers: ouside and inside.

When adrenal goes to ACTH, it releases hormone

While ACTH goes to Adrenal cortex, it can release one of the 3 classes of hormone

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Thyroid Hormones Regulate Growth and Metabolism

Thyroid hormones

1. Amines act (bind) like steroids ( meaning for amines to bind to receptor it has to go through the cell membrane to bind to receptor)

2. Main hormone: thyroxine, triothyronine

3. Production of thyroid hormones requires iodine in order to be made.

Without iodine, thyroid may enlarge goiter in an attempt to produce more hormones

4. Thyroid deficiency may result in stunted growth and reduced brain size

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Gonads Produce steroid Hormones

Regulating Reproduction

1. Trigger reproductive behavior and gamete production.

Testes:

Leyodig= cells produce and secrete testosterone

Ovaries: 2 main classes of hormones

1. Progestin: EX: progesterone

2. Estrogen: EX: Estradiol

Progestines--Angrogens--Estrogen

But the sexes differ in the proportion of each hormone

LH and FSH goes through the Gonals

Progestion turns into androgens turns in estrogens

There is no really a female hormone or a male hormone

Male have more of estrogen and female have more of androgens. But everybody have a little bit of both

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Hypothalamus produces

1. gondrotropin hormone= releasing, GnRH

2. Anterior pituitary (LH and FSH)

Produces Testes

Hypothalamus produces (GnRH)

Anterior Pituitary

LH and FSH

goes on to produce

Ovaries

Hypothalamus is always the one releasing hormone. The released hormone always go into the anterior pituitary and pituitary makes Gonalds hormone and those hormone goes and become testes

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Sexual Differentiation

Process by which individuals develop either male or female bodies/ behavior

It takes multiple steps and multiple influences

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Sexual Determination

event that decides whether an individual becomes male or female ( is one time event)

1. Sex is determined early in life

Mammals' sex is determined at conception ( sperm and egg meet only one time)

2. Egg contributes X Chromosomes;

Sperm contributes X or Y

XX--Female

XY--male

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Sexual differentiation of the gonads

makes a male and female different

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Sex Chromosomes Direct

Sexual Differentiation of Gonads

1. Gonads are indifferent early in development (can develop into either testes or ovaries)

2. Mammals: Y chromosomes contain SRY (Sex determining region of Y chromosome)

SRY is responsible for developing testes

No Y chromosome/ no SRY protein= ovaries will develop instead=female

Male determine the sex of the baby

The first step is genetic and everything else after is hormone

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Gonadal Hormones

Direct Sexual Differentiation of the rest of the body

Two ducts: Wolffan ducts and mullerian ducts

Wolffan ducts= male sex organs and develops epididymis, vas deferens, and seminal vesicles

Mullerian ducts= female sex organs and develops fallopians tubes, uterus, and vagina

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6 weeks undifferentiated

Everybody have a wolffan duct and mullerian duct while in the womb. But once they are born, the male develop wolffan duct and female develop mullerian duct

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So You've Got Testes, Now what?

1. Males: wolffian ducts develop b/c of testosterone produced by testes

2. Mullerian ducts shrink b/c anti-mullerian (AMH), a protein hormone flourishes

3. Non-wolffian structures are masculinized b/c 5 alpha reductase (an enzyme) locally converts testosterone into dihydrotestoterne (DHT)= stronger version of testosterone and after DHT penus form

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What happens when XY chromosome/ SRY is expressed

1. Genetic Sex: Gene Expression

Gonadal Sex= (sex hormone secretion):

2. Anti-mullerian hormone (AMH) occurs and testosterone (T) is produced

3. Phenotypic Sex:

1. AMH causes mullerian duct to shrink

2. Testosterone induces Wolffian ducts to form epididymis, vas deterns, and seminal vesticles, and other tissues to form prostate and bulbourethrat gland (1, 2 are happening internally)

5 alpha reeductase : converts testosterone into DHT (external)

DHT induces skin to form scrotum; tubercle forms penis (External)

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What happens when SRY does not develop

1. Genetic Sex: Gene expression

2. No SRY expressed

3. Ovaries produce, no AMH, no T

4. in absence of AMH, mullerian ducts form fallopian tubes, uterus, and inner vagina

5. In absence of testosterone, wolffan ducts regress, and no prostate or bulbo-urethral gland forms (4 and 5 happen internally)

6. 5 alpha reductase= in absence of DHT, skin forms labia and outer vagina; tubercle forms ditoris