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295 Cards in this Set
- Front
- Back
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Learning vs memory |
Learning: creating changes in the brain, based on experience. -this is actually making the neurological pathways. Memory: how those changes are stored in the brain. -when things are connected, we activate these paths and keep them. |
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Physiological ways we change our brain to learn: |
Reorganization. -new synapses, myelination, neurons and dendritic branching -occurs with experience - enhances with enrichment |
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What enhances learning? |
An enriched environment! |
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How changes are stored in the brain(memory); |
-Synapses fuse together -synchronized firing for same concepts. This ties together what we know. |
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What stage of neurogenesis is memory involved in? |
Survival |
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What did HM have removed? |
Bilateral hippocampus removal -to eliminate/reduce severe epilepsy |
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Behavior results from HM’s surgery: |
Mild retrograde amnesia - 2 years prior Severe anterograde amnesia -continued for the rest of his life |
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External Cue |
Triggers that reactivate a memory that are outside your body. Something you see, hear or sense. |
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Evidence of contribution 2, being able to have unconscious memories: |
Classical conditioning trials -eye blink task Incomplete pictures test -seeing varying levels of incomplete pictures (average person can tell what the image is by slide 3) |
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Categories of Long Term Memories (LTM) |
Explicit Memories Implicit Memories |
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What are explicit memories? |
-Conscious memories -can talk about the memories |
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Two divisions of explicit memories: |
Semantic memories( or declarative): knowledge of facts Episodic Memories: Events. -these can be feelings, visual or senses -we can lose episodic memory very easily |
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Implicit memories |
Unconscious Memories Still affect our behavior |
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Two divisions of Implicit memories: |
Procedural Memories: muscle memory -involves the basal ganglia (and a bit of the cerebellum) and is involved in procedural memories Classical Conditioning: learned responses |
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How memories are reactivated later: |
Internal and External cues. -triggers that pull memories out. -The closer the cue is to the memory, the better it is for retrieval |
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Internal cue |
Trigger that reactivates a memory, these are emotions, visualization, and feelings. |
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External Cue |
Triggers that reactivate a memory that are outside your body. Something you see, gear or sense. |
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Best sense for triggering memories: |
Olfactory |
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What neurotransmitters play a large role in memory? |
Glutamate, Acetylcholine and epinephrine. |
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When there is a high rate of cell division, there is a high chance of _________ |
Mutation -areas with high change of cells (such as the neurogenesis found in the hippocampus, and medial temporal lobe) are common places for epilepsy |
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Retrograde Amnesia |
Loss of memory prior to a traumatic event |
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Anterograde Amnesia |
Memories lost after a traumatic event -inability to form new memories, occurs for awhile after the trauma until you become “normal” again |
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Which memories are generally safe after a traumatic experience? |
Memories from the distant past, they are normally not affected. |
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Evidence of Long Term Memory |
HM: Hippocampi removed severe anterograde amnesia -no new explicit memories Mild retrograde amnesia -retained most of old explicit memories KC Hippocampi and PFC damaged (damage to medial temporal lobes) -severe anterograde amnesia No new explicit memories -severe retrograde amnesia For episodic memory only; semantic memory intact! |
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Amnesia behavior characteristics in Alzheimer’s disease: |
-Major anterograde amnesia for explicit memory -newest episodic memories lost first (older memories preserved longest) |
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Amnesia physiological explanation in Alzheimer’s disease: |
Acetylcholine deficiency -affected area: basal forebrain |
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When we start to lose acetylcholine, we have trouble _________ |
Packing in and making new memories |
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One of the earliest signs of Alzheimer’s: |
Not being able to remember stuff! They talk about the past well, but have trouble with new info. -episodic memory is most fragile |
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Amnesia in Korsakoff’s Syndrome, behavioral characteristics: |
-Major anterograde amnesia for ALL types of memories -major retrograde amnesia for all types of memories |
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What causes Korsakoff’s Syndrome? |
Results from alcoholism! -it is less about the alcohol, and more from diet. There are Thiamine deficiencies, and alcoholics generally don’t buy foods with it in there! |
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Where is Thiamine found? |
Things high in vitamin B! |
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Prominent person with Korsakoff’s syndrome? |
Dennis Rodman |
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Amnesia in Korsakoff’s Syndrome, physiological explanation: |
Thiamine deficiency -area of concern is the thalamus. Without its use, we end up kinda brain dead, no info is being sent throughout the brain. |
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Common place damaged that causes amnesia: |
Medial Temporal Lobe |
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Transient Global Amnesia |
Sudden onset amnesia, with severe anterograde amnesia, and mild retrograde amnesia for explicit episodic memories. -generally lasts 4-6 hours. -can be caused by stroke and anesthetic. |
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Evidence of contribution 3, that there are different types of long term memory: |
HM retained new procedural memories, but no event memories. -must be different areas of the brain. |
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What are concept cells: |
Found throughout the medial temporal lobe, surrounding the hippocampus. -these respond to multiple items (somehow related) -respond to multiple sensory modalities (vision, auditory, etc) Respond=neuron fires |
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Jennifer Aniston Neurons |
These are single neurons located throughout the hippocampus. -respond to one item! -respond to only one sensory modality! -all called Jennifer Aniston neurons! |
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Concept cells have what name in front of them? |
Name of the stimuli/object! (Unlike Jennifer Aniston neurons) |
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What are the three parts of the hippocampus? |
Posterior and anterior hippocampus and the dentate gyrus |
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Place cells (spatial view cells) |
Located in the posterior hippocampus. -these fire in a specific way to represent parts of a familiar environment. -they fire to where the animal thinks it is. -this firing makes a map of this location for future usage. It’s how we make mental maps, and feel familiar. |
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How does information get into the posterior hippocampus? |
It is forwarded from areas in the medial temporal lobe |
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Name the cortex’s under the hippocampus (in the MTL) |
Parahippocampal Cortex: forwards spatial information Entorhinal cortex: “groups” memory information together to relay into the hippocampus for sorting Perirhinal cortex: forwards object information |
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Pathway for spatial memories: |
Posterior parietal lobe> parahippocampal cortex> entorhinal cortex>posterior hippocampus |
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How is the Hippocampus like the thalamus? |
In some cases it takes incoming information and distributes it for consolidation through the brain. -but it also stores some memory. |
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Where is spatial memory stored? |
Hippocampus, specifically the posterior hippocampus. |
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Which subcortical system is the hippocampus part of? |
Limbic System |
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What are the three parts of the hippocampus? |
Posterior and interior hippocampus and the dentate gyrus |
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What does the anterior hippocampus do? |
Responsible for explicit memory encoding, and forwarding. |
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What does the posterior hippocampus do? |
Spatial memory encoding |
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Which part of the hippocampus has “ridges” on it? |
The dentate gyrus |
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Name the cortex’s under the hippocampus (otherwise noted as in the medial temporal cortex) |
Parahippocampal Cortex: forwards spatial information Entorhinal cortex: “groups” memory information together to relay into the hippocampus for sorting Perirhinal cortex: forwards object information |
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Types of hippocampal cells: |
Concept Cells Jennifer Aniston Neurons Place Cells (spatial view cells-humans) |
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What do concussions show us about memories? |
That memories must be consolidated to be kept long term Evidence Only most recent memories surrounding the trauma are lost (older memories are fjne) |
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What determines the degree of retrograde amnesia after a concussion? |
It varies based on the severity. -some can forget minutes prior to trauma, some forget days. |
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Where are memories stored? |
1. Inferior Temporal Cortex -processes visual object information. (I.e. v4 and fusiform face area) 2. Prefrontal cortex -Episodic memory -> anterior hippocampus > PFC ( memory consolidation) -this is storage not working memory! 3. Cerebellum -memories related to classical conditioning (ex. eye blink test) 4. Dorsal Striatum - habit formation and procedural memory 5. Medial temporal Lobe -concept cells *6. Amygdala -does not store memories, but strengthens emotional significance 7. Cortex -semantic memory |
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Damage to where causes loss to episodic memories? |
Prefrontal cortex |
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What is the gateway to storing new info throughout the cortex? |
Anterior hippocampus |
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Where is memory related to visual object kept? |
Inferior Temporal cortex |
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What kinds of memory is kept in the prefrontal cortex? |
Episodic memories |
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Where is memories related to classical conditioning stored? |
Cerebellum |
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What kinds of memories are stored in the dorsal striatum? |
Habit formation and procedural memories |
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Where are concept cells found? |
Medial temporal lobe |
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What does the amygdala do in regard to memory? |
Strengthens memories as they go for consolidation, adding emotion. -if you form a memory and the amygdala is firing you will remember it really well (or suppress it!) |
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Where is semantic memory found? |
Throughout the cortex! |
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Lobotomy vs. lobectomy |
Lobotomy is a surgical operation on the brain, intent on treating mental illness. Lobectomy is the removal of a lobe or organ |
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Front (Term) |
1. Perirhinal Cortex 2. Entorhinal Cortex 3. Parahippocampal cortex 4. Lateral fissure |
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LTP |
Long-Term potentiation -process by which neurons connect more substantially by making synapses more sensitive to signals. |
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Three stages of LTP |
Induction, maintenance and expression |
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MAMAWAMA |
Sometimes referred to as the mamawama complex. -femininity and masculinity are mutually exclusive. -this is more social construct garbage. |
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Biological sex: |
Objectively measurable; gonads, hormones, chromosomes |
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Sexual orientation: |
Who you are physically/emotionally attracted to -you can be emotionally attracted to one type of person and physically attracted to another. |
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Gender Identity |
How you view yourself
-FYI a transgender is a man identifying as a woman. Transsexual is after surgery. |
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Gender Expression |
How you demonstrate your gender (based on gender roles) |
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What are endocrine glands? |
Glands (tissue) in the peripheral nervous system that release hormones into the circulatory system (blood) -circulatory system carries hormones to target tissues (bones, muscles for growth, etc) |
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Endocrine Gland: Gonads |
These are glands that: A) release steroid hormones B) they create/contain sex cells |
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Male gonads |
Testes Sex cells: sperm |
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Female gonads: |
Ovaries Sex cells: ova |
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Zygote: |
Sperm + ova (fertilization) = zygote |
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Male and female sex chromosome pairs: |
Female XX Male XY |
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What are the three classes of Hormones? |
Amino Acid Derivatives Steroid Hormones Peptides & proteins |
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Amino Acid Derivatives: |
Synthesized out of Amino Acid Molecules -epinephrine (synthesized from tyrosine) — released from the adrenal medulla |
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What does vasopressin do? |
Regulates water retention and adult male protective behavior |
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What does oxytocin do? |
Body activities during labor. Also implicated in social bonding. (Helps body heal) |
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The anterior and posterior pituitary are both controlled by: |
Nuclei in the hypothalamus -dysfunction in the hypothalamus can lead to major effects on body and mind |
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What connects the pituitary gland to the hypothalamus? |
Infundibulum |
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Is the anterior or posterior pituitary gland involved in a multi step process? |
Anterior! Tropic hormones travel to other glands to tell them to release their hormones. -hormones from the posterior pituitary just go straight to their target tissues. |
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Does the pituitary gland release testosterone or estrogen? |
No |
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What is the path involved in regulation of gonadal hormones? |
1. hypothalamus -> anterior pituitary -via gonadotropin-releasing hormone (GRH) 2. Anterior pituitary -> Gonads -via gonadotropin 3. Gonads -> body tissue -via sex steroid hormones |
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For posterior pituitary, vasopressin goes: |
To the kidneys! |
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Do males and females have the same types of sex steroid hormones? |
Yes! They are just at different levels at different times - females are cyclical - males are at a steady state |
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What are the the cycle phases for females? |
In uterus: 1. Menstrual phase 2. Proliferation phase 3. Secretory Phase In ovaries: Day 1-13 (1& 2) is the Follicular phase Day 14: ovulation (sexual desire peaks) Day 15-28 (3) is the Luteal phase |
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Where is the adrenal gland found? |
The kidneys! (On the top technically anterior) |
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What uterus phases align with the ovaries Follicular Phase? |
Menstrual phase and the proliferation phase |
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What uterus phase aligns with the ovaries Luteal phase? |
Secretory Phase |
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What day does ovulation occur? |
14 |
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What do women experience during the menstrual phase? |
Lowest pain tolerance Emotional variability Least social |
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What do women experience during the proliferation phase? |
Highest pain tolerance Highest confidence & energy Most social (Best phase for pushing yourself!) |
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What do women experience during the start of the secretory phase? |
High pain tolerance Calmest mood Moderately social |
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What do women experience towards the end of the secretory phase? |
Lower pain tolerance Most irritation, anxiety and fatigue Less social |
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What do birth control pills do? |
Increase estrogen and progesterone -gives higher pain tolerance -better mood -but you can get anxious, gain weight, etc. |
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Steroid Hormones |
Synthesized from cholesterol (fat) -released from testes, ovaries and adrenal cortex -has three main classes |
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What are the three main classes of steroid hormones? |
1. Androgens: testosterone 2. Estrogens: estradiol 3. Progestins: Progesterone -in females it prepares the body for pregnancy - in males it is involved in sperm cell metabolism. |
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Why don’t men hear much about progesterone? |
We have less flexibility of it in our bodies, and do not see any many big swings as females do. So we see less changes due to it. -this is involved in some behaviors (none listed specifically) |
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What do women experience during the menstrual phase? |
Lowest pain tolerance Emotional variability Least social -day 1-7 |
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What do women experience during the proliferation phase? |
Highest pain tolerance Highest confidence & energy Most social (Best phase for pushing yourself!) Day 7-14 |
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What do women experience during the start of the secretory phase? |
High pain tolerance Calmest mood Moderately social Day 14-28 |
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What does the Anterior Pituitary do? |
Produces tropic hormones. -these travel to other endocrine glands to make them release their Hormones. -“master gland” is really only appropriate for the Anterior pituitary. |
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What does the posterior pituitary do? |
Produces vasopressin And oxytocin -this is more needed for day to day life. |
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Cramping is due to? |
The uterus shedding its lining |
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Sexual development at 6 weeks (from fertilization): |
1. Bipotential primordial gonads 2. Have both male and female ducts |
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Sexual development at 12 weeks from fertilization |
Major differentiation occurs - 1st hormone surge! - If nothing else happens or XX: - mullerian system matures, Wolffian degrades. -this becomes the Female ducts: uterus, Fallopian tubes, upper part of vaginal canal |
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What are the female ducts? |
Uterus, Fallopian tubes, upper part of the vaginal canal. |
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What are the male set of ducts called? |
Wolffian System |
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What are the female set of ducts called? |
Mullerian System |
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Sexual development at 7 weeks (from fertilization) |
Differentiation begins -if nothing else happens, or if XX then gonads turn into ovaries - if XY then the SRY gene on the Y chromosome secretes SRY protein transforming gonads into testes. |
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What is bipotential? |
When gonads can turn into either testes or ovaries |
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What do the ducts do? |
Channel sex hormones |
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What needs to happen for gonads to become testes? |
There must be a functioning SRY gene on the Y chromosome. This produces the SRY protein that binds to the bipotential primordial gonads to convert it into testes. |
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Sexual development at about 7-12 weeks from fertilization: |
Genital development -both types of genitals develop out of the same bipotential precursor -if nothing happens or XX then it develops into a labia/clitoris If XY then the SRY on Y -> binds to testes -> releases 5-alpha-reductase (5- AR). —this converts testosterone into DHT (dihydrotestosterone. [an androgen]) —— this turns the bipotential precursor into a penis. |
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What transforms the bipotential precursor into a penis? |
SRY on Y chromosome binds to testes -> this releases 5 alpha-reductase (5-AR) -> 5-AR converts testosterone into DHT (dihydrotestosterone) -> DHT transforms the bipotential precursor into a penis |
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What does DHT stand for? |
Dihydrotestosterone this in an androgen |
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Sexual development at 12 weeks from fertilization |
Major differentiation occurs - 1st hormone surge! - If nothing else happens or XX: - mullerian system matures, (Wolffian degrades) -this becomes the Female ducts: uterus, Fallopian tubes, upper part of vaginal canal If XY: Testes secrete testosterone -matures wolffian system- becomes male ducts: seminal vesicles, vas deferens - testes secrete mullerian-inhibiting substance (degrades mullerian system) |
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What are the ducts in the male system? |
Seminal vesicles, and vas deferens |
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What is the second hormone surge? |
Puberty! |
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Chemical changes in puberty |
Anterior pituitary releases: Human Growth Hormone: -this is for bone/muscle tissue growth (growth spurt) Gonadotropin & adrenocorticotropin (ACTH): -goes to gonads and adrenal cortex triggering sex steroid hormones |
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What do sex steroid hormones do in puberty? |
1. Matures genitals 2. Motivates sexual activity and menstruation 3. Develop secondary sex characteristics (like an Adam’s apple). |
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Ages of surge of hormones (puberty) for males and females: |
Females: 9-12 Males: 10-14 |
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Where does Gonadotropin and Adrenocorticotrophin (ACTH) come from, and go? |
Comes from: Anterior Pituitary Goes to: Gonads & Adrenal Cortex |
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Front (Term) |
A. Testicle B. Urethra C. Prostate Gland D. Rectum E. Seminal Vesicle F. Bladder G. Vas Deferens H. Penis I. Vagina J. Uterus K. Fallopian Tubes L. Ovaries |
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Front (Term) |
A. Seminal vesicle B. Vas Deferens C. Developing gonad D. Wolffian System E. Mullerian System F. Uterus G. Fallopian Tubes H. Upper part of the vagina |
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What are the 4 structures that participate in the mechanisms of sexual behavior? |
1. The cerebral cortex 2. Hypothalamic nuclei 3. Amygdala 4. Ventral Striatum |
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What chemical is released after orgasm more in males? |
Vasopressin (This May cause men to be sleepy) |
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What is the role of the cerebral cortex in sexual behavior? |
cortex mediates the most complex aspects of sexual experience, specifically: altered perceptions of time, self-awareness, and “feels -endorphins cause euphoria as it binds throughout the brain/cortex |
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What part of the brain is suppressed during orgasm? |
The Frontal Lobe |
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Why are we less likely to interpret sensations as painful during sex? |
Endorphins binding to the periaqueductal gray, providing pain relief. - this also allows us to do things that would otherwise be very uncomfortable. |
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What is released during orgasm? |
Dopamine (pleasure) Endorphins (euphoria/out of body experience) |
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What is the role of the hypothalamic nuclei during sex? |
Different nuclei in the hypothalamus are involved in male and female sexual behavior. -damage to these areas can cause sexual dysfunction. |
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What hypothalamic nuclei is involved in female sexual behavior? |
Ventromedial Nucleus -in rats, this part of the brain causes them to arch their back to allow the male to penetrate. |
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What hypothalamic nuclei is involved in male sexual behavior? |
Medial Preoptic Nucleus -involved in mounting, thrusting, etc. -this part of the brain is larger in males. -damage to this area does not mean that they engage in female sexual behavior, just not male sexual behavior. That is a different area. |
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Erectile Dysfunction, or lack of sexual drive in women can be caused by?... |
Hypothalamic dysregulation or possibly even a tumor. |
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What chemical is released after orgasm more in women? |
Oxytocin (This May be why the talking and cuddling) |
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What is A and B? |
A. Medial Preoptic Nucleus B. Ventromedial Nucleus |
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Examination of Anne S. Showed: |
Externally: normal physical female, with a 4-cm vaginal canal Internally: undescended testes, no ovaries/uterus Blood test: male level testosterone Cheek scrape: XY chromosomes |
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What did Anne S. Have? |
Androgen Insensitivity Syndrome -mutation on the androgen receptor gene. -she had no places for androgens to bind, so no masculine changes could occur! |
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Without androgen receptors, what could not develop in Anne S? |
Penis (DHT cannot bind to bipotential precursor) Wolffian System (androgens cannot mature the Wolffian system) -still had the mullerian-inhibiting substance so female ducts would not develop either |
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What happened to Anne S. At puberty? |
No male secondary sex characteristics because there are no androgen receptors! |
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What is the cause of the Guevedoces Phenomenon? |
5-Alpha-reductase Deficiency -there is no 5-AR to convert testosterone into DHT so no penis develops -BUT, the hormone surge at puberty continues unfinished maturation. (So long as androgen receptors are still in place, the testosterone will overcome the female traits) 1 in 9 have this in the Dominican Republic |
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What is the role of the amygdala in sexual behavior? |
Fear and identifying potential mates -rats use more olfaction -humans use more vision (but still some smell) |
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Men have a ________ response time viewing graphic sexual images compared to women. |
Higher -there is a lot of amygdala activity in an fMRI when those images are seen! |
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Kulver-Bucy Syndrome |
Flat Affect (dead in the eyes-emotionally void) Hyper sexuality (you will sexually approach everyone!) -we can mimic this when we lesion the amygdala
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Takeaway function of the amygdala from Kulver-Bucy Syndrome |
The amygdala plays a role in who we cannot/shouldn’t approach. -it is kind of a sexual barrier. -without it everyone is fair game and you mount everyone! |
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What is the role of the ventral striatum (nucleus accumbens) in sexual behavior? |
It is active when experiencing pleasureable sexual activity or expecting it! -see through activity in the mesocorticolimbic pathway |
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What is the pathway of the mesocorticolimbic dopaminergic pathway? |
Dopamine travels from: Ventral Tegmental Area (VTA) -> nucleus accumbens |
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Scientific name for, and reason for wet dreams: |
“Nocturnal emissions” -these experiences are very real to the brain because the same pleasure pathway is active during sex as when thinking about sex! -men and women both get wet dreams |
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What are the two phenomenal cases of human sexual development? |
1. Anne S. 2. The Guevedoces Phenomenon |
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Pathways for testosterone with 5-Alpha Reductase deficiency: |
Back (Definition) |
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Current Sex cases: |
1. Castor Semenya -no penis, other male physical traits, XY cheek swab -identifies as female -left running to play football cause didn’t want to take testosterone suppressants 2. Dutee Chand -similar to castor, but allowed all the invasive testing |
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Castors testosterone levels compared to Olympic standard for women: |
Castor: T levels > 5nmol/L Norm: 1-1.8 nmol/L |
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What class of hormone are vasopressin and oxytocin? |
Peptide |
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What are the two theories of sleep? |
1. Recuperation theory 2. Adaptation theory |
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What is recuperation theory? |
Tells us why we sleep! - The purpose of sleep is to restore optimal functioning to the cells in our bodies and minds that get worn down during the day |
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What is adaptation theory? |
Tells us when we sleep. -we sleep at night when the most of our natural predators were out. |
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How do we measure sleep? |
EEG -electroencephalogram |
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Why is REM sleep paradoxical? |
Because the person is asleep but the brain is firing as if they are awake! |
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What is REM? |
-Rapid eye movement -brain activity similar to wakefulness (oxygen consumption&glucose metabolism) -loss of muscle tone (core muscle Antonia) -emotional, creative dreams |
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What does an EEG measure? |
It measures electrical activity in the brain. -translates neural activity into wave lengths |
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What do wave lengths during deep sleep look like? |
Longer wave lengths and higher amplitude |
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What do the wave lengths during wakefulness look like? |
Shorter waves and lower amplitude (The shorter and lower the waves, the more awake you are) |
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In what stage are Gamma waves (30-100+Hz) seen? |
Hyper-alertness -stimulant use, extreme fear |
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When are Beta waves (12-30Hz) seen? |
Normal alertness -paying attention in class or talking |
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When are Alpha waves (8-12Hz) seen? |
Stage 1 (NREM) -relaxed wakefulness/daydreaming -often don’t know you’re asleep |
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What stage are Theta waves (4-7Hz) seen? |
Stage 2 -drifting down into unconsciousness -deep meditation -Hypnic Jerks and falling sensations |
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What is a hypnic jerk? |
Sudden movement/jerk while falling asleep. This is the brain stem sensing the heart rate is decreasing and low oxygen levels. It sends a pulse to make sure the body is alive. |
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What stage are Delta wavs (0-Hz) seen? |
Stage 3 (NREM) -deep, dreamless sleep; HGH high -goal: stay in this stage the longest! -most important stage of sleep |
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Why are gamma waves rarely seen for long periods of time? |
They are exhausting and possibly damaging. |
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Way to track your sleep? |
With something like a Fitbit, Maybe Apple Watch. Not the sleep app. It’s crap. -Fitbit based on heart rate and oxygen consumption. App based on movement |
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Why is REM important? |
Helps consolidate memories (contentious) Body shows a REM rebound effect |
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What do antidepressants show us about REM sleep and memory? |
Antidepressants often block the ability for REM (accidentally-it’s a side effect) and we see no apparent lapses in memory. -REM May not be involved in memory consolidation. |
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What is the REM Rebound effect? |
Once deprived of REM for a night, then next 2-3 days will have much higher levels of REM to make up for it. -must be important if the body compensates. We have a certain amount of REM we need each night to feel right. |
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How long do short sleepers sleep? |
4-6 hours. -they spend most of their time in stage 3 -they get there faster and stay there longer! Net the same amount of stage 3 but in fewer cycles. |
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Who has more dreams, short or long sleepers? |
Long sleepers! |
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Ways to increase sleep efficiency: |
-room set to 68 degrees (colder is better! They help push through the first phases of sleep) -no food/light within an hour of sleep -6 hour minimum -have a consistent sleep pattern for 2,weeks with no caffeine -keep naps to less than 20 minutes or the length of a full sleep cycle |
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Why does light (even blue light) effect sleeping? |
Light tells the pineal gland to not release melatonin. |
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What is sleep inertia? |
Waking up groggy. -this is waking up in stage 3. You can design your sleep to avoid this! |
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How do we know when people are dreaming? |
We wake them up during different stages of sleep! |
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The Thalamus is least active during what stage/wave length? |
Stage 3-Delta |
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What are dreams like during NREM? |
Only 7% have dreams. -Falling, isolated experience and boring (like daily routines) |
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What are dreams like during REM? |
80% time had dreams -stories, narratives, and imaginative-most creative dreaming. |
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Do we incorporate external stimuli into our dreams? |
Yes! -saw when misting sleepers. They dreamed they were in rain. |
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True or false: Dreams only last an instant and the brain alters perception of time |
Unclear. When woken up 5 or 15 minutes into REM people generally knew how long they were asleep. -this does ask the wrong question. It doesn’t gauge how long their dream was. Just how long they were asleep. |
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Do some people not dream at all? |
People who think they don’t dream are just good at not waking up in REM. -in tests, if woken up in REM most have dreams. |
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Why doesn’t sleep walking happen in REM? |
Core-muscle Atonia occurs. -nuclei in the brain stem (reticular formation) fire during REM, making GABA bind to the neurons in the primary motor cortex. This locks down movement. |
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What is inhibited during core-muscle atonia? |
Glutamate and acetylcholine |
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Theory behind REM dreams? |
Activation-Synthesis Theory -during REM there is random brain stem activity, and the thalamus becomes uninhibited. -the thalamus then acts without being controlled and sends messages through the cortex -the cortex is forced to “interpret” the signals and that is our dreams. -cortex sometimes uses established pathways to translate dreams. So they may have common elements, or involve things we know of significance. |
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How does Activation-Synthesis Theory explain hyper-emotional and creative dreams? |
Prefrontal Cortex is is shut down during REM (to restore), but the limbic system is not and It runs unbridled sending and interpreting information that is hyper-emotional. -the prefrontal cortex isn’t there to regulate emotions. |
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How do we know that stage 3 is helpful for repair/restoration of the brain? |
Human Growth Hormone is released into the body during this phase, allowing uninterrupted repair. -Thalamus is least active, giving the brain a break from firing. |
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What is the biological explanation of Eyes moving during REM? |
Dreams are visual, and eyes are used for vision. They are Linked, so it is an impulsive move. -or maybe so we can keep track of what is happening in the room so we can pick up on potential threats while we sleep. |
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Do we descend into REM? |
No. It looks more like stages: 1-2-3-2-1-REM |
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How long is a sleep cycle? |
About 90 minutes (+/-30 min). -it depends on the person. |
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How many sleep cycles per night? |
About 5 |
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How do the first 4 hours compare to the last 4 hours of sleep? |
The first 4 hours is more restorative because there is more stage 3 present. The last 4 is more light sleep and REM. |
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Why doesn’t sleeping longer help you feel better? |
The most restorative sleep happens at the start of sleeping. The longer you sleep the more REM and light sleep you experience. REM is exhausting for the brain. |
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What is a graph of sleep called? |
Hypnogram or a somnogram |
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Why are gamma waves rarely seen for long periods of time? |
They are exhausting and possibly damaging. |
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Way to track your sleep? |
With something like a Fitbit, Maybe Apple Watch. Not the sleep app. It’s crap. -Fitbit based on heart rate and oxygen consumption. App based on movement |
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Why is REM important? |
Helps consolidate memories (contentious) Body shows a REM rebound effect |
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What do antidepressants show us about REM sleep and memory? |
Antidepressants often block the ability for REM (accidentally-it’s a side effect) and we see no apparent lapses in memory. -REM May not be involved in memory consolidation. |
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What is the REM Rebound effect? |
Once deprived of REM for a night, then next 2-3 days will have much higher levels of REM to make up for it. -must be important if the body compensates. We have a certain amount of REM we need each night to feel right. |
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How long do short sleepers sleep? |
4-6 hours. -they spend most of their time in stage 3 -they get there faster and stay there longer! Net the same amount of stage 3 but in fewer cycles. |
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Who has more dreams, short or long sleepers? |
Long sleepers! |
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Ways to increase sleep efficiency: |
-room set to 68 degrees (colder is better! They help push through the first phases of sleep) -no food/light within an hour of sleep -6 hour minimum -have a consistent sleep pattern for 2,weeks with no caffeine -keep naps to less than 20 minutes or the length of a full sleep cycle |
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Why does light (even blue light) effect sleeping? |
Light tells the pineal gland to not release melatonin. |
|
|
What is sleep inertia? |
Waking up groggy. -this is waking up in stage 3. You can design your sleep to avoid this! |
|
|
How do we know when people are dreaming? |
We wake them up during different stages of sleep! |
|
|
The Thalamus is least active during what stage/wave length? |
Stage 3-Delta |
|
|
What are dreams like during NREM? |
Only 7% have dreams. -Falling, isolated experience and boring (like daily routines) |
|
|
What are dreams like during REM? |
80% time had dreams -stories, narratives, and imaginative-most creative dreaming. |
|
|
Do we incorporate external stimuli into our dreams? |
Yes! -saw when misting sleepers. They dreamed they were in rain. |
|
|
True or false: Dreams only last an instant and the brain alters perception of time |
Unclear. When woken up 5 or 15 minutes into REM people generally knew how long they were asleep. -this does ask the wrong question. It doesn’t gauge how long their dream was. Just how long they were asleep. |
|
|
Do some people not dream at all? |
People who think they don’t dream are just good at not waking up in REM. -in tests, if woken up in REM most have dreams. |
|
|
Why doesn’t sleep walking happen in REM? |
Core-muscle Atonia occurs. -nuclei in the brain stem (reticular formation) fire during REM, making GABA bind to the neurons in the primary motor cortex. This locks down movement. |
|
|
What is inhibited during core-muscle atonia? |
Glutamate and acetylcholine |
|
|
Theory behind REM dreams? |
Activation-Synthesis Theory -during REM there is random brain stem activity, and the thalamus becomes uninhibited. -the thalamus then acts without being controlled and sends messages through the cortex -the cortex is forced to “interpret” the signals and that is our dreams. -cortex sometimes uses established pathways to translate dreams. So they may have common elements, or involve things we know of significance. |
|
|
How does Activation-Synthesis Theory explain hyper-emotional and creative dreams? |
Prefrontal Cortex is is shut down during REM (to restore), but the limbic system is not and It runs unbridled sending and interpreting information that is hyper-emotional. -the prefrontal cortex isn’t there to regulate emotions. |
|
|
How do we know that stage 3 is helpful for repair/restoration of the brain? |
Human Growth Hormone is released into the body during this phase, allowing uninterrupted repair. -Thalamus is least active, giving the brain a break from firing. |
|
|
What is the biological explanation of Eyes moving during REM? |
Dreams are visual, and eyes are used for vision. They are Linked, so it is an impulsive move. -or maybe so we can keep track of what is happening in the room so we can pick up on potential threats while we sleep. |
|
|
Do we descend into REM? |
No. It looks more like stages: 1-2-3-2-1-REM |
|
|
How long is a sleep cycle? |
About 90 minutes (+/-30 min). -it depends on the person. |
|
|
How many sleep cycles per night? |
About 5 |
|
|
How do the first 4 hours compare to the last 4 hours of sleep? |
The first 4 hours is more restorative because there is more stage 3 present. The last 4 is more light sleep and REM. |
|
|
Why doesn’t sleeping longer help you feel better? |
The most restorative sleep happens at the start of sleeping. The longer you sleep the more REM and light sleep you experience. REM is exhausting for the brain. |
|
|
What is a graph of sleep called? |
Hypnogram or a somnogram |
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What is sleep taking called? |
Somniloquy |
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What is sleep walking called? |
Somnambulism |
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Types of drugs that effect sleep: |
Hypnotic, anti-hypnotics |
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Purpose of a hypnotic drug |
Help you fall asleep or feel sleepy |
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What is Melatonin? |
Hormone synthesized from the Pineal Gland and released when it gets dark. -exogenous, Chronobiotic & soporific -but does not improve sleep quality! Many who take it wake up groggy and sleepy. |
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Where are receptors found? |
On ligand gated ion channels |
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What are the 4 steps of GABA agonists functioning? |
1. GABA binds to GABA binding site on the receptor 2. Ion channel opens 3. Makes Chloride (CL-) rush into the cell 4. Hyperpolarizes neuron |
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What is CL-? |
Chloride |
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Benzodiazepines |
Specific MoA-Binds to benzodiazepines sites on the ligand gated ion channel -prescribed for insomniacs and anxiety |
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Examples of benzodiazepines |
Diazepam (Valium), alprazolam (Xanax), Clonazepam (Klonopin), Chlordiazepoxide (Librium) |
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3 GABA agonist drug classes |
Benzodiazepine, imidazopyridines, and Barbituates |
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Imidazopyridines |
Specific MoA binds to Imidazopyridine site on receptor -used for sedation |
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Example of an Imidazopyridine |
Zolpidem (this is a sedative with much less pleasure than benzodiazepines) |
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Imidazopyridines are more or less addicting than benzodiazepines? |
Less! That is why they were engineered from benzodiazepines. Same effect, less addictive and pleasurable. |
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Barbituates |
Specific MoA binds to Barbituate site -this is a sedative |
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What is exogenous mean? |
An exogenous supplement is taken from outside the body. |
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Example of a barbituate |
Phenobarbital |
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Benzodiazepines, Imidazopyridines and barbituates all have the same result by doing what? |
They all open the ion channel and bring CL- into the cell, but how they get there is a little different. |
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Does an agonist increase the neurotransmitter or the effects of the neurotransmitter? |
The effects! It does not need to increase the neurotransmitter to be considered an agonist |
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What are anti-hypnotics? |
They are designed to wake you up! Stimulants |
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Anti-hypnotic drugs from class: |
Cocaine and Amphetamines |
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What catecholamines are cocaine and amphetamines agonists to? |
Dopamine and norepinephrine (also endorphins!) |
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General MoA of cocaine and Amphetamines? |
Catecholamine agonist |
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Specific MoA of cocaine and amphetamines? |
Blocks re-uptake of catecholamines! -secondarily increases endorphins |
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What is Na+? |
Sodium! |
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When dopamine binds to its receptors, what ion enters the cell? |
Sodium! Na+ |
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What does soporific mean? |
Sleep promoting |
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Blocked re-uptake causes? |
The dopamine neurotransmitter (or whatever is blocked) to bind to the receptors multiple times, causing it to fire again. -this is temporal post synaptic summation |
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Why are anti-hypnotics bad when used regularly? |
They cause the neurons to fire an unnatural amount of times. This re-firing is bad for them and can cause damage or neural death. |
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Three categories of sleep disorders? |
Insomnias, Hypersomnias, REM sleep disorder |
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Causes of insomnia: |
1. Iatrogenic (doctor creates from prescriptions) 2. Classical conditioning (ex. Don’t do homework on your bed!) 3. Physiological mechanisms |
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Types of insomnia: |
1. Onset (falling asleep) 2. Maintenance (staying asleep) 3. Sleep inertia (waking up the next day) |
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Sleep Apnea |
Stop breathing several times while sleeping (normal is 5x per hour, severe is 30x an hour!) -awake and fall back asleep-no memory of it -unaware of the problem |
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2 types of sleep apnea: |
1. Obstructive sleep apnea -pharyngeal collapse (back of tongue collapses on the airway creating a snoring sound. (Snoring) 2. Central sleep apnea -lungs told not to move from the medulla! No snoring! |
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What can help with sleep apnea? |
A CPAP machine |
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Other physiological causes of insomnia: |
1. Periodic limb movement disorder -legs twitch excessively (person unaware!) they may complain of tiredness or soreness 2. Restless leg Syndrome -rippling tension/uneasiness in the legs (like they have anxiety!) -they know they have it! -L-Dopa (dopamine agonist) and Gabapentin (GABA) agonist are pharmacological treatments |
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What makes all insomnias worse? |
Stimulants, depressants and extreme exercise |
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What is chronobiotic? |
It adjusts timing of internal rhythms |
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Why does dopamine help with restless leg syndrome? |
Too little dopamine in the nigrostriatle pathway means inability to control movements. Increasing dopamine should increase control. |
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Why does Gabapentin help with restless leg syndrome? |
Gabapentin increases GABA in the primary motor cortex and spinal cord, telling them not to move the legs. |
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Types of hypersomnias |
1. Sleep Paralysis 2. Narcolepsy |
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Behavioral symptoms of sleep paralysis: |
1. Core muscle atonia 2. Alertness (wakefulness) 3. Terrifying, realistic dreams -called hypnagogic hallucinations |
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What causes core muscle atonia and where is it found? |
Nucleus Magnocellularis in the reticular formation. -this blocks efferent motor neurons from passing to the spinal cord. |
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Physiological explanation for sleep paralysis: |
1. nucleus magnocellularis stays on too long during transition to wakefulness 2. Uninhibited thalamus (theta waves) stimulates the cortex making crazy dreams! 3. DMT (dimethyltryptamine) from pineal gland causes hallucinations |
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Where does DMT come from? |
Pineal gland |
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Where does DMT bind to? |
Serotonin “hallucinatory” receptors in the cortex |
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What stage of sleep does sleep paralysis occur in? |
REM |
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When are you more likely to have sleep paralysis? |
If you are younger, take a depressant before sleep, sleeping on your back, naps because of fast sleep cycling. -rushing through stages can cause it, fast sleep cyclers get it more than slow! |
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What division of the brain is the pineal gland located in? |
Diencephalon |
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Two primary behavior symptoms of narcolepsy: |
1. Sleep episodes-they are repeated and brief (10-15 minutes) - fall directly into REM (actually work through the stages quickly) 2. Cataplexy -sudden loss of muscle tone -usually precipitated by strong emotions |
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How many of the primary behavioral symptoms must you have to have narcolepsy? |
At least 1. They most commonly appear together. |
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Physiological explanation of narcolepsy: |
Too little oxytocin (wakefulness promoting hormone) release from the hypothalamus |
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Treatments for narcolepsy |
Anti-hypnotic drug modafinil |
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What does an agonist do? |
Increases the effect of a Neurotransmitter it is targeting |
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What three ways do drugs work? |
1. They pretend to be the neurotransmitter by binding to their receptors 2. Block re-uptake of the desired neurotransmitter 3. They can bind to receptors that are specifically made for them |
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What is Mechanism of Action (MoA)? |
It is what we use to describe what neurotransmitter is being affected and if it is increasing or decreasing its effects |
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What is an antagonist? |
Decreases the effects of a neurotransmitter |
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What is a ligand-gated ion channel? |
Also known as a transporter. It is a channel that is blocked until a specific neurotransmitter binds to it. (Ligand means neurotransmitter) |
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Physiological explanation of narcolepsy: |
Too little orexin (wakefulness promoting hormone) release from the hypothalamus -normally present throughout your cortex, CNS and spinal cord |
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What is REM sleep disorder? |
Damage or lesions in the Nucleus Magnocellularis causes it not to be able to block outgoing motor signals! -we act out our REM dreams! |
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What are the pharmacological treatments for restless leg syndrome? |
L-dopa Gabapentin |
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What area of the brain is implicated in the physiological explanation of narcolepsy? |
Lateral hypothalamic area -too little orexin released from the hypothalamus |
