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Neuro Biology > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

What is genetic sex?

A
  • x/y chromosome complement
  • x chromosome inactivation and escape
  • sry gene
  • epigenetics
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2
Q

Which partner determines sex?

A

fathers in humans

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3
Q

How many genes does the x chromosome have?

A

500

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4
Q

How many genes does the y chromosome have?

A

50 genes

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5
Q

What are the female chromosomes ?

A

XX

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6
Q

What are the male chromosomes ?

A

XY

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7
Q

What is gonadal sex?

A
  • internal reproductive systems (testes and ovary formation)
  • consequences of testicular testosterone surge and aromatization in early life, puberty and adult hormone cycles
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8
Q

What is gonadal sex directed by?

A
  • early hormone exposure
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9
Q

What is the SRY?

A
  • sex determining region
  • encodes testes determination factor (TDF) on y-chromosome
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10
Q

What does the SRY do?

A
  • causes embryonic undifferential tissue to develop into testes instead of ovary
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11
Q

What do embryonic testes secrete?

A
  • testosterone and MIH
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12
Q

What can testosterone do?

A
  • can bind to endocrine receptors or can be metabolized into estrogen
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13
Q

What is MIH?

A
  • mullerian-inhibiting hormone
  • causes regression of mullerian ducts
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14
Q

Are humans female by default?

A
  • no, instead of SRY females have other inhibitory hormones maintaining the ovary
  • there is active repression of transdifferentiating genes
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15
Q

Can gonadal sex and genetic sex be disassociated?

A

yes

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16
Q

What is phenotypic sex?

A
  • external genitals
  • secondary sex characteristics,
  • behavior and neuron properties
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17
Q

What is gender identity?

A

individuals perception of their sex

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18
Q

What mediates the effects of biological sex?

A
  • neural and gonads
  • these influences can permanently sexually differentiate neurons or induce temporary, sex-specific changes
  • environment can also change
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19
Q

Where do sex steroid hormones come from?

A
  • synthesized from cholesterol
  • can be produced by gonads under the direction of HPG- axis or locally synthesized neurosteroids in brain
  • fatty structure allows for action at nuclear receptors or membrane receptors
  • concentrations may vary based on brain region
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20
Q

What hormone is the most abundent in males?

A

testosterone

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21
Q

When do the testes release androgens?

A
  • early development and adulthood
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22
Q

Are testosterone levels constant?

A

vary over the course of a day

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23
Q

How is T converted into estradiol?

A
  • conversion happens in the brain by aromatase
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24
Q

When do ovaries release estrogen?

A

starting at puberty

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25
Q

What hormones are most prominent in females?

A
  • estradiol and progesterone
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26
Q

Are estradiol and progesterone levels constant?

A
  • no, vary based on cycle
  • menstrual cycle is around 25 days
  • estral cycle (rodents) is around 4 days
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27
Q

What can estradiol do?

A
  • can act on multiple extranuclear receptor types to change neuron function
  • effect depends on what receptor and where
  • localization of receptors allows for a localized effect of steroid hormones
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28
Q

Is the neruoendocrine environment the same for all people?

A

no dynamic and varies by sex

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29
Q

What are the direct/ acute effects of sex steroid hormones?

A
  • alter membrane excitability, sensitivity to NT, NT Release, especially in the presynaptic terminal
  • modulate functions of enzymes, channels, NT receptors
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30
Q

What are the indirect/ long term effects of sex steroid hormones

A
  • promote or inhibit gene transcription through action of cytoplasm
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31
Q

What is organizational hormone action?

A
  • permanent, irreversible
  • happens in specific developmental pyramids like early in life
  • hormone binds, causes change, leaves, change stays
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32
Q

Where does organizational hormone action occur?

A
  • brain and reproductive organ development
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33
Q

What is activational hormone action?

A
  • temporary
  • usually associated with adulthood, but can occur in any developmental pyramid
  • hormone leave and change goes away
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34
Q

Where does activational hormone action occur?

A
  • estrous and other mammalian sexual cycles
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35
Q

What happens if estradiol is metabolized?

A

it can be masculinized

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36
Q

What is the organizational / activational hypothesis posits?

A
  • early hormone exposure organizes neural substrates subserving behaviors and later exposure activates the sexually differentiated the neural substances
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37
Q

Where is testosterone converted into estradiol by aromatase

A

cytoplasm

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38
Q

Do female gonads produce estrogen durin the early stages of deveopment?

A

no

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39
Q

What triggers the masculinization of the nervous system?

A

estradiol binding to estrogen

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40
Q

What can testosterone do?

A
  • bind to androgen receptors to masculinize
  • be converted to estradiol by aromatase
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41
Q

How can masculinization occur?

A
  • through androgen receptors alone
  • through estrogen receptors alone
  • both
  • which one is highly specified
  • animal study: newborn female rats are treated with estrogen develop masculine behaviors and brain morpholgy as adults
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42
Q

What is neural sex differentiation dependant on?

A
  • genetics
  • epigenetics (environment)
  • hormone exposure
  • hard to generalize between neuron types
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43
Q

What are activational effects of basic hormone action?

A
  • naturally occurring fluctuation in dendritic spine density on adult hippocampal pyramidal neurons
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44
Q

Where is the site of excitatory synapse formation on dendrites that have spines?

A

the dendritic spines

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45
Q

What happens in adult female rats with changes is estradiol and progesterone levels over the estrous cycle?

A
  • the number of dendritic spines fluctuates
  • increase in the hippocampal spine number coincides with female rat peak fertility
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46
Q

What are sex dimorphisms?

A

-clearly defined unconditional physical or behavioral differences between male and female individuals of the same species

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47
Q

What is an example of a sex dimorphism?

A
  • lion’s mane or spinal nucleus of the bulbocaernosus (SNB)
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48
Q

What is the SNB?

A
  • a neural sex dimorphism in rats
  • SNB neurons innervate bulbovacernosus (BC) muscles at the base of the penis
  • during early life more SNB neurons die in femaes than males
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49
Q

What is onuf’s nucleus?

A
  • neural sex dimorphism in humans that is analogous to the SNB in rats
  • located in sacral spinal cord
  • innervate BC mucles surrounding the vagina and the base of the penis
  • male is bigger because males have more motor neurons there
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50
Q

What are latent sex dimorphism mechanisms of E2-induced synaptic potentiation in the hippocampus?

A
  • in females the presynaptic releases beta and post releases alpha
  • in males the postsynaptic releases beta and the pre releases alpha
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51
Q

What is a latent sex dimorphism?

A
  • one aspect of a trait is the same for females and males, but the mechanisms underlying the trait are different
  • just the effect is the same
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52
Q

What is a sex difference?

A
  • physical or behavioral difference between male and female individuals of the same species that vary along a continuum, data overlaps
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53
Q

What are examples of sex differences?

A
  • height, differences in cognition
  • ESPC frequency rat nucleus acumens core
  • connectome
  • dendritic spine density in hippocampal neuron
  • a lot of unknown because not widely studied
  • drug abuse
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54
Q

What are the sex differences in the connectome?

A
  • males have greater ipsilateral connectivity and females have greater contralateral connectivity
  • males and females differ in brain connectivity as a whole
  • 100% of documented differences in neuroanatomy
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55
Q

What are some sex differences in drug abuse?

A
  • higher rates of drug abuse in men, but sex differences in experiences and progression of addiction
  • female rats acquire self- administration ore rapidly than males (willing to do a task for the drug more)
  • discrete trial
  • progressive ratio schedule
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56
Q

What is the discrete trial procedure for sex differences in drug abuse?

A
  • rats have access to drug at certain periods of the day
  • female rats exhibit extended binging and increased drug intake
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57
Q

What is the progressive ratio schedule for sex differences in drug abuse?

A
  • progressive increase in responses required for drug infusion
  • intact female rats reach higher final ratios than males
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58
Q

Where do sex differences occur?

A
  • gentic, molecular, anatomical/physiological level
  • occur in every organ measured so far
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59
Q

What two organs differ the most in terms of gene-expression between males and females?

A
  • liver and brain
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60
Q

What is the problem with sex differences in trials?

A
  • sex is widely undrported, we need more trials to record sex
  • we need more trials to include both males and females (trials are going back to strictly male
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61
Q

What can sex differences at the neural level do?

A
  • increase or decrease sex differences in observed behavior
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62
Q

What does the hypothalamus do?

A

-regulates all basic physiological needs
- maintains homeostasos

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63
Q

How does the hypothalalmus maintain homeostasis?

A
  • gets info from internal sensors and nucleus of solitary tract (autonomic)
  • compares info with set biological points
  • integrates somatic behavioral info with autonomic visceral and endocrine responses
    -makes adjustments where needed
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64
Q

How does the hypothalamus make adjustments to maintain homeostasis?

A
  • behavior responses (somatic)
  • ANS responses (visceral)
  • endocrine responses (hormonal)
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65
Q

What are the parts of the hypothalamus?

A
  • dorsal striatum
    -NA
  • hypothalamic nucleus
  • many more
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66
Q

What does the dorsal striatum control?

A

motor control

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67
Q

What does the NA control?

A
  • reward and motivation
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68
Q

What does the hypothalamus control neuroendocrinally?

A

-feeding and reproduction

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69
Q

What is the hypothalamic nuclei?

A
  • can be sexually dimorphic
    -ex. SDN preoptic area controls male copopulatory info
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70
Q

How is the pituitary gland divided?

A
  • anterior and posteriorly
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71
Q

What origin does the anterior pituitary have?

A
  • non-neural origin
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72
Q

What origin does the posterior pituitary have?

A

neural origin

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73
Q

What are the two groups of neurosecretory neurons?

A
  • magnocellular
  • parvocellular
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74
Q

Where is the magnocellular gland?

A

-posterior pituitary

75
Q

What does the posterior pituitary do?

A
  • diancephalic structure
  • releases neurohormones into circulatory system
76
Q

What are examples of posterior pituitary hormones?

A
  • oxytocin
  • vasopressin
77
Q

What does oxytocin control?

A
  • uterine contraction
    milk production
78
Q

What does vasopressin control?

A
  • blood volume and salinity by working with kidneys
79
Q

What are neurohormones?

A

hormones released by a neuron

80
Q

Where are the parvocellular glands?

A
  • pituitary stalk
81
Q

What do parvocellular glands do?

A
  • releases hormones into portal circulation to act on cells in anterior pituitary, to make cells increase or decrease release
82
Q

What are parvocellular homrone examples?

A
  • gnrh
    -somatostatin
  • anterior pituitary hormones like GH, LH, FSH
83
Q

Is the anterior pituitary part of the CNS?

A

no

84
Q

What is the parvocellular pathway?

A
  • neural- non neural - effect
85
Q

What is the HPG axis?

A
  • example of parvocellular
  • hypothalamus relesases GNRH into the antetrior pituitary which releases LH and FSH causing the gonads to release androgens and estrogens
  • androgens and estrogens produced for both genders
  • regulates gonadal hormone production in a negative feedback loop
86
Q

What is the HPA axis?

A
  • parvocellular
  • paraventricular hypothalamus releases CFH into the anterior pituitary which releases ACTH leading to the adrenal cortex releasing cortisol
87
Q

Is the HPA axis fast or slow?

A
  • slow because it has to go through the bloodstream and the body needs to process what is happening
88
Q

What does cortisol do?

A
  • stress response
  • mobilixes energy systems, supresses immune system
  • cortisol crosses BBB
89
Q

How do diffuse modulatory system work?

A
  • metabotropic receptors
90
Q

How are diffuse modulatory systems named?

A

after the primary NT used

91
Q

What are diffuse modulatory systems made of?

A
  • large number of neurons
  • small number of cell bodies ( around 1000) in 1 or a few nuclei
  • typically in or around the brainstem
    -axon connections are formed by individual neurons, a single neuron can innervate different targets
92
Q

What is the dopamine system?

A

-controls motivation and reqard
- goes from SNPC to dorsal striatum and other places

93
Q

What does the ventral tegmental area do?

A
  • sends dopamine to ventral striatum and NA
94
Q

What is motivation?

A
  • change in behavioral response to a consistent stimulus due to a change in endogenous state
  • encompassses feeding, sex, affilative behavior, drug seeking
95
Q

What is the appetitive stage of motivation ?

A
  • anticipatory stage of motivation
    -search phase
  • more variable and spontaneous
96
Q

What is the consumatory stage of motivation?

A
  • sterotypic phase that results in termination of behavior sequence
97
Q

How is domapine measured?

A
  • using electrochemical or micro dialysis techniques
98
Q

Where does the NA get inputs from?

A
  • PFC, HC, BLA, CTA, VP
99
Q

Where does the NA send input to?

A
  • VTA and VP
100
Q

What part of the NA get D1 and D2?

A
  • the core and the shell
101
Q

How can you increase a DA response?

A
  • put an electrode in the mesolimbic projection because it is more direct and doesn’t have the same inhibitory synapses the VTA could have, nd other effects NA could have
  • also gets DA where it needs to go
102
Q

What does serotonin control?

A
  • emotion
  • heavily innervates the limbic system
  • general arousal
    -sleep-wake
  • mood (especially aggression)
  • emotional expression (physiology)
  • emotional experience (feeling and cognitive)
103
Q

Where is serotonin produced?

A
  • dorsal ralphe
104
Q

What does the limbic system include?

A
  • prefrontal cortex, cingulate gyrus/cortex, anygdala, parahippocampal gyrus, basal ganglia, NA
105
Q

What is the NE system?

A
  • in charge of general arousal, sleep wake cycle, attentiveness
106
Q

Where does NE come from?

A
  • locus correolus and other brainstem nuclei
107
Q

What is the ACH system?

A
  • in charge of sleep-wake and learning and memory
  • part of basal forebrain complex
108
Q

What does cocaine do to the mesolimbic system?

A
  • blocks DA reuptake by Da transporter on NAC
  • BLOCKS
  • side effect is less sleep
109
Q

What does amphetamine do to the mesolimbic system?

A
  • reverses DA transporter in NAc so DA comes out
  • REVERSES
  • side effect: less sleep
110
Q

What does PCP do to the mesolimbic system?

A
  • blocks glutamate receptors in NAc including projections from the amydgala
  • associated with a lack of fear
111
Q

What does nicotine do to the mesolimbic system?

A
  • acts on ACHRs present of NA presynaptic terminals
112
Q

What do opiates like heroin do to the mesolimbic system?

A

-inhibit neurons that release GABA onto VTA neurons

113
Q

What does alcohol do to the mesolimbic system?

A
  • complex effects
  • includes inhibition of GABAergic neurons
114
Q

What does ecstasy (NMDA) do to the mesolimbic system?

A
  • may block DA reuptake and inhibit GABAergic neurons
  • cold be used to help fear disorders like PTSD
115
Q

What do cannabinoids do to the mesolimbic system?

A
  • increase excitatory input into VTA
116
Q

What do addictive drugs do to the mesolimbic system?

A
  • individual effects are different from acute effects
  • affects addictive pheontyps and liabilities
  • there is s spectrum of addiction likelyhood
  • all drugs hijack a part of the mesolimbic system
117
Q

What is learning?

A
  • acquisition of new knowledge/skill
118
Q

What is memory?

A
  • retention of learned knowledge
  • short and long term and working
119
Q

What is short-term memory?

A
  • temporary like seconds or minutes
120
Q

What is long-term memory?

A
  • held in brain for days weeks or years
121
Q

What is working memory?

A
  • what we keep in mind but lose if distracted
122
Q

What are the phases of learning?

A
  • encoding
  • consolidation
  • storage
  • retrieval
123
Q

What is encoding?

A

-info first gets into brain and processed

124
Q

What is consolidation?

A
  • info moved into storage
  • takes time
125
Q

What is storage?

A
  • builidng and strengthening of networks of neurons to store info
126
Q

What is retrieval?

A
  • access to info when needed
127
Q

What is the story of HM?

A
  • severe epilepsy led to bilateral temporal lobe resection
  • lost short-term memory, kept some long-term
  • still had sequential memory
  • he couldn’t remember anything but could still learn
  • his hippocampus lost the ability to consolidate info
  • still had good working memory
128
Q

What is explicit memory?

A
  • facts, events,
  • requires deliberate consciouss effort
129
Q

What is non-declarative/implicit memory?

A
  • procedural memory
  • classical conditioning
  • no conscious awareness
  • more reflexive than reflective
130
Q

What is procedural memory?

A
  • skills and habits
131
Q

What are the types of classical conditioning?

A
  • motor
  • perceptual
  • emotion
132
Q

What is retrograde amnesia?

A
  • a loss of memory- access to events that occured or info that was learned before an injury or disease onset
133
Q

What is Anterograde amnesia?

A

-loss of ability to create new memories after an event leading to a partial or incomplete ability to remember new events and recent past.
- still have long term memory

134
Q

How can you test declaritive memory?

A
  • how many numbers can you remember
  • delayed match: put out three objects, switch objects, try and remember which ones were og
135
Q

What does the chemical structure of a drug determine?

A
  • binding
  • location
  • affinity
  • strength
136
Q

Does the timing and type of drug administration matter?

A

yes it determines the strength of drug

137
Q

What are the basic categories of neuropeptides?

A
  • amino acids (small organic molecules)
  • amines (small organic molecules)
  • peptides (proteins)
138
Q

What is a drug?

A
  • any substance your body doesn’t produce that binds to the receptors in your body
139
Q

What does a drug do?

A
  • depends on the receptors they can bind to
  • mimic or block the actions of our endogenous NT
140
Q

Are natural drugs safer than man made ones?

A

no it depends on the actions on the body

141
Q

What is binding affinity?

A
  • the degree of chemical attraction between a ligand and a receptor
142
Q

What is efficacy?

A
  • the ability of a bound ligand to activate the receptor
143
Q

What are competitive ligands?

A

-drugs that bind to the same receptor site as the NT

144
Q

What is a noncompetitive ligand?

A
  • binds instead to a modulatory site on the receptor
145
Q

Are competitive or noncompetitive ligands agonists or antagonists?

A
  • could be either
146
Q

What is a dose-response curve?

A
  • a graph of the relationship between drug doses and the effects
147
Q

What are pharmacodynamics?

A

the relationship between drugs and their targets

148
Q

What is potency?

A
  • the amount of drug needed to produce and effect
149
Q

What is efficacy?

A
  • the amount of response a drug has at a specific dose
150
Q

What is a metabolic tolerance?

A
  • organ systems become more effective at eliminating the drug
151
Q

What is functional tolerance?

A
  • target tissue may show altered sensitivity to the drug
152
Q

What can cause tolerance?

A
  • changes in numbers of receptors can alter sensitivity in a direction opposite to the drugs effects
  • down regulate or up-regulate
153
Q

What is down regulation?

A

-turn down the number of receptors that can bind
- more common than upregulating

154
Q

Why is upregulating uncommon?

A
  • energy consuming
  • not needed as often
155
Q

What is cross-tolerance?

A
  • tolerance to a whole class of chemically similar drugs
156
Q

What is sensitization?

A

-drug effects become stronger with repeated treatment

157
Q

What happens when there is too much glutamate or excitation?

A

-seizures and convulsions

158
Q

What point in the synaptic transmission process do drugs affect?

A
  • can affect literally all points pre-synaptic or post-synaptic
159
Q

What type of drug administration is the fastest?

A
  • IV is fastest. inhalation is a very quick second best
160
Q

What type of drug administration is the slowest

A

transdermal diffusion

161
Q

What type of drug is used for schizophrenia?

A
  • d2 receptor antagonists
  • sometimes serotonin receptors
162
Q

What type of drug is used to treat anxiety?

A
  • GABA receptors
163
Q

What type of drug is used to treat depression?

A
  • monoamine NT increasing
  • MAOI
    -tricyclics
  • SSRIs
164
Q

What does alcohol affect?

A

-gaba receptors
- biphasic - initial stimulant followed by prolonged depression
- lowering of inhibitions

165
Q

What is the main ingredient in cannabanoids?

A

delta 9 thc

166
Q

What are the cannabanoid receptors?

A

cb1 cb2

167
Q

What are nicotine receptors?

A
  • ACH
168
Q

What does cocaine do?

A
  • locks reuptake of monoamine transporters
169
Q

What is a dissociateive drug?

A
  • produces feelings of depersonalization and detachment from reality
170
Q

What is the dissociative drug receptors?

A
  • antagonists to nmda receptors
171
Q

What are examples of dissociative drugs?

A

-pcp ketamine

172
Q

Where is memory of faces stored?

A
  • vetral visual stream
  • temporal cortex
173
Q

What does more neurons mean in terms of memory?

A

more neurons= stronger memory

174
Q

What is the halle berry experiment?

A
  • showed faces of celebs and saw if people could recognize them
  • measured medial temporal cortex and amount of AP firing with each face
  • measured medial temporal cortex and amount of AP firing with each face
  • used to find the pathway for face recognition
175
Q

How does face recognition and memory work?

A
  • strengthening requires synaptic plasticity
  • LTP is for declarative memory
  • must be activity on both sides of the synapse
  • what wires together fires together
176
Q

What can some forms of NMDA antagonists do?

A
  • block declaritive memory because it has to do with hippocampus
177
Q

What does short term memory have to do with LTP?

A
  • if something can be forgotten there is a back and forth or on and off of LTP
    -LTP and LTD
  • more Ca2+ correlates to more LTD which can be seen with shorter more powerful stimmuli
178
Q

What can affect long term memory?

A
  • genetics
  • gene expression
  • neurons
  • dendrite structure changes
179
Q

What is the most common type of memory loss?

A
  • alzheimers
180
Q

What is dementia?

A
  • a loss of cognitive funciton
181
Q

What is alzheimeres caused by?

A
  • amyloid plaque build up
  • can see senile plaques from estracellular deposits of amygdaloid
  • tau tangles
  • disease of the synapse?
182
Q

What is the least affected lobe when it comes to alzheimers?

A
  • occipital lobe and broadmans area 17
183
Q
A

Neuro Biology (4 decks)

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