bio235 exam 1

two main control systems

nervous system and endocrine system

what is the nervous system?

an organized group of cells conducting electrical signals within and among cells

centralization

CNS has evolved over time to have central “control center”

cephalization

evolutionary observation of the brain being in the head

larger brain region…

more complex

three main phases of communication in nervous system

sensory input, integration, motor output

sensory input

information gathered with sensory receptors, afferent neurons carry info through PNS

integration

nervous system processes/analyzes information in the CNS (brain/spinal cord)

motor output

response carried out by efferent neurons (muscles contract, hormones release, etc)

central nervous system

brain and spinal cord

peripheral nervous system

nerves connecting brain and spinal cord with the body’s glands, muscles, etc

afferent

PNS to CNS, sensory input

efferent

CNS to PNS, motor output

divergence

one presynaptic (sending) neuron sends signals to multiple postsynaptic (receiving) neurons

convergence

multiple presynaptic (sending) neurons send signals to one postsynaptic (receiving) neuron

synapse

where neurons “link” together

action potential

rapid and temporary change in voltage across a cell membrane that allows neurons and cells to communicate

how do neurons produce electricity?

bodies are full of positive and negative ions, opposite charges attract, attraction creates electricity

resting membrane potential

voltage/charge is different across the cell membrane when the cell is at rest, maintained by sodium-potassium pumps on the membrane

stages of an action potential

1. resting state: membrane is polarized (-70mV), higher Na outside and K inside

2. depolarization: voltage moves into threshold (-50mV), channels open, Na floods cell, spikes to 40mV

3. repolarization: voltage drops back into negative, Na channels close and K channels open, neuron repolarizes

4. hyperpolarization (undershoot): refractory period, voltage dips below normal

5. return to resting state: neuron returns to polarized state, K channels are closed

refractory period

recovery time where neuron cannot fire again

intensity of action potentials

reflected through frequency, not magnitude/amplitude

brain maps

measure/record structure and electrical activity in the brain, can see how parts of the brain connect/work

hormone

chemical released into bloodstream by endocrine cell, regulates function of target cells

amines

derived from amino acid tyrosine (T3/T4), catecholamines, and tryptophan (melatonin)

peptides/proteins

made of amino acids linked by peptide bonds, short chains, control metabolism, growth, fluid balance, and reproduction

steroids

adrenal cortex, gonads, placenta, cholesterol

dissolve in bloodstream (water soluble), bind to receptors on cell surface, faster acting (seconds to minutes to hours)

most peptide/all catecholamine hormone transport

cannot dissolve in blood, need chaperone proteins (bound hormones), CAN pass through lipid membrane, slower acting (hours to days)

lipid based steroid/thyroid hormones, amines hormone transport

hormone cascade

one hormone triggers the release of another, creating a chain reaction. self regulating, negative feedback

neurons in hypothalamus

receive stimulatory/inhibitory inputs and influence secretion of pituitary hormones

posterior pituitary

neural extension of hypothalamus, hormones secreted are synthesized in hypothalamus

anterior pituitary

receives input from hypothalamus through portal blood vessels, hypothalamic hormones cause the release of pituitary hormones into bloodstream

hormones produced in posterior pituitary

oxytocin, vasopressin

hormones produced in anterior pituitary

growth hormone, TSH, ACTH, LH, FSH, prolactin (releasing/inhibiting hormones)(lowkey all da hormones)

releasing hormones

stimulate anterior pituitary to secrete hormones (growth hormone, TRH, GnRH, CRH)

inhibiting hormones

slow down/stop pituitary from releasing specific hormones (growth hormone inhibiting hormone, dopamine (prolactin inhibiting))

direct acting hormone

control non-endocrine tissue (growth hormone, prolactin)

tropic hormone

control other endocrine tissues (TRH, ACTH, LH, FSH)

HPT axis

hypothalamic-pituitary-thyroid, controls metabolism, energy balance

TRH TSH T3 & T4

hypothalamus releases TRH (thyrotropin releasing hormone) —> anterior pituitary releases TSH (thyroid stimulating hormone) —> thyroid releases T3 and T4

CRH ACTH glucocorticoids (cortisol)

hypothalamus releases CRH (corticotropin releasing hormone) —> CRH travels to anterior pituitary —> anterior pituitary releases ACTH (adrenocorticotropic hormone) into bloodstream —>ACTH travels to adrenal cortex and produces glucocorticoids like cortisol

HPA axis

hypothalamic-pituitary-adrenal axis, controls stress respones

HPG axis

hypothalamic-pituitary-gonadal axis, controls reproduction

GnRH LH & FSH androgens and estrogens

hypothalamus releases GnRH (gonadotropin releasing hormone) —> anterior pituitary releases LH (luteinizing hormone) and FSH (follicle stimulating hormone) into bloodstream —> gonads produce sexual hormones (androgens and estrogens)

HPS axis

hypothalamic-pituitary-somatotropic axis, controls growth

GHRH growth hormone

hypothalamus releases GHRH (growth hormone releasing hormone) —> anterior pituitary releases growth hormone into bloodstream —> grow

MSH

melanocyte-stimulating hormone, skin darkening, etc

prolactin

mammary glands, caring for young

thyroid hormones

stimulate metabolic rate through cellular respiration and O2 consumption, important for growth/early development, development of CNS in wildlfie

why does iodine deficiency affect thyroid hormone production?

iodine is a critical building block of thyroid hormones

what organs do thyroid hormones impact most?

liver, kidneys, nervous system, skeletal muscles

hypothyroidism causes/symptoms

symptoms: excessive weight gain, sluggishness/fatigue (low MR), cretenism, myxedema, goiter

caused by: iodine deficiency, developmental defects, autoimmune disorders

hyperthyroidism causes/symptoms

symptoms: excessive weight loss, tension/anxiety, goiter, fatigue (catabolism)

caused by: Graves Disease (autoimmune)

insulin

secreted in response to high glucose levels (after eating), increases uptake of glucose in liver, muscle, and fat cells

glucagon

secreted in response to low blood glucose levels (haven’t eaten), mobilize glucose from liver, muscle, and fat cells

how are insulin/glucagon antagonists?

counteract each other, glucagon rises when insulin decreases to ensure stable glucose levels

synergistic hormone interaction

one hormone amplifies the effect of another (insulin + glucagon + epinephrine)

type 1 diabetes

(mellitus) loss of insulin producing cells = decreased production of insulin

type 2 diabetes

loss of receptors/receptor sensitivity for insulin, metabolic disease, production of insulin is often normal but could be reduced

stressors in animal kingdom

weather, predators, hierarchy, energetically costly behaviors

immediate response

(catecholamines) adrenal medulla (higher up in kidney), seconds to minutes (fight/flight), increased blood glucose and supply of O2

delayed response

(glucocorticoids) from adrenal cortex, minutes to days, increase blood glucose levels, suppress unnecessary physiological processes, redirect behavior towards survival

chronic stress causes

heart disease/strokes, muscle wasting, insulin insensitivity, reproductive inhibition/infertility, ulcers, IBS, inhibition of immune system