NEUR 201 UNit 3

proprioception

body’s ability to balance

• dependent on info from the visual system, vestibular senses and touch senses

cardiac mucle cell

can contract rhythmically without innervation

regulated by autonomic NS (involuntary movement)

skeletal muscle cell

muscle fibers are individually innervated by axon branches from the CNS

smooth muscle cells

innervated by the autonomic nervous system (involuntary movement)

somatic motor system

moving different muscle groups produces a different type of movement in a different direction using flexion and extension of Synergistic and Antagonistic muscle groups

by knowing where our body is located in space + intention of movement- our brain can automatically determine what muscles to activate in order to achieve a movement

what is the pathway for extension?

1. biceps brachii (flexor)

2. brachialis (flexor)

3. triceps brachii (extensor)

4. anconeus (extensor)

what is the pathway for flexion?

1. anconeus (extensor)

2. triceps brachii (extensor)

3. brachialis (flexor)

4. biceps brachii (flexor)

what are characteristics of slow fibers (Type I, oxidative)

• glycogen content: low

• rate of fatigue: slow

• ATPase activity: low

• Fiber diameter: small

• Motor unit size: small, slow

• innervating by: small neurons

what are the two types of fast fibers?

fast oxidative (IIa) and fast glycolytic (IIb)

what are characteristics of fast oxidative (IIa) fibers

• glycogen content: intermediate

• rate of fatigue: intermediate

• ATPase activity: high

• Fiber diameter: intermediate

• Motor unit size: intermediate, fast fatigue-resistant

• innervating by: intermediate sized neurons

what are the characteristics of fast glycolytic fibers (IIb)?

• glycogen content: high

• rate of fatigue: fast

• ATPase activity: high

• Fiber diameter: large

• Motor unit size: large, fast fatigue

• innervating by: large neurons

what determines the amount of force that the muscle produces? how?

• firing rate of the motor neuron

• input to the (efferent) motor neuron is sent from upper motor neurons in the brain and sensory input from the muscles

how do motor neurons communicate with muscles?

neuromuscular junction

sarcolemma

excitable membrane around the muscle fiber

myofibrils

found within the muscle fiber

contract when an AP moves down the sarcolemma

what does the sarcoplasmic reticulum store?

calcium

how is the sarcoplasmic reticulum accessed by APs?

T-tubles within the sarcolemma that act like tunnels

how does the t-tubule carry APs?

when depolarized, a tetrad of voltage-sensitive calcium channels open allowing calcium to flow out of the sarcoplasmic reticulum leading to myofibril contraction

what happens when we want to contract our muscle?

excitation-contraction coupling

what are the steps of excitation

1. AP runs though a motor neuron and releases ACh at the NT junction

2. ACh binds to nicotinic receptors on the sarcolemma allowing Na+ to enter the cell causing depolarization called the end point potential (EPP)

3. Sarcolemma becomes depolarized moving into the T-tubules causing Ca2+ release from the sarcoplasmic reticulum

What are the steps of contraction?

1. Ca2+ binds to troponin (a protein that is covering attachment sites on actin within the thin filaments)

2. tropomyosin is shifted revealing binding sites on actin

3. myosin heads from the thick filament bind to actin and pivot, causing the filaments to slide along each other and the muscle to contract

4. ATP binds to each myosin head and detaches from actin

5. the cycle continues as long as Ca2+ and ATP are present

muscle spindles

type of stretch receptor that sends info to alpha motor neurons for sensory feedback

sensory info is about muscle stretch —> causes contraction producing reflex

intrafusal fibers

modified fibers within the muscle spindle

inntervated by gamma motor neurons instead of alpha motor neurons

golgi tendon organ

provides info about stretch of the tendon attached to the muscle

uses Ib afferent axon instead of Ia like mucle spindle

as muscle contracts, firing rate of teh Ia axon is decreased, but the firing rate of the Ib axon is increased

what are the steps for the patellar reflex?

1. tap on patellar ligament excites nerve endings of muscle spindle in quadriceps femoris

2. stretch signals travel to spinal cord via afferent nerve fiber and posterior root

3. afferent neuron excites motor neuron in spinal cord

4. efferent signals in motor nerve fiber stimulate quadriceps to contract, producing knee jerk

5. at same time, a branch of the afferent nerve fiber stimulates inhibitory motor neuron in spinal cord

6. that neuron inhibits motor neuron that supplies hamstring muscles

7. hamstring contraction is inhibited so hamstrings (knee flexors) do not antagonize quadriceps (knee extensor)

spinal interneurons function

• excitatory or inhibitory

• allow for reflexes to coordinate proper muscle contraction or relaxation

homeostasis

maintenance of body’s internal environment with a narrow physiological range (temp, bp, etc)

Autonomic NS

function automaticcaly w/o conscious, voluntary control

Sympathetic division of the ANS

fight or flight —> prepare by dilating pupils, inc heart rate, dec digestion, etc

parasympathetic division of the ANS

rest + digest —> slow heart rate, inc intestinal and gland activity, relaxes spincter muscles in the GI tract

humoral response

hypothalamic neurons respond to sensory signals by stimulating or inhibiting the release of pituitary hormones in the bloodstream

visceromotor response

neurons in the hypothalamus respond to sensory signals by adjusting the balance of sympathetic and parasympathetic outputs of the ANS

somatic motor response

hypothalamic neurons (lateral hypothalamus) respond to sensory signals by inciting an appropriate somatic motor behavioral response

secretory hypothalamus

secretes chemicals into the bloodstream for long range impact on the brain and entire body

integrates somatic + visceral response depending on what the brain needs

recieves signals about the body and sends info to appropriate place to help maintain temp

neurosecretory cells

found in periventricular zone of the hypothalamus

extend axons to pituitary stalk —> release neurohormones into the blood (not normal NT)

which hormones are received by the posterior pituitary from what?

magnocellular neurosecretory cells: oxytocin + vasopressin/ADH

what is the function of teh anterior pituitary

actual gland that synthesizes and secretes many hormones to regulate other gland secretions in the endocrine system (thyroid, adrenal, mammary, etc)

controlled by the hypothalamus w/ parvocellular neurosecretory cells which secrete hypophysiotropic hormones into the blood

what is the function of oxytocin

social bonding + maternal instinct, contracts uterus to facilitiate delivery of baby + ejection of milk from mammary glands for feeding

what happens if too much oxytocin?

benigh prostatic hyperplasia

what happens if too little oxytocin?

prevent milk ejection + breast feeding

linked to autism + depressive disorder

what is the function of vasopression/ADH?

regulates BP, volume, salt concentration + water volume in tissues

acts on kidneys to retain water in the body

too much ADH?

caused by drug side effects + diseases of the lungs, chest wall, hypothalamus/pituitary

lung cancer can also lead to it

low levels ADH?

kidneys exrete too much water leading teh dehydration + fall in bp

indicate damage to hypothalmus/pituitary gland or excessive water drinking

diabetes insipidus

associated with inc thirst, urine production

cortisol function?

secreted from adrenal cortex of adrenal gland

mobilize energy reserves, supress immune system in a fight/flight situation stimulated by stress

CRH —> ACTH → adrenal cortex —> secrete cortisol

too much cortisol?

Cushing’s syndrome

rapid weight gain concentrated to the face, chest, abdomen, flushed round face, high BP, oseoporosis, immune suppression, sleeplessness, memory impairment/irritability

high levels in women —> dec sex drive + irregular/missed menses

too little cortisol?

Addison’s disease

fatigue, dizziness, weight loss, muscle weakness, mood changes, hyperpigmentation

life threatening condition

function of follicle stimulating hormone?

anterior pituitary —> targets gonads cause ovulation in women, spermatogenesis in men

too mcuh FSH?

hypergonadotrophic-hypogonadism

primary ovarian/testicular failure

Klinefelter’s syndrome (men), Turner syndrome (women)

rise naturally during menopause

too little FSH?

hypogonadotrophic-hypogonadism

incomplete development at puberty, ovarian failure

ovarian follicles don’t grow properly —> infertility

Kallman’s syndrome

lutenizing hormone function?

anterior pituitary —> act on gonads to regulate function and maturation of ovaries and sperm

Men: stimulates leydig cells —> prod testosterone

Women: easy in the cycle prod estradiol, later releases egg from ovary (ovulation), also required to prod progesterone