EXAM 3 Flashcards

(35 cards)

1
Q

HOMEOSTASIS

A

All animals maintain constancy in their internalenvironment- that is they control
or regulate such parameters as blood O2levels, chemistry, pH, and body
temperature.
This is done against a changing external environment.

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2
Q

Regulators

A

use mechanisms of homeostasis to
moderate changes in the internal environment
even though the external environment might be
changing

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3
Q

Conformers-

A

allow body parameters to track those
of the environment

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4
Q

Negative feedback loops-

A

changes in the monitored parameter (body
temp for example) cause the control mechanism to work to
counteract further changes of the parameter in the same
direction

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5
Q

Positive feedback loops

A

trigger changes that amplify rather the
reverse the the change in a parameter

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6
Q

Homeostatic control systems

A
  1. Receptors- sense changes in the internal environment
  2. Control center- processes information gathered from
    receptors and sends a response to the effectors
  3. Effector- adjusts the regulated parameter
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7
Q

NEGATIVE FEEDBACK
EXAMPLE

A

Body temp increases— control
circuit counteracts further
heating and activates effectors
which tend to cool the body
NEGATIVE FEEDBACK
EXAMPLE

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8
Q

bioenergetic strategy

A

*Endotherms: (mammals and birds) use metabolic
heat to maintain a high stable body temperature
that differs from that of the surrounding
environment.
*Ectotherms: (reptiles, fishes, most other animals)
use energy from the environment to adjust body
temperature- regulate and/or conform.

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9
Q

Basal Metabolic Rate (BMR)

A

the minimum cost of living in
an endotherm. Measured on resting, fasted animals with
no thermal stress during their rest phase

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10
Q

Standard Metabolic Rate (SMR)

A

the same as BMR except
that the temperature at which the measurements are
made is specified- (for ectotherms)

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11
Q

Total ATP

A

29 ATPs
1. Glycolysis (cytosol) produces 2 ATP
2. Citric acid cycle- Krebs cycle (mitochondrial matrix)- 2 ATP
3. oxidative phosphorylation- electron transport chain and
hydrogen pumping: produces approximately 25 ATP

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12
Q

Q10

A

Q10 = MR(t+ 10) /MRt
MR = metabolic rate – this is only an example – we could
be looking at heart rate (HR) or breathing rate (BR) or any
other function

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13
Q

Energy balance equation

A

NET HEAT PRODUCTION M -lE= C*(Tb-Ta) HEAT LOSS/GAIN
M = metabolic heat production
lE = evaporative heat loss
C = thermal conductance
Tb = body temperature
Ta = air or environmental temperature

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14
Q

Functions of the nervous system

A
  1. Sensory input-information gathering
  2. Integration-processing information
  3. Motor output-sends response to information to
    muscles or glands
  4. Interacts with the endocrine system to effect
    longer regulation of body functions
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15
Q

Neuronal characteristics

A

Direct information to specific sites (target cells)
*Allow for rapid communication (150m/sec) -brain
to hand in a few milliseconds
*Allow for multiple or single inputs and outputs

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16
Q

Types of neurons

A

*Sensory neurons-collect information-ears, eyes,
nose, mouth have specialized neurons that collect
environmental information
*Motor neurons-transmit signals to muscles or
glands (effectors)
*Interneurons-neurons that connect the PNS to the
CNS

17
Q

How do neurons work?

A
  1. Membrane potentials- imbalance in ions across a
    membrane produces a potential-measured as a voltage
    difference
  2. Ions move across membranes down electro-chemical
    gradients
  3. Changes in membrane potential lead to impulses- action
    potentials (AP)
  4. Action potentials (AP) propagate undiminished!!!! along
    an axon
  5. Chemical or electrical communication allows for the
    transfer of information between neurons (at synapses).
18
Q

The Nernst equation

A

converts energy stored
as a concentration gradient to energy stored as electrical
potential for a single ion!
Eion= 2.3 xRT/zFxln [ion]o/[ion]I
R= gas constant z =Valence number
T= Temperature F= Faraday constant
Eion= 58xlog10[ion]o/[ion]I

19
Q

Goldman Equation

A

takes all ions into account to
provide an equilibrium potential for the membrane.
Vm= 58mV x Log10Pk[K+]o+ PNa[Na+]o+ PCl[Cl-]i
Pk[K+]i+ PNa[Na+]i+ Pk[Cl-]o

20
Q

excitatory postsynaptic potentials (EPSPs)

A

Na+ flows inward or K+ outward
Changes in membrane potential that increase the probability of an action potential

21
Q

inhibitory postsynaptic potentials (IPSPs)

A

Cl- flows inward
Changes in membrane potential that decrease the probability of an action potential

22
Q

The Action Potential - propagation

A
  1. The influx of Na+causes positive charges to spread away
    from Na+channels
  2. Positive feedback occurs, which causes more voltage-
    gated Na+channels to open
  3. The action potential does not propagate back up the axon
  4. Speed of propagation is enhanced by either large axon
    size or myelination or increased temperature
23
Q

Trans-membrane resistance

A

how easily charge leaks across the membrane –
high resistance = low leakage and charge travels farther inside the membrane

24
Q

Membrane capacitance

A

the ability of the membrane to store charge –
unlike charges attract across the membrane –attraction decreases with distance
between charges across the membrane. Low capacitance and charge travels
farther inside the membrane surface

25
Action potential velocities on the axon are affected by several traits
Axon diameter -increases the distance local potentials travel by reducing Transmembrane and Axoplasmic resistance Myelination –saltatory conduction means that the axon depolarized only at specific points (nodes of Ranvier) and thus jumps down the axon quickly Temperature of the axon –increasing temperature by 10°C doubles conduction velocity
26
Myelinated fibers and the Length Constant
*Myelination greatly increases trans-membrane resistance, thus reducing current leakage across the membrane and increasing current flow along inner and outer membrane surfaces. *Myelination also decreases capacitanceby providing a greater distance between ions across the membrane. This reduces the membrane’s ability to store charge and results in more rapid charging and discharging of membrane capacitance. This results in increased current flow along the membrane surfaces
27
The Synapse
1. Neurotransmitters are stored in synaptic vesicles at the ends of axons. 2. The action potential causes calcium channels to open. 3. Calcium triggers exocytosis of neurotransmitters into the synapse. 4. Many receptors for neurotransmitters are ligand- gated channels.
28
PROPERTIES OF NEUROTRANSMITTERS
1. When substance is applied to post-synaptic membrane it must have the same effect as pre-synaptic stimulation. 2. Substance must be released when the pre-synaptic neuron is active. 3. Action of the substance must be blocked by the same agents that block natural transmission at that synapse. Two types of neurotransmitters: those that directly affect ion channel conductances and those that work through second messengers to change conductances
29
Be able to describe the sequence of events that leads to a contraction and relaxation of a muscle fiber from the arrival of an action potential at the neuro-muscular junction
1. Plasma membrane of the fiber is depolarized by AP. AP in skeletal muscle is generated by postsynaptic potentials so neuronal input is needed 2. The AP is conducted deep into the muscle fiber along the T-tubules 3. Dihydropyridine receptors (DHPR) in T-tubules respond to depolarization and undergo a conformational change that —through a direct linkage to ryanodine receptors (RyR) in the sacroplasmic reticulum (SR), causes the ryanodine receptor’s Ca2+channels to open4. Ca2+flows into the myoplasm of the fiber and causes further opening of uncoupled ryanodine Ca2+receptor channels. Free Ca2+levels inside the cell rise from 10-7M to about 10-6M; Ca2+channels in the SR membrane then close because Vmof the T-tubules has returned to Vrest. 5. Most of the Ca2+entering the myoplasm immediately binds to troponin inducing a conformational change in the troponin molecules. This change in position causes an unmasking of the myosin binding sites by the tropomyosin allowing myosin cross-bridges to bind to Actin. 6. Myosin cross-bridges attach to the actin filaments and the myosin head rotates against the actin filament and pull on the thinner actin filaments which shortens the sarcomere. 7. ATP binds to the ATPase site on the myosin head causing the myosin head to detach from the thin filament. ATP is then hydrolyzed and the energy of hydrolysis is stored as the myosin head re-cocks, which then attaches to the next open site on the actin filament. During a single contraction each cross-bridge attaches, pulls, and detaches as it “rows”along the thin filament. 8. Finally, calcium pumps in the SR membrane actively transport Ca2+from the myoplasm back into the SR lumen. As the level of Ca2+is reduced troponin releases the Ca2+from its binding site and the associated shift in conformation causes the attached tropomyosin the cover the myosin binding sites on the actin thin filaments.
30
Be able to describe the importance of Calcium ions in the cycle of muscle contraction and how Ca2+ is regulated
Ca2+ is what initiates the conformation change in order to block myosin binding sites and therefore lead to relaxation
31
Know how ATP is used by skeletal muscle and source of ATP synthesis for different activities (table 20.1)
TABLE
32
Be able to describe the factors that determine the contractile properties muscle fibers and how they vary to affect contraction velocity, force and time to fatigue – see muscle type characterization slide
1. Electrical properties: responsive to graded potentials or just Action Potentials. 2. Rates at which cross-bridges detach from actin - determines max rate of contraction. Fast myosin isoforms. Troponin isoform with weak Ca2+ affinity 3. Densities of Calcium pumps in SR determines how fast calcium levels are reset to resting values. Presence of parvalbumin in the cytoplasm. 4. # of mitochondria and density of blood vessels determines max rate of oxidative ATP production and time to fatigue.
33
Be able to describe the properties of SO, FOG and FO muscle fibers (table 10-1and 20.2)
Slow twitch (SO type 1) fibers- contract slowly - fatigue slowly. Slow to moderate Vmax; Responds to AP and used for moderately fast repetitive movements. Contain high numbers of mitochondria and very vascular. Slow Calcium kinetics. Red in color due to high levels of myoglobin Fast twitch oxidative (FOG type 2a) fibers. Used for rapid repetitive movements- sustained locomotion. High Vmax; High numbers of mitochondria. Flight muscles of migratory birds. Red in color. Fast twitch glycolytic (FG type 2x) fibers. Very rapid contraction, but fatigue rapidly too. Rapid calcium kenetics; few mitochondria. Muscles of vertebrate ectotherms. White in color. Chicken breasts
34
What are the two types of neurotransmitters and how does their mechanism of action differ?
Small molecule: act directly ob neighboring cells neuropeptides: adjust how cells communicate at the synapse.
35
Know at least two ways that neurotoxins work to block neuron function with examples
ACETYLCHOLINE:excitatory to vertebrate skeletal muscles TETRODOXIN: Works as a Na+ channel blocker