nerve signal transmission raise your right hand. easy, right? you don’t even have to think twice...
TRANSCRIPT
Nerve Signal Transmission
Raise your right hand.
Easy, right?
You don’t even have to think twice and your right arm is moving….
But what makes it happen???
How does your brain tell your body what to do?
The Nervous System
Central nervous system (CNS)– brain and spinal cord
Peripheral nervous system (PNS)– sensory and motor
neurons
Nerves – bundles of neurons
wrapped in connective tissue
Simple Nerve CircuitReflex: simple response-- sensory to motor neurons – Involuntary; not analyzed or
interpreted by brain
Ganglion (ganglia): cluster of nerve cell bodies in the PNSGlia: cell that provides support, insulation, and protection– astrocytes, radial glia,
oligodendrocytes, Schwann cells
Information Processing
- External stimuli detected- sight, sound, touch,
smell, taste, etc.- Information sent to the
CNS - analysis and
interpretation- Motor output is relayed
to the effector cells- muscle/ endocrine cells
Neuron StructureCell body~ nucelus and organellesDendrites~ receiving signalsAxons~ transmitting signals– Hillock~ connects
axon to cell body; generates signal
Synaptic terminals~ communicates w/ another cell (releases neurotransmitters)– Synapse~ neuron
junction (site of cell communication)
Neuron Diversity
Sensory neuron: convey information to spinal cordInterneurons: information integrationMotor neurons: convey signals to effector cell (muscle or gland)
Schwann Cells and Myelin
Schwann cells– PNS support cells– Wraps around axon,
creating layers of myelin
Myelin sheath– supporting, insulating
layers
Nodes of Ranvier– Gaps between Schwann
cells
Membrane Potential- Intracellular/extracellular ionic concentration
difference - K+ diffuses out/Na+ in; large anions cannot follow
(selective permeability of the plasma membrane)- Voltage difference between -60 and -80 mV
It has potential….
Resting potential~ membrane potential of a neuron that is not transmitting
Equilibrium potential~ magnitude of membrane voltage at equilibrium– Nernst equation- Eion = 62mV (log [ion]outside / [ion]inside
Gated Ion ChannelsOpen/ Close in response to stimuli…
Photoreceptors– Changes in light intensity
Vibrations in air – sound receptors
Chemical – neurotransmitters
Voltage – membrane potential changes
Graded PotentialsDepend on strength of stimulus– Threshold potential must be reached for reaction to occur
Hyperpolarization (outflow of K+); increase in electrical gradient; cell becomes more negative
Depolarization (inflow of Na+); reduction in electrical gradient; cell becomes less negative
Threshold potential: if stimulus reaches a certain voltage (-50 to -55 mV)….The action potential is triggered….
1. Resting state – Both Na+ and K+ voltage-gated channels are
closed
2. Threshold – a stimulus opens some Na+ channels
3. Depolarization – action potential generated – Na+ channels open– cell becomes positive (K+ channels
closed)
4. Repolarization – Na+ channels close, K+ channels open; K+
leaves – cell becomes negative
5. Undershoot – both gates close, but K+ channel is slow;
resting state restored
Refractory period~ insensitive to depolarization due to closing of Na+ gates
Conduction of Action Potential
Movement of the action potential is self-propagating– Depolarization of one part
of axon triggers the action potential in the next part
Regeneration of “new” action potentials only after refractory period– This keeps signal moving
in the forward direction only
Action Potential Speed
Axon diameter (larger = faster; 100m/sec)
Nodes of Ranvier (concentration of ion channels)– saltatory conduction- transmission “jumps” from one
node to the next– 150m/sec
Synaptic communicationDepolarization of the membrane (from a.p.) causes Ca+ influx (voltage gated channel)Ca+ causes vesicles to fuse with the presynaptic membrane and release neurotransmittersNeurotransmitters bind w/ ligand-gated ion channels on postsynaptic membraneNeurotransmitter releases from the receptor and the channels close
Postsynaptic Potential
EPSPs- excitatory postsynaptic potentials
IPSPs- inhibitory postsynaptic potentials
Indirect Transmission
Neurotransmitters bind with specific receptors instead of ion channels
Much slower reaction time but last longer
Different neurotransmitters produce diverse effects
Psychological drugs interact at the location of these receptors
Muscles contractMuscles move by shortening, or contracting… they cannot extend on their ownEach muscle has an antagonistic muscle that contracts to move in the opposite direction
What’s in a Muscle?Muscles are a bundle of muscle fibers.
Muscle fibers: single cell w/ many nuclei composed of myofibrils
Myofibrils: longitudinal bundles composed of myofilaments
Myofilaments:– Thin~ 2 strands of actin protein
and a regulatory protein
– Thick~ myosin protein
Sarcomere: repeating unit of muscle tissue within a myofibril
Sarcomere Structure
Z lines~ sarcomere border
I band~ only actin
A band~ actin and myosin overlap
H zone~ central sarcomere; only myosin
Sliding-filament model
Theory of muscle contraction
Sarcomere length reduced
Z line length becomes shorter
Actin and myosin slide past each other (overlap increases)
Actin-myosin interaction1. Myosin head hydrolyzes
ATP to ADP and inorganic phosphate (Pi)-- “high energy configuration”
2. Myosin head binds to actin; forming a “cross bridge”
3. Releasing ADP and P, myosin relaxes sliding actin; “low energy configuration”
4. Binding of new ATP releases myosin head
Creatine phosphate~ supplier of phosphate to ADP
Contraction Regulation
Relaxation: – tropomyosin blocks
myosin binding sites on actin
Contraction: – calcium binds to
toponin complex– tropomyosin
changes shape, exposing myosin binding sites
ACTION!Acetylcholine released from synaptic terminal of motor neuron
Acetylcholine binds w/ receptors and causes an action potential in the muscle fiber
A.P travels down the T (transverse) tubules and triggers release of Ca+ from the sarcoplasmic reticulum– Modified endoplasmic
reticulum
Contraction begins when Ca+ reaches the sarcomere and binds to troponin