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85 Cards in this Set

  • Front
  • Back
Functions of Nervous Tissues
1. sensing changes with sensory receptors (sensation)
2. interpreting & remembering changes (integration center)
3. reacting to those changes with effectors
In short: communication system, regulator/control system, and command system)
What is a ligand?
ion molecule that bind with protein
2 types of Ion Channels
1. Leakage (non-gated) channel)
2. Gated channels:
- voltage gated
- ligand gated
- mechanically gated
Leakage (non-gated) Channel
* passive (facilitated diffusion)
* always open
* nerve cells have more K+ than Na+ leakage channel
* resulting membrane permeability to K+ is higher
* resting membrane potential is -70mV in nerve tissue
Gated Channels
1. active open/close in response to a stimulus resulting in neuron excitability
2. Types of Gated Channels:
a. Voltage channel:
* open/close in response to change in voltage
* in membranes of sarcolemma/axolemma (skeletal muscle cells), not in motor-end plates
b. Ligand Gated:
* open/close in response to particular chemical stimuli (hormone, neurotransmitter) bind on receptors
* only on motor-end plates
c. Mechanically-gated channel:
* open/close with mechanical stimulations (stretching, pressure, vibrations)
* on smooth muscle cells
Electrical Signals in Neurons
* Neurons are highly excitable due to Voltage Difference Across the Membrane
* Communicate with 2 types of electrical signals:
1. Action-Potential: all/nothing, travel long distances
2. Graded Potential: local membrane changes only
* In living cells, flow of ions occurs via ion channels in the cell membranes
Resting Membrane Potential
* Is the negative ions along inside of cell membrane and positive ions along the outside
--potential energy difference at rest is -70mV
--cell is then "polarized"
Resting Membrane Potential Exist Because:
1. concentration of ions is different inside and outside
--ECF si rich in Na+ and Cl-
--Cytosol is full of K+, Phosphate and amino acids

2. Membrane permeability is different between Na+ and K+
-- greater permeability for K+ (50-100)
-- inflow of Na+ can't keep up with outflow of K+
-- Na/K pump removes Na+ as it leaks into cell
-- Na/K pump ejects 3Na+ for each 2K+ ions into the cell (ratio is 3:2 for Na+ entry to K+loss via passive channels)
--Resting membrane potential is -90mV (equilibrium potential for K+)
--Typical neuron has resting membrane potential of -70mV
Graded Potentials
= Small deviations from resting potential of -70mV
* hyperpolarization = membrane has become more negative
* depolarization =
membrane has become more positive (less negative)
Local Potentials:
= Local disturbances in membrane potential
-- aka: graded potentials caused by depolarizing of the inside of plasma membrane
-- happens when neuron is stimulated by chemicals, light, heat or mechanical disturbance.
-- depolarization decreases potential across cell membrane due to opening of gated Na+ channels
* Na+ rushes in down concentration and electrical gradients
* Na+ diffuses for short distance inside membrane producing a change in voltage called a LOCAL POTENTIAL
Local Potential (L/P or G/P)
Action Potential (A/P)
* L/P are graded (vary in magnitude accord. to stimulus strength)
* L/P are decremental (get weaker the farther they spread)
* L/P are reversible as K+ diffuses out of the cell
* L/P can either excitatory or inhibitory
How do Graded Potentials Arise?
1. Source of stimuli:
-- mechanical stimulation of membranes with mechanical gated ion channels (pressure)
-- chemical stimulation of membranes with ligand gated ion channels (neurotransmitter)
2. Graded/post-synaptic/ receptor or generator potential
-- ions flow through ion channels and change membrane potential locally
-- amount of change varies with strength of stimuli
3. Flow of current (ions) is local change only
Action Potential
-- Series of rapidly occurring events that change and then restore the membrane potential of a cell to its resting state
-- Ion channels open, Na+ rushes in (depolarization), K+ rushes out (repolarization)
-- All-or-none principal = with stimulation, either happens one specific way or not at all (lasts 1/1000 of a second)
-- Travels (spreads) over surface of cell without dying out
Depolarizing Phase of Action Potential
-- Chemical or mechanical stimulus causes a graded potential to reach at least threshold (-55mV)
-- Voltage-gated Na+ channels open & Na+ rushes into cell
* in resting membrane, inactivation gate of sodium channel is open & activation gate is closed (Na+ can not get in)
* when threshold (-55mV) is reached, both open & Na+ enters
* inactivation gate closes again in few ten-thousandths of second
* only a total of 20,000 Na+ actually enter the cell, but they change the membrane potential considerably (up to +30mV)
--Positive feedback process
Re-polarizing Phase of Action Potential
* When threshold potential of
-55mV is reached, voltage-gated K+ channels open
* K+ channel opening is much
slower than Na+ channel
opening (which causing depolarization)
* When K+ channels finally do open, the Na+ channels have already closed (Na+ inflow stops)
* K+ outflow returns membrane potential to -70mV
* If enough K+ leaves the cell, it will reach a -90mV membrane potential and enter the after-hyperpolarizing phase
* K+ channels close and the membrane potential returns to the resting potential of -70mV
What is Refractory Period of Action Potential?
period of time during which neuron can't generate another action-potential
Types of Refractory Periods
1. Absolute refractory period
-- even very strong stimulus will not begin another AP
-- inactivated Na+ channels must return to the resting state before they can be reopened
-- large fibers have absolute refractory period of 0.4 msec and up to 1000 impulses per second are possible
2. Relative refractory period
-- a supra-threshold stimulus will be able to start an AP
-- K+ channels are still open, but Na+ channels have closed
Summary of Action Potential
* Resting membrane potential is -70mV
* Depolarization is the change from -70mV to +30 mV
* Repolarization is the reversal from +30 mV back to -70 mV)
Propagation of Action Potential
= An action potential spreads (propagates) over the surface of the axon membrane
* as Na+ flows into the cell during depolarization (voltage of adjacent areas is effected and their voltage-gated Na+ channels open)
* self-propagating along the membrane

-- The traveling action potential is called a NERVE IMPULSE
(Local) Anesthetics
-- Prevent opening of voltage-gated Na+ channels
-- Nerve impulses cannot pass the anesthetized region
-- i.e: Novocaine and lidocaine

Regional Anesthetics:
-- chemicals given @ spinal cord/plexus to affect several nerves (ie: epidural)
General Anesthetics:
-- affect synaptic transmission some ESPS (depolarized), some are IPSP (hyper-polarized) >>deals with perception
Continuous Conduction
Saltatory Conduction
1. Continuous conduction (unmyelinated fibers):
step-by-step depolarization of each portion of the length of the axolemma
2. Saltatory conduction
-- depolarization only at nodes of Ranvier where there is a high density of voltage-gated ion channels
-- current carried by ions flows through extracellular fluid from node to node (conduction hops between node of Ranvier
Speed of Impulse Propagation
the propagation speed of a nerve impulse is not related to stimulus strength
>> larger, myelinated fibers conduct impulses faster due to the size and saltatory conduction
Fiber types
1. Type A fibers
-- largest (5-20 microns, 130m/sec)
-- myelinated somatic sensory and motor to skeletal muscle
2. Type B fibers
-- medium (2-3 micron, 15m/sec)
-- myelinated visceral sensory and autonomic pre-ganglionic fibers
3. Type C fibers
-- smallest (.5-1.5 micron, 2m/sec)
-- un-myelinated sensory and autonomic motor fibers
How do we differentiate a light touch from firmer touch?
(Encoding of Stimulus Intensity)
1. Frequency of impulses
-- firm pressure generates impulses at a higher frequency
2. Number of sensory neurons activated
-- firm pressure stimulates more neurons than does a light touch
Action Potentials in Nerve and Muscle
1. Entire muscle cell membrane versus only the axon of the neuron is involved
2. Resting membrane potential
-- nerve is -70mV
-- skeletal & cardiac muscle is closer to -90mV
3. Duration:
-- nerve impulse is 1/2 to 2 msec
-- muscle action potential lasts 1-5 msec for skeletal & 10-300msec for cardiac & smooth
3. Fastest nerve conduction velocity is 18 times faster than velocity over skeletal muscle fiber
Comparison of Graded & Action Potentials
1. Origin
-- GPs arise on dendrites and cell bodies
-- APs arise only at trigger zone on axon hillock
2. Types of Channels
-- AP is produced by voltage-gated ion channels
-- GP is produced by ligand or mechanically-gated channels
3. Conduction
-- GPs are localized (not propagated)
-- APs conduct over the surface of the axon
4. Amplitude
-- amplitude of the AP is constant (all-or-none)
-- amplitude of GP vary depending upon stimulus
5. Duration
-- The duration of the GP is as long as the stimulus lasts
6. Refractory period
-- AP has a refractory period due to the nature of the voltage-gated channels, and the GP has none.
Signal Transmission @ Synapses -- 2 Types of Synapses
1. Electrical
-- ionic current spreads to next cell through gap junctions
-- faster, two-way transmission & capable of synchronizing groups of neurons
2. Chemical
-- one-way information transfer from a presynaptic neuron to a postsynaptic neuron
* axodendritic: from axon to dendrite
* axosomatic: from axon to cell body
* axoaxonic: from axon to axon
Chemical Synapses
-- Action potential reaches end bulb and voltage-gated Ca+ 2 channels open
-- Ca+2 flows inward triggering release of neurotransmitter
-- Neurotransmitter crosses synaptic cleft & binding to ligand-gated receptors
(the more neurotransmitter released, the greater the change in potential of the postsynaptic cell)
-- Synaptic delay is 0.5 msec
-- One-way information transfer
Nervous System Divisions
1. Central nervous system (CNS): brain and spinal cord
2. Peripheral nervous system (PNS): cranial and spinal nerves that contain both sensory and motor fibers
-- connects CNS to muscles, glands & all sensory receptors
Subdivisions of PNS
1. Somatic (voluntary) nervous system (SNS):
-- neurons from cutaneous and special sensory receptors to the CNS (voluntary effectors)
-- motor neurons to skeletal muscle tissue
2. Autonomic (involuntary) nervous systems
-- sensory neurons from visceral organs to CNS
-- motor neurons to smooth & cardiac muscle and glands:
a. sympathetic division (speeds up heart rate)
b. parasympathetic division (slow down heart rate)
3. Enteric nervous system (ENS)
-- involuntary sensory & motor neurons control GI tract
-- neurons function independently of ANS & CNS
* Functional unit of nervous system
* Have capacity to produce APs (electrical excitability)
* Cell body
-- single nucleus with prominent nucleolus
-- Nissl bodies (chromatophilic substance)
-- abundant rough ER & free ribosomes for protein synthesis
-- neurofilaments give cell shape and support
-- microtubules move material inside cell
-- lipofuscin pigment clumps (harmless aging)
* Cell processes = dendrites & axons
* Amitotic (your cell is as old as you are)
-- Conducts impulses towards the cell body
-- Typically short, highly branched & unmyelinated
-- Surfaces specialized for contact with other neurons
-- Contains neurofibrils & Nissl bodies
-- Conduct impulses away from cell body
-- Long, thin cylindrical process of cell
-- Arises at axon hillock (trigger zone)
-- Impulses arise from initial segment (trigger zone)
-- Side branches (collaterals) end in fine processes (=axon terminals)
-- Swollen tips called synaptic end bulbs (synaptic terminals/ boutons) contain vesicles filled with neurotransmitters
Axonal Transport (Axoplasmic Flow Diffusion)
* Cell body is location for most protein synthesis
-- neurotransmitters & repair proteins
* Axonal transport system moves substances
1. slow axonal flow
-- movement in one direction only: away from cell body (remove waste)
-- movement at 1-5 mm per day
2. fast axonal flow
-- moves organelles & materials along surface of microtubules (200-400 mm per day)
-- transports in either direction
-- for use or for recycling in cell body
Axonal Transport & Disease
-- Fast axonal transport route by which toxins or pathogens reach neuron cell bodies
1. Tetanus (Clostridium tetani bacteria)
-- disrupts motor neurons causing painful muscle spasms
-- bacteria enter the body through a laceration or puncture injury
-- more serious if wound is in head or neck because of shorter transit time
Functional Types of Neurons
1. Sensory (afferent) neurons
-- receptors detect changes in body and external environment
-- this information is transmitted into brain or spinal cord
2. Interneurons (association neurons)
-- lie between sensory & motor pathways in CNS
-- 90% of our neurons are interneurons
-- process, store & retrieve information
3. Motor (efferent) neuron
-- send signals out to muscles & gland cells
-- organs that carry out responses called effectors
Functional Classification of Neurons
1. Sensory (afferent) neurons
-- transport sensory information from skin, muscles, joints, sense organs & viscera to CNS
2. Motor (efferent) neurons
-- send motor nerve impulses to muscles & glands
3. Interneurons (association) neurons
-- connect sensory to motor neurons
-- 90% of neurons in the body
Variation in Neuronal Structure
1. Multipolar neuron
-- most common
-- many dendrites/one axon
2. Bipolar neuron
-- one dendrite/one axon
-- olfactory, retina, ear
3. Unipolar neuron
-- sensory from skin & organs to spinal cord
4. Anaxonic neuron
-- many dendrites/no axon
-- help in visual processes
Structural Classification of Neurons
Based on number of processes found on cell body:
1. multipolar = several dendrites & one axon
most common cell type
2. bipolar neurons = one main dendrite & one axon
found in retina, inner ear & olfactory
3. unipolar neurons = one process only(develops from a bipolar)
are always sensory neurons
Neuroglial Cells
* Half of the volume of the CNS
* Smaller cells than neurons
50X more numerous
* Cells can divide
-- rapid mitosis in tumor formation (gliomas)
* 4 cell types in CNS
-- astrocytes
-- oligodendrocytes
-- microglia
-- ependymal
* 2 cell types in PNS
-- schwann cells
-- satellite cells
* Star-shaped cells
* Form blood-brain barrier by covering blood capillaries
* Metabolize neurotransmitters
* Regulate K+ balance
* Provide structural support
* Most common glial cell type
* Each forms myelin sheath around more than one axons in CNS
* Analogous to Schwann cells of PNS
Microglia (smallest)
* Small cells found near blood vessels
* Phagocytic role -- clear away dead cells
* Derived from cells that also gave rise to macrophages & monocytes
Ependymal Cells
* Form epithelial membrane lining cerebral cavities & central canal
* Modify cerebrospinal fluid (CSF)
-- Coroid Plexus produces CSF
Satellite Cells
* Flat cells surrounding neuronal cell bodies in peripheral ganglia
* Support neurons in the PNS ganglia
Schwann Cells
* Cells encircling PNS axons
* Each cell produces part of the myelin sheath surrounding an axon in the PNS
Axon Coverings in PNS
* All axons surrounded by a lipid & protein covering (myelin sheath) produced by Schwann cells
* Neurilemma is cytoplasm & nucleus of Schwann cell
(gaps are called nodes of Ranvier)
* Myelinated fibers appear white
-- jelly-roll like wrappings made of lipoprotein (myelin is 20% protein, 80% lipid)
-- acts as electrical insulator
-- speeds conduction of nerve impulses
* Unmyelinated fibers
-- slow, small diameter fibers
-- only surrounded by neurilemma but no myelin sheath wrapping
Myelination in PNS
* Schwann cells myelinate (wrap around) axons in the PNS during fetal development
* Schwann cell cytoplasm & nucleus forms outermost layer of neurolemma with inner portion being the myelin sheath
* Tube guides growing axons that are repairing themselves
Un-myelinated Axons
* Schwann cells hold small nerve fibers in grooves on their surface with only one membrane wrapping
Myelination in CNS
* Oligodendrocytes myelinate axons in the CNS
* Broad, flat cell processes wrap about CNS axons, but the cell bodies do not surround the axons
* No neurilemma is formed
* Little regrowth after injury is possible due to the lack of a distinct tube or neurilemma
Regeneration and Repair
1. Plasticity maintained throughout life
-- sprouting of new dendrites
-- synthesis of new proteins
-- changes in synaptic contacts with other neurons
2. Limited ability for regeneration (repair)
-- PNS can repair damaged dendrites or axons
-- CNS no repairs are possible
Neurogenesis in the CNS
1. Formation of new neurons from stem cells was not thought to occur in humans
-- in 1992 a growth factor was found that stimulates adult mice brain cells to multiply
-- in 1998 new neurons found to form within adult human hippocampus (area important for learning)
2. Factors preventing neurogenesis in CNS
-- inhibition by neuroglial cells, absence of growth stimulating factors, lack of neurolemmas, and rapid formation of scar tissue
Repair Within the PNS-- part I
1. Axons & dendrites may be repaired if
-- neuron cell body remains intact
-- schwann cells remain active and form a tube
-- scar tissue does not form too rapidly
2. Chromatolysis
-- 24 to 48 hours after injury, Nissl bodies break up into fine granular masses
Repair Within the PNS -- part II
3. Between 5 to 5 days:
-- Wallerian degeneration occurs (breakdown of axon & myelin sheath distal to injury)
-- retrograde degeneration occurs back one node
4. Within several months, regeneration occurs
-- neurolemma on each side of injury repairs tube (schwann cell mitosis)
-- axonal buds grow down the tube to r
Gray and White Matter
* White matter = myelinated processes (white in color)
* Gray matter = nerve cell bodies, dendrites, axon terminals, bundles of unmyelinated axons and neuroglia (gray color)
-- In the spinal cord = gray matter forms an H-shaped inner core surrounded by white matter
-- In the brain = a thin outer shell of gray matter covers the surface & is found in clusters called nuclei inside the CNS
Excitatory Cholinergic Synapse
* Nerve signal opens voltage-
gated calcium channels
* Triggers release of ACh which crosses synapse
* ACh receptors trigger opening of Na+ channels producing local potential (postsynaptic potential)
* When reaches -55mV, triggers AP
Inhibitory GABA-ergic Synapse
* Nerve signal triggers release of GABA (GamaAminoButyric Acid) which crosses synapse
* GABA receptors trigger opening of Cl- channels producing hyper-polarization
* Postsynaptic neuron now less likely to reach threshold
Excitatory Adrenergic Synapse
* Neurotransmitter is NE (Norepinephrine)
* Acts through 2nd messenger systems (cAMP: cyclic AMP)
* Receptor is an integral membrane protein associated with a G protein, which activates adenylate cyclase, which converts ATP to cAMP
* cAMP has multiple effects
-- synthesis of new enzymes
-- activating enzymes
-- opening ligand gates
-- produce a postsynaptic potential
Cessation & Modification of the Signal
1. Mechanisms to turn off stimulation
-- diffusion of neurotransmitter away from synapse into ECF where astrocytes return it to the neurons
-- synaptic knob reabsorbs amino acids and monoamines by endocytosis & breaks them down with monoamine oxidase
-- acetylcholinesterase (AChE) degrades ACh in the synaptic cleft (choline reabsorbed & recycled)
2. Neuromodulators modify synaptic transmission
-- raise or lower number of receptors
-- alter neurotransmitter release, synthesis or breakdown
>> nitric oxide stimulates neurotransmitter release
Neural Integration
1. More synapses a neuron has the greater its information-processing capability
-- cells in cerebral cortex with 40,000 synapses
-- cerebral cortex estimated to contain 100 trillion synapses
2. Chemical synapses are decision-making components of the nervous system
-- ability to process, store & recall information is due to neural integration
3. Neural integration is based on types of postsynaptic potentials produced by neurotransmitters
Post-synaptic Potentials
1. Excitatory postsynaptic potentials (EPSP)
-- a positive voltage change causing postsynaptic cell to be more likely to fire (result from Na+ flowing into the cell)
-- glutamate & aspartate are excitatory neurotransmitters
2. Inhibitory postsynaptic potentials (IPSP)
-- a negative voltage change causing postsynaptic cell to be less likely to fire (hyper-polarize) >>result of Cl- flowing into the cell or K+ leaving the cell.
-- glycine & GABA are inhibitory neurotransmitters
3. ACh & norepinephrine vary depending on cell
Excitatory & Inhibitory Potentials
* The effect of a neurotransmitter can be either excitatory or inhibitory
1. a depolarizing postsynaptic potential is called an EPSP
-- it results from the opening of ligand-gated Na+ channels
-- the postsynaptic cell is more likely to reach threshold
2. an inhibitory postsynaptic potential is called an IPSP
-- it results from the opening of ligand-gated Cl- or K+ channels
-- it causes the postsynaptic cell to become more negative or hyper-polarized
-- the postsynaptic cell is less likely to reach threshold
Removal of Neurotransmitter
1. Diffusion
-- move down concentration gradient
2. Enzymatic degradation
-- acetylcholinesterase (AChE)
3. Uptake by neurons or glia cells
-- neurotransmitter transporters
-- Prozac = serotonin reuptake
Spatial Summation
Summation of effects of neurotransmitters released from several end bulbs onto one neuron (at once), multipolar neuron
Temporal Summation
Summation of effect of neurotransmitters released from 2 or more firings of the same end bulb in rapid succession onto a second neuron (over time/ in succession)
Three Possible Responses
1. Small EPSP occurs
-- potential reaches -56 mV only
2. An impulse is generated
-- threshold was reached
-- membrane potential of at least -55 mV
3. IPSP occurs
-- membrane hyper-polarized
-- potential drops below -70 mV
Strychnine Poisoning
* In spinal cord, Renshaw cells normally release an inhibitory neurotransmitter (glycine) onto motor neurons preventing excessive muscle contraction
* Strychnine binds to and blocks glycine receptors in the spinal cord
*Massive tetanic contractions of all skeletal muscles are produced
-- when the diaphragm contracts & remains contracted, breathing can not occur
Neurotransmitter Effects
1. Neurotransmitter effects can be modified
-- synthesis can be stimulated or inhibited
-- release can be blocked or enhanced
-- removal can be stimulated or blocked
-- receptor site can be blocked or activated
2. Agonist (work with)
-- anything that enhances a transmitters effects
3. Antagonist (work against)
-- anything that blocks the action of a neurotransmitter
Small-Molecule Neurotransmitters (part I)
1. Acetylcholine (ACh)
-- released by many PNS neurons & some CNS
-- excitatory on NMJ but inhibitory at others
-- inactivated by AChE (acetylcholinesterase)
2. Amino Acids
-- glutamate released by nearly all excitatory neurons in the brain (inactivated by glutamate specific transporters)
-- GABA is inhibitory neurotransmitter for 1/3 of all brain synapses (Valium is a GABA agonist -- enhancing its inhibitory effect)
Small-Moleculle Neurotransmitters (part II)
3. Biogenic Amines
-- modified amino acids (tyrosine)
* norepinephrine: regulates mood, dreaming, awakening from deep sleep
* dopamine: regulating skeletal muscle tone
* serotonin: control of mood, temperature regulation, & induction of sleep
-- removed from synapse & recycled or destroyed by enzymes (monoamine oxidase or catechol-0-methyltransferase)
Small-Molecule Neurotransmitters (part III)
4. ATP and other purines (ADP, AMP and adenosine)
-- excitatory in both CNS & PNS
-- released with other neurotransmitters (ACh & NE)
5. Gases (nitric oxide or NO)
-- formed from amino acid arginine by an enzyme
-- formed on demand and acts immediately
**diffuses out of cell that produced it to affect neighboring cells
**may play a role in memory & learning
-- first recognized as vasodilator that helps lower blood pressure
* 3-40 amino acids linked by peptide bonds
* Substance P: enhances our perception of pain
* Pain relief
-- enkephalins: pain-relieving effect by blocking the release of substance P
-- acupuncture may produce loss of pain sensation because of release of opioids-like substances such as endorphins or dynorphins
Neuronal Circuits
* Neurons in the CNS are organized into neuronal networks
* A neuronal network may contain thousands or even millions of neurons.
* Neuronal circuits are involved in many important activities
-- breathing
-- short-term memory
-- waking up
Types of Neuronal Circuits
1. Diverging -- single cell stimulates many others
2. Converging -- one cell stimulated by many others
3. Reverberating -- impulses from later cells repeatedly stimulate early cells in the circuit (short-term memory)
4. Parallel-after-discharge -- single cell stimulates a group of cells that all stimulate a common postsynaptic cell (math problems)
Multiple Sclerosis (MS)
* Autoimmune disorder causing destruction of myelin sheaths in CNS and PNS
-- sheaths becomes scars or plaques
-- 1/2 million people in the U.S
-- appears between ages 20 and 40
-- females twice as often as males
* Symptoms include muscular weakness, abnormal sensations or double vision
* Remissions & relapses result in progressive, cumulative loss of function
* The second most common neurological disorder
-- affects 1% of population
* Characterized by short, recurrent attacks initiated by electrical discharges in the brain
-- lights, noise, or smells may be sensed
-- skeletal muscles may contract involuntarily
-- loss of consciousness
* Epilepsy has many causes, including;
-- brain damage at birth, metabolic disturbances, infections, toxins, vascular disturbances, head injuries, and tumors
Pre-Synaptic Inhibition
One presynaptic neuron suppresses another one.
-- Neuron I releases inhibitory neurotransmitter GABA
prevents voltage-gated calcium channels from opening in neuron S so it releases less or no neurotransmitter onto neuron R and fails to stimulate it.
Neural Coding
* Qualitative information (salty or sweet) depends upon which neurons are fired
* Qualitative information depend on:
-- strong stimuli excite different neurons (recruitment)
-- stronger stimuli causes a more rapid firing rate
>>CNS judges stimulus strength from firing frequency of sensory neurons (600 APs /sec instead of 6 APs/sec)
Learning & Memory
* Learning is acquiring new knowledge
* Memory is retaining that knowledge:
1. short-term memory:
-- recall phone number while dialing
-- depends upon electrical events (reverberating circuits)
2. long-term memory
-- frequent retrieval of specific information helps with memory consolidation (learning)
-- structural or biochemical changes occurs (ie: increase in dendrites, enlarge end bulbs, increase in presynaptic terminals or formation of additional membrane receptors)
* Recently acquired memory lost first with coma or shock treatments
Memory & Synaptic Plasticity
* Memories are not stored in individual cells
* Physical basis of memory is a pathway of cells (aka: memory trace/engram)
-- new synapses or existing synapses have been modified to make transmission easier (synaptic plasticity)
* Synaptic potentiation
-- process of making transmission easier
-- correlates with different forms of memory (immediate, short term, and long term memory)
Immediate Memory
* Ability to hold something in your thoughts for just a few seconds
* Feel for the flow of events (sense of the present)
* Our memory of what just happened “echoes” in our minds for a few seconds
-- reverberating circuits
Short Term Memory
1. Lasts from a few seconds to several hours
-- quickly forgotten if distracted with something new
2. Working memory allows us to keep something in mind long enough search for keys, dial the phone
-- reverberating circuits
3. Facilitation causes memory to longer lasting
-- tetanic stimulation (rapid, repetitive signals) causes Ca+2 accumulates & cell becomes more likely to fire
4. Post-tetanic potentiation (to jog a memory)
-- Ca+2 level in synaptic knob has stayed elevated long after tetanic stimulation, so little stimulation will be needed to recover that memory
Long Term Memory
* May last up to a lifetime
* Types of long-term memory
1. Declarative: retention of facts as text/words
2. Procedural: retention of motor skills (ie:keyboard)
* Physical remodeling of synapses with new branching of axons or dendrites
* Molecular changes called long-term potentiation
-- Tetanic stimulation causes ionic changes (Ca+2 entry)
1. neuron produces more neurotransmitter receptors
2. synthesizes more protein used for synapse remodeling
3. releases nitric oxide signals presynaptic neuron to release more neurotransmitter
Alzheimer Disease
* 100,000 deaths/year
* 11% of population over 65; 47% by age 85
* Symptoms
-- memory loss for recent events, moody, combative, lose ability to talk, walk, and eat
* Diagnosis confirmed at autopsy
-- atrophy of gyri (folds) in cerebral cortex
-- neurofibrillary tangles & senile plaques
* Degeneration of cholinergic neurons & deficiency of ACh and nerve growth factors
* Genetic connection confirmed for some forms
Parkinson's Disease
* Progressive loss of motor function beginning in 50’s or 60’s -- no recovery
-- degeneration of dopamine-releasing neurons in substantia nigra (prevents excessive activity in motor centers/ basal ganglia)
-- involuntary muscle contractions (pill-rolling motion, facial rigidity, slurred speech, illegible handwriting, slow gait)
* Treatment is drugs and physical therapy
-- dopamine precursor can cross blood-brain barrier
-- deprenyl (MAO inhibitor) slows neuronal degeneration
-- surgical technique to relieve tremors