Differences between Axon and Dendrites:

Axon Dendrites
Take information away from the cell body Take information to the cell body
Smooth surface Rough surface (dendritic spine)
1 axon per cell Usually more than one
No ribosome Have ribosomes
May be myelinated No myelin insulation
Branch further from cell body Branch near the cell body

Which parts of a neuron are shown by a Golgi stain and are not shown by a Nissl stain?
Nissl Stain shows nissl body (actually Rough ER), which are the clumps of stained
material around the neural cell nuclei. It differentiates neuron from glia and enables the
study of cytoarchitecture, the arrangements of neuron in brain.
Nissl Stain only shows the surrounding of nuclei in neuron, and it look like protoplasm
with nuclei. Golgi Stain however stains the entirety of the neural cell. It shows that
neuron cell have cell bodies, axon and dendrites.
What is myelin and what does it do? Which cells provide myelin to the central nervous system?
Myelin is a membranous wrapping around axons. It insulates the axon and increase the
transmission speed of information along the axon. Oligodendroglial cells provide myelin
in CNS while Schwann Cells provide the myelin in PNS.
Neuroskeleton
Consist of Microtubule, Neurofilament and microfilament.
Axoplasmic Transport
All proteins are manufactured by the machinery in the cell body. Axon possessing no
protein manufacturing capabilities has to transport everything from the cell body.
Transports directed toward Axon terminal are called anterograde transport while
backward to cell body are called retrograde transport.
In anterograde transport material are carried inside a vesicle which is then transported by
a protein called kinesin that walk-over on microtubule to the axon terminal. Retrograde
transport use the same pathway but with different protein, dynein.

Differences between Glia and Neuron:
1. Neurons have TWO "processes" called axons and dendrites. Glial cells only have ONE.
2. Neurons CAN generate action potentials. Glial cells CANNOT, however, do have a resting
potential.
3. Neurons HAVE synapses that use neurotransmitters. Glial cells do NOT have chemical
synapses.
4. Neurons do NOT continue to divide. Glial cells DO continue to divide.
5. There are many MORE (10-50 times more) glial cells in the brain compared to the
number of neurons.
Properties of Blood Brain Barriers:
1. Presence of tight junctions between the endothelial cells
2. One of the notable features of endothelial cells in comparison to other cell is the lack of
pinocytic vesicles
3. Selective permeability to molecules based on their molecular weight and lipid solubility
4. Presence of specific markers

Atrocytes Star Shaped Cells that provide physical and nutritional support for neurons. 1)
regulate chemical content of ECF 2) transport nutrient to neurons 3) hold
neurons in place
Microglia Macrophage of the CNS. Digest parts of dead neurons
Oligodendroglia Myelination
Satellite Cells Physical support to neurons in PNS
Schwann Cells Myelination

Which ions carry the early inward and late outward currents during the action potential?
Sodium ions carry the early inward current while Potassium ions carry the late outward
currents.

Why is an excitatory synapse on the soma more effective in evoking action potentials in the
postsynaptic neuron than an excitatory synapse on the tip of a dendrite?
Differing from axons action potential which is all-or-none phenomenon, Dendrites and
Soma use Graded Potential to carry the impulse. Graded potential created from
excitatory synapse will travel until it reaches the axon hillock and if when reaching the
hillock the potential is higher than the threshold it will trigger Action Potential. However,
Graded Potential diminishes along the journey it takes to Axon Hillock. The further it is
from the hillock, the more potential are diminished, and thats why EPSP on the soma
which is nearer to the hillock than the tip of dendrites are more effective.
Two properties of Ion Channels: Ion Selectivity and Gating. Ion selectivity is determined by
Diameter of the pore and the nature of the R groups lining it. Gating refer to the closing and
opening of the channel by changes in the local environment.
Resting Potential is usually -65mV. Protein inside the cell creates negative charge. [K+] is higher
inside the cell while [Na+] is higher outside the cell. Resting potential is created when K+ moved
out of the cell because of the concentration gradient but also moved to the inside by electric force.
And the reverse happens for Na+. This creates electric and concentration movement equilibrium.
Na-K-ATPase is there to maintain the concentration of each ion constant.
Action Potential is generated when the depolarization passes the threshold and will create an all-
or-none response. Voltage gated Na+ channel will open and create Sodium influx and make the
inside of the cell positively charged. There is no delay in the opening of the channel and they
remain open for 1 msec and then inactivates. Meanwhile delayed rectifier voltage gated
potassium channel will open after about 1 msec delay. This will cause potassium efflux and
polarized the membrane. After that Na-K-ATPase will return the concentration to normal.
Synapse: Specialized contact between neurons for the transfer of information from one neuron to
another. Electrical synapse and chemical synapse.
Characteristic of gap junction (electrical synapse):
a. Narrow gap only about 3 nm,
b. Very fast transmission,
c. Bidirectional transmission,
d. Synchronization of activities,
e. Existence not only in nervous system, but also in cardiac muscle, liver cells and in
intestine smooth muscle,
f. Presence in animals of lower class, but rare in the nervous system of mammals.

Characteristic Chemical Synapse
1. A synaptic cleft of 20 50 nm wide,
2. The presynaptic element (axon terminal) contains active zone, synaptic vesicles storing
neurotransmitters,
3. The postsynaptic density contains the neurotransmitter receptors,
4. One way transmission from presynaptic side to postsynaptic side,
5. Synaptic transmission in the mature mammal nervous system is chemical.

Difference between Electrical and Chemical Synapse:
Electrical Chemical
Distance between cell 3.5nm 20-40nm
Cytoplasmic continuity Yes No
Ultrastructural Component Gap-junction channel
(connexon)
Presynaptic Vesicles and
Postsynaptic Receptor
Agent of transmission Electrical Current Chemical transmitter
Synaptic delay Virtually absent At least 0.3ms; 1-5ms or longer
Direction Bidirectional unidirectional

According to the thickness of postsynaptic density:
(a) Asymmetrical, Grays type I, excitatory
(b) Symmetrical, Grays type II, inhibitory

Neurotransmitter are produced in the rough ER and further modified and packed in a vesicle by
Golgi apparatus. It will be transported into the synaptic terminal. Depolarization of the terminal
membrane will activate voltage gated calcium channel and trigger influx of Ca2+ ions. The vesicles
are docked at the active zones of presynaptic terminal. Presence of high concentration calcium will
induce the fusion of vesicle and the membrane causing exocytosis. Neurotransmitter will be
release and bind to the postsynaptic receptor and cause potential changes. Neurotransmitter in
the cleft will diffused away, reuptake, or destroy enzymatically.


Synaptic Integration: process in which multiple synaptic transmissions ends on one postsynaptic
neuron and cause summation of input. Spatial or temporal summation. Temporal Summation
happens when multiple synaptic transmissions from a single presynaptic neuron are fired rapidly.
While Spatial summation occurs during multiple presynaptic neuron send impulse at the same
time to the same cell.
Shunting inhibition. EPSP at the dendrite and IPSP near the soma. EPSP cannot move to the soma.
List the criteria that are used to determine whether a chemical serves as a neurotransmitter.
a. There are precursors and/or synthesis enzymes located in the presynaptic side of
the synapse.
b. The chemical is present in the presynaptic element.
c. It is available in sufficient quantity in the presynaptic neuron to affect the
postsynaptic neuron.
d. There are postsynaptic receptors and the chemical is able to bind to them.
e. A biochemical mechanism for inactivation is present.
What are three methods that could be used to show that a neurotransmitter receptor is
synthesized or localized in a particular neuron?
Immunocyochemistry. The neurotransmitter candidate are purified and injected to the
bloodstream where it will invoke immune response and generation of Ab. Ab is taken
from blood and tagged and applied to brain tissue.
In Situ Hybridization. If we knew the mRNA sequence for the transmitter we can use a
chemically labeled probe and apply it to brain tissue. The probe will bind to the mRNA in
the cell.

Acetycholine:
1. Synthesized by Choline acetyltransferase.
2. Degraded by Acetylcholinesterase
3. Muscarinic receptor- G-protein receptor
4. Nicotinic Receptor- Ligand gated ion channel



Catecholamine
1. All catecholamine are synthesized from tyrosine by tyrosine hydroxylase into
L-dopa.
2. L-dopa is then converted to dopamine by dopa decarboxylase.
3. Dopamine beta-hydroxylase changed dopamine into Norepinephrine
4. Phentolamine N-methyltransferase converts NE to epinephrine
5. Degraded by Monoamine Oxidase
Serotonergic
1. Derived from tryptophan and converted by tryptophan hydroxylase and 5-HTP
decarboxylase
2. Degraded by MAO
GABA synthesized from Glutamic Acid by Glutamic Acid Decarboxylase.
Glutamate and Glycine are synthesized from glucose.
NO synthesized from Arginine.
AMPA and NMDA. Both are receptors for glutamate. AMPA are permeable to Na and K but not Ca.
NMDA are permeable to Ca. NMDA need the postsynaptic membrane to be depolarized to be
active because Mg2+ clogged them. AMPA activation will bring depolarization and open the NMDA.
NMDA will let Ca in to cause long term effect.
Neuropeptides: Small Protein like molecules used by neurons to communicate with each other
distinct from the larger neurotransmitter. They are neuronal signaling molecules, influence the
activity of brain in specific ways and are thus involved in particular brain functions, like analgesia,
reward, food intake, learning and memory.
Glutamate activates a number of different metabotropic receptors. The consequence of
activating one subtype is the inhibition of cAMP formation. A consequence of activating a
second subtype is activation of protein kinase C. Propose mechanisms for these different effects.
Glutamate may activate G-linked protein receptors. When activated alpha subunit will
inhibit adenylyl cyclase and inhibit production of cAMP from ATP. Beta and gamma
subunit may also activate phospholipase C. PLC will split Phosphatidylinositol-4,5-
biphosphate or PIP2 into inositol-1,4,5-triphosphate (IP3) and Diacyglycerol (DAG). DAG
will activate Protein Kinase C. IP3 binds to receptor in smooth ER and invoke elevation of
Ca2+ from SER.




Ca2+ ions are considered to be second messengers. Why?
Second messengers are substances which act within a cell to trigger a response which is
triggered by the activation of receptor by the first messenger. Calcium concentration in
cytosol is very low. Activation of G-protein linked receptor will activate the PLC and
cleave PIP2 into DAG and IP3. IP3 will cause elevation of Ca2+ in cytosol. Calcium then
will bind to various protein such as calcium-calmodulin-dependent protein kinase and
give out response.

Tyrosine Kinase receptor. When 2 ligand bind to 2 receptors, the receptors will autophosphorylate
and also cause the phosphorylation of target protein and bring out response.
List of second messengers:
1. cAMP. From ATP by adenylyl cyclase
2. cGMP. From GTP by guanylate cyclase
3. IP3 (inositol triphosphate). From PIP2 by PLC
4. DAG (diacylglycerol).From PIP2 by LPC
5. Calcium. Elevated by IP3.
Third Messenger, basically a transcription factor, bind to specific DNA sequence and control its
transcription rates.
What is the fate of tissue derived from the embryonic neural tube? Neural crest?
The entire CNS comes from the wall of neural tube while the entire PNS come derive
from neural crest.
Children are often able to learn several languages apparently without effort, while most adults
must struggle to master a second language. From what you know about brain development, why
would this be true?
Maturation of brain, lose plasticity.

Why might performing bilateral amygdalectomy on a dominant monkey in a colony result in that
monkeys becoming subordinate?
Bilateral amygdalectomy will reduce aggression in the dominant monkey. The other
monkey will see these changes and feel that the dominant monkey has become more
placid and less difficult to challenge. As a result the dominant monkey will become the
subordinate.

Theories of emotion:
James-Lange theory: we experience emotion in response to physiological changes in our
body. E.g. we feel sad because we cry.
Cannon Bard theory: emotional experience can occur independently of emotional
experience. Cannon bard proposed that stimulus-response neural loop are devoid of
emotion, when the signals reach the thalamus, it will create emotions.
Limbic lobe is the collection of cortex around the corpus callosum which is the cingulate gyrus and
the medial side of temporal lobe including the hippocampus.
Papez circuit, a neural circuit that links the thalamus and neocortex in bidirectional way.

Kluver-Bucy Syndrome is caused by bilateral removal of temporal lobes. They are psychic blindness,
oral tendencies, hypermetamorphosis, hypersexuality and decrease in fear and aggression.
Bilateral amygdalectomy will reduce fear and aggression. While stimulation cause increased
vigilance or attention.

Sham rage: the animal show the behavioral manifestation of rage but in a situation that normally
would not cause anger. It is observed when anterior hypothalamus is destroyed along the
telencephalon but disappear when posterior hypothalamus is also destroyed.
Stimulation of medial hypothalamus produces affective aggression while stimulation of lateral
hypothalamus produces predatory aggression.
Fibers from lateral hypothalamus makes up the medial forebrain bundle and directed toward the
ventral tegmental area, producing predatory aggression.
Fibers from medial hypothalamus directed towards periaqueductal gray matter through dorsal
longitudinal fasciculus and produce affective aggression.
Serotonin-containing neurons are located in the raphe nuclei of brain stem. Drugs that block the
synthesis or release of serotonin increase aggressive behavior. Serotonin precursor and reuptake
inhibitor will decrease the aggression.
Dopaminergic neurons in the ventral tegmental area are associated with the reward system. When
the rats are given dopamine agonist, they will increase self-stimulation and vice versa. This
reinforce that dopamine are linked with reinforcement behavior.
-wave blocking: -wave are temporarily blocked by an influx of light and mental activities and
replaced by -wave.
EEG rhythms:
Beta waves, f>14Hz, signal an activated cortex
Alpha waves, f=8-13Hz, associated with quiet, waking states, closed eyes.
Theta waves, f=4-7Hz, occur during some sleep states
Delta waves, f<4Hz, large amplitude, hallmark of deep sleep
Synchronous EEG rhythms may be created in 2 ways:
They may all be led by a pacemaker cells
They may share or distribute the timing among themselves by exciting or inhibiting one
another


The most extreme form of synchronous brain activity is in the form of seizures. General Seizures
involved both hemispheres while partial seizures involve only a circumscribed area of the cortex.
Repeated seizures are called epilepsy.
Behaviorally, sleep is:
1. Reduce motor activity
2. Decreased response to stimulation
3. Stereotypic postures
4. Relatively easy reversibility
Non-REM sleep:
1. Reduced muscle tension, minimal movement
2. Temperature and energy consumption lowered
3. Increase in parasympathetic activity
4. Brain- rate of energy use and the general firing rates are low
5. Dreams are rare
6. High GH secretion
REM sleep:
1. High oxygen consumption in brain
2. Incapable of movement
3. Rapid eye movement
4. Low core temperature
5. Irregular heart and respiration rates.
6. Dreaming
7. Low GH secretion
Sleep Cycle:
1. Stage 1 Non-REM:
a. Transitional sleep, lightest stage
b. Short duration
c. Eyes make slow rolling movement
2. Stage 2 Non-REM:
a. Slightly deeper
b. Occasional sleep spindle wave
c. K-complex in EEG observed
d. Eyes movement almost cease

3. Stage 3 Non-REM:
a. Deeper stage
b. Large amplitude slow delta rhythm
c. No eye or body movement
4. Stage 4 Non-REM
a. Deepest stage
b. Larger amplitude and slower wave
5. Sleep progress from stage 1-2-3-4 and then reverses to 3-2-1 and then enters into
REM state and the cycle starts anew.
6. REM stage (see above) characterized by fast, low voltage rhythm.
Functions of sleep:
1. Restoration theory: sleep to rest and recover and to prepare to be awake again
2. Adaptation theory: Sleep to keep ourselves out of trouble, to hide from predators
when we are most vulnerable or from other harmful features of the environment or to
conserve energy
Lesion in the ascending reticular activating system induces sleep and coma while its stimulation
caused an aroused state. Several sets of neurons increase their firing rate in wakeful states such as
serotonin neurons of raphe nuclei, NE neurons of locus coeruleus and Ach neurons in the brain
stem. Ach neurons activity levels are also high in REM sleep, unlike the other two. Ach neurons are
REM-on neuron that is they induce REM sleep while spike activity in NE and 5-HT neurons cause
REM sleep to ceases, they are REM-off neuron.
Sleep promoting factors, muramyl dipeptide, IL-1, and adenosine which are antagonize by caffeine.
Environmental time cues such as the light and dark and variations in temperature are collectively
termed zeitgebers.
When mammals are completely deprived of zeitgebers, they settle into a rhythm of activity and
rest that is more than 24 hours, that is they make their own rhythm and the rhythm are in free run.
Suprachiasmatic Nuclei in the hypothalamus regulates the circadian clock. SCN have a
photosensitive mechanism in regulating the clock via the retinohypothalamic tract. Axons from
retina directly synapse with dendrites of SCN and provide the information of light-dark cycles.
Each SCN cells are a clock cells. They have clock gene that when translated into protein, the sama
protein will inhibit further transcription. As time passes, the protein will decrease and
transcription increase in a 24 hour cycle.

Where within the body can pain be modulated and what causes its modulation?
Afferent Regulation: At the level of spinal cord, pain evoked by activity of nociceptors
can be reduced by simultaneous activity of mechanoreceptors (A fibers). Nociceptor
stimulates the projection neuron in the dorsal horn which axons project to the
spinothalamic tract. Mechanoreceptor neurons also activate the interneuron which
inhibits the projection neuron.
Descending Regulation: In the midbrain exist an area called Periaqueductal Gray Matter.
PAG send descending neuron to raphe nuclei and in turn to dorsal horn where they will
inhibit the activity of nociceptive neuron.
Mechanoreceptors are sensitive to physical distortion. They have unmyelinated axon branches
which have mechanosensitive ion channels. These channels gating depend on stretching or
changes in tension.
Meissner and Pacinian corpuscle respond quickly but then stop firing (rapidly adapting), while
merkels disk and ruffini ending are slowly adapting as they generate a more sustained response.
Meissner corpuscle and merkels disk have small receptive size and vice versa.
The layered capsule makes the pacinian corpuscle sensitive to vibrating, high frequency stimuli.
Primary afferent axons enter through the dorsal roots. Depending on the size differentiated into
(from largest to smallest) A, A, A and C. For axons that carry information from muscle it is
grouped into I, II, III, IV.
The area of skin innervated by right and left dorsal roots of a single spinal segment is called a
dermatome.
Pathway of touch is dorsal colum-medial lemniscus pathway.
Ascending branc of A axons enter the dorsal column of spinal cord, move up and terminate at the
dorsal column nuclei at the junction between medulla and spinal cord. Axon from dorsal column
nuclei arches toward ventral and medial medulla and decussates and ascends within medial
lemniscus. They terminate at Ventral Posterior nucleus of thalamus, and then axon from VP
terminate at Primary somatosensory cortex or S1.

Touch from face is carried by Trigeminal Pathway. The axon terminates at trigeminal nucleus, and
then the axon from trigeminal nucleus decussate and project into VP and S1.





Primary Somatosensory Cortex, S1:
1. Receive direct input from VP nucleus
2. Responsive to somatosensory stimulus
3. Lesion impair somatic sensation
4. Stimulated evoke sensory experience

Most inputs from VP end in area 3a, 3b and these areas project into area 1 and 2 and to S2.
Area 3b is concerned with texture, size and shape. Projection to area 1 include the texture while
the rest are to the area 2.

Somatotropy are mapping of body sensation to structure in brain. Properties:
1. Upside down, except head
2. Crossing over, except head
3. Area related to sensitivity

Posterior Parietal Cortex (area 5 and 7). Lesion in this part cause agnosia, the inability to recognize
object even though simple sensory skill are normal. May also cause neglect syndrome, in which a
part of the body or a part of the world is ignored or suppressed and its very existence is denied.

Pain information depend on the free, branching and unmyelinated nerve endings (C fiber).
Pain is the feeling of irritation, sore, aching, etc. while nociception is the sensory process that
trigger pain. Nociceptive neurons are C fiber or lightly myelinated A fibers.

Nociceptive neurons are usually polymodal nociceptors that is theyrespond to mechanical,
thermal and chemical stuff. Specific also exist, mechanical, thermal and chemical nociceptors.

Hyperalgesia: excessive response to noxious stimuli. E.g. touch on burned area.
Examples of sensitizing chemical, bradykinin, prostaglandin and substance P.

Preceptions of pain: A fast, sharp first pain by A fiber and a duller, long-acting second pain by C
fiber. Nociception is mediated by glutamate neurotransmitter and Substance P neuropeptide.
Referred pain is a phenomenon where visceral pain is perceived as cutaneous pain. It occur
because pain nociceptive neurons are mixed with cutaneous nociceptive neurons.

Ascending Pain pathways: Spinothalamic Pathways. The afferent fibers enter the dorsal horn and
travel a short distance up and down in the Zone of Lissauer. They will synapse on the cell in
substantia gelatinosa. Axons from substantia gelatinosa will immediately decussate and ascend
through spinothalamic tract and end on thalamus.

Trigeminal pain Pathways mediate pain from face. Nociceptive fibers synapse with spinal
trigeminal nucleus of the brain stem and axons from these cells will ascend to thalamus.

Ascending pain pathways end on the VP nucleus and also in the small intralaminar nuclei of
thalamus.

Difference between Pain and touch:
Touch Pain
Receptor Specialized structure Free nerve ending
Axon A A and C
Connection in Spinal Cord In the deep dorsal horn Substantia Gelatinosa
Pathway Ascending then decussate Decussate and Ascend

Thermoreceptors are divided into 2: Warm receptors and Cold Receptors. Warm receptors start
firing in 30C and increase their firing rates until 45C. While cold receptors fire receptors from 35
to 10C. They use the same pathway as pain.

Define motor unit in one sentence. How does it differ from motor neuron pool?
One alpha motor neuron and all of the muscle fibers it innervates collectively make up
the motor unit. The collection of alpha motor neuron that innervates a single muscle is
called motor neuron pool.
Lower motor neurons are divided into alpha motor neuron and gamma motor neuron. They are
situated at the ventral horn of the spinal cord.
Alpha motor neurons are directly responsible for muscle contraction. They innervate the
extrafusal fibers of skeletal muscle.
There are 3 sources of input to alpha motor neurons:
1. Muscle spindle, input about muscle length
2. Upper motor neurons
3. Interneurons in the spinal cord
Red (dark) muscle fibers are characterized by large number of mitochondria, they are slow to
contract but can sustain contraction for a long time. Example in the antigravity muscle and make
up the slow motor unit.
White muscle fibers contain fewer mitochondria, contract rapidly and powerfully but fatigue easily.
Usually in reflex and make up the fast motor units.
Excitation-contraction coupling:
1. AP in alpha motor neurons
2. Release of Ach
3. Opening of Nicotinic receptor and generation of EPSP
4. AP is transmitted along the t-tubule
5. Depolarization of T tubule cause Ca2+release from sarcoplasmic reticulum
6. Ca2+ bind to troponin
7. Myosin binding sites are open
8. Myosin heads bind to actin
9. Myosin heads rotate
10. Myosin heads disengage at the expense of ATP
11. Myosin cycle continues as long as there are calcium
12. Ca2+ are pumped back to sarcoplasmic reticulum
13. Troponin returned and closed the myosin binding sites

Muscle spindles:
1. Located deep within skeletal muscle.
2. Consist of several types of specialized skeletal muscle contained in a fibrous
capsule.
3. Group Ia sensory axon
4. Roles are:
a. Detection in muscle length
b. Proprioception, body sense, informs how our body are positioned
Myotatic reflex:
1. When muscle is lengthened, the Ia neurons are depolarized
2. This depolarization will depolarized alpha motor neurons and cause contraction
Gamma Motor Neurons:
1. Innervates intrafusal muscle fiber (muscle inside muscle spindle)
2. When extrafusal fiber contract, if the muscle spindle do not contract, it will slacken
and muscle spindle will not give information about length anymore. To prevent this
gamma motor neuron will activate and contract the poles of muscle spindle and
pulling the muscle spindle and keeping the Ia neurons active.
3. Gamma loop (feedback loop):
a. Gamma motor neuron intrafusal fiber Ia afferent alpha motor neuron
extrafusal fiber
Golgi tendon organs:
1. Located at the junction between muscle and its tendon
2. Innervated by Ib neurons
3. Functions:
a. Monitor muscle tension, esp. when handling fragile objects.
Spinal Interneurons:
1. Generate the coordinated motor neurons:
2. Roles:
a. Inhibitory input (reciprocal inhibition), in reflex the flexing of muscle have to
be paired with the relaxation of the antagonist muscle
b. Excitatory input (flexor reflex), when raising leg from a thumbtack, all flexor
muscle are recruited.
c. Crossed extensor reflex, activation of flexor on one side is accompanied by
inhibition of flexor on the other side.
Lateral pathways: corticospinal and rubrospinal tract. Control voluntary movements of the distal
musculature.
Corticospinal tract.
Motor Cortex internal capsule thalamus cerebral peduncle base of the medulla
decussation at the junction between medulla and spinal cord lateral column of spinal cord
(lateral corticospinal tract) ventral horn

Rubrospinal tract:
Red nucleus in midbrain decussation at the pons lateral column of spinal cord ventral horn

Ventromedial Pathway: Vestibulospinal tract, tectospinal tract, pontine reticulospinal tract,
medullary reticulospinal tract. Control Posture muscles.

Vestibulospinal and tectospinal tracts keep the head balanced on the shoulders as the body
moves and when the head is turned to new stimuli.

Vestibulospinal tracts:
Vestibular nuclei in medulla project bilaterally to the spinal cord and activate cervical spinal
circuits
Another project to the lumbar spinal and maintain upright and balance by facilitating the
extensor muscle of legs

Tectospinal tracts originate from superior colliculus in midbrain. Activation leads to orienting
response that directs heads and eyes to move so that the appropriate point of space is imaged
on the fovea.

Pontine reticulospinal tract enhance antigravity reflex and maintained body posture while
medullary reticulospinal tract liberates antigravity muscle from reflex control.

Primary motor cortex area 4 precentral gyrus
Area 6 consist of premotor area and supplementary motor area, they play an important role in
planning movement.

Basal ganglia: consist of caudate nucleus, putamen, globus pallidus, subthalamic nuclei and
substantia nigra. Motor loop facilitates the initiation of movement. Cortex striatum (putamen
and caudate nucleus) globus pallidus Vlo (Ventral lateral nucleus of thalamus) SMA(cortex)

The cerebellum is important for fine control of voluntary movement. Motor loop through lateral
cerebellum: axons from cortex (prefrontal area, area 4, 6 and sensory cortex) pontine nuclei
cerebellum ventral lateral nuclei of thalamus (VLc) motor cortex.

How do the diffuse modulatory and point to point synaptic communication systems in the brain
differ? List 4 ways.

Diffuse modulatory Point to point
Diffuse, unspecific Precise and specific
Long duration Brief transmission
Slow Fast
Regulate behavior Regulate movement, sensation

Homeostasis: Maintenance of bodys internal environment within a narrow physiological range.

Hypothalamus can be divided into lateral, medial and periventricular. Lateral and medial zones
regulate behavior. Periventricular zone lie right next to the 3
rd
ventricle. The Suprachiasmatic
nucleus in this zone lies just above the optic chiasm regulate the circadian clock. Other cells
control the ANS. The 3
rd
kind of cells is neurosecretory neurons.

Magnocellular neurosecretory neurons (large) have axons that extend down to the posterior
pituitary. They release oxytocin and Vasopressin. Oxytocin release during labor cause the uterus to
contract and facilitates the delivery of newborn. Vaspressin (ADH) increase the water absorption
in the collecting tubule.

Parvocellular neurosecretory neurons (small) communicate with the anterior pituitary by
bloodstream. They secrete hormones that regulate the hormone secretion by the endocrine cells
in the anterior lobe. Corticotropin releasing hormone induce the release of Adrenocorticotropic
hormone, Thyrotropin releasing hormone induce release of TSH. Gonadotropin Releasing
Hormone induces the release of FSH, LH. Etc.

ANS, Autonomic Nervous System. Divided into Sympathetic system which is important in fight or
flight situation and Parasympathetic system which works for maintaining normal visceral function.





Diffuse modulatory System:
Noradrenergic neuron at Locus coeruleus. Locus coeruleus are located at the pons. They are
involved in the regulation of attention, arousal and sleep-wake cycles, as well as learning and
memory, anxiety, pain, mood and brain metabolism.

Serotonergic neuron at Raphe nuclei. Raphe nuclei are located at the midline of brain stem.
Involved in the modulation of pain, regulation of sleep-wake cycles and regulation of mood and
behaviors.

Dopaminergic Neurons at substantia nigra and Ventral Tegmental Area.
Axons from substantia nigra project to the striatum where they facilitate the initiation of voluntary
movement.
Ventral Tegmental Area are located at midbrain. It is involved in the reward and reinforcement
system.

Cholinergic Neurons at Basal Forebrain and Brain Stem Complexes.
Basal Forebrain complex. Cells in this complex are among the first to die in AD. They are also
involved in the arousal and sleep wake cycles.
Brain Stem Complex, mainly acts on the dorsal thalamus and regulates the excitability of sensory
relay nuclei.

Bilateral lesion of the lateral hypothalamus leads to reduced feeding behavior. Name three
types of neuron, distinguished by their neurotransmitter molecules that contribute to this
syndrome.

1. MCH (melanin-concentrating hormone) as neurotransmitter.
2. Orexin as neurotransmitter.

Obesity is the result when energy intake and storage consistently exceed the usage where the
body fat increase. The reverse is starvation.
Lipostatic Hypothesis. The brain monitors the amount of body fat and acts to defend this energy
store against perturbations.
Leptin. Hormone that are produced by the ob gene. This hormone will decrease the eating
behavior. It is produced by the adipocytes.
Leptin molecules activate leptin receptors in the arcuate nucleus. Activated neurons because of
the leptin will cause the secretion of neurotransmitter MSH (alpha Melanocyte Stimulating
Hormone) and CART (cocaine-and-amphetamine regulated transcript). High leptin will activate
humoral response (increase TSH and ACTH, result in increased of metabolic rates), visceromotor
response (sympathetic activation, increase in metabolic rates and body temperature), and somatic
motor response (decrease feeding behavior).
Fall in leptin molecules decrease activation of MSH and CART neuron and also activate NPY
(Neuropeptide Y) and AgRP (agouti-related peptide) neuron. They inhibit secretion of TSH and
ACTH, activate parasympathetic, and stimulate feeding behavior.
Lesion in the lateral hypothalamic area cause decreased feeding behavior while stimulation
increase feeding behavior. There are 2 sets of neurons MCH (melanin concentrating hormone) and
orexin neurons. They are activated when the leptin levels are low.
Satiety signal, a signal that terminate the meal and inhibit feeding afterword.
1. Gastric distension. Vagal sensory axon activate neuron at the nuclei of solitary tract
2. CCK. Cholecystokinin is secreted in response to fatty food in the intestine.
3. Insulin. They are important for glucose uptake and decreasing blood glucose level by
anabolism into glycogen.
Dopamine neurons in the ventral tegmental area project ot the basal forebrain area was believed
to serve hedonic reward. Lesion in this system will reduce the craving of food and stimulation will
result in the reverse.
Serotonin levels are low during postabsorptive period and rise in anticipation of food and spike at
meal. The elevation of serotonin cause mood-elevating effects.
What does the Wernicke-Geschwind language processing model explain? What data are
inconsistent with this model?
Sound: When sound reach the ears, neural signal reach onto the auditory cortex, but the
speech is not comprehended until it reaches the Wernickes area. To repeat the words,
the brain passes word-based signals from Wernickes area to Brocas area via Arcuate
fasciculus. Brocas area will processed these signals to a code for muscular movement
required for speech.
Vision: When reading words, the information are processed into the visual cortical
system and then passed into angular gyrus. Angular gyrus will transform the information
so that it evokes the same pattern from Wernickes area as if the words were spoken.
And the same pathway occurs.
Visual information can reach the brocas area without making a stop at angular gyrus.
Aphasia is also influenced by the damage to subcortical structure such as thalamus and
caudate nucleus. Other cortical areas may also compensate in the recovery of language
after stroke. Most aphasia involves both comprehension and speech deficit and not as
specific as the model explained.

Aphasia is the partial or complete loss of language abilities following brain damage, often without
the loss of cognitive faculties or the ability to move the muscles used in speech.
Brocas aphasia: Motor or nonfluent aphasia, because the person has difficulty speaking even
though he can understand language heard or read. Due to damage in the frontal lobe near the
representative area of mouth and lips of precentral gyrus (motor cortex).
Wernickes aphasia: Speech is fluent but comprehension is poor. Due to damage on the superior
surface of the temporal lobe near primary auditory cortex.
Conduction aphasia: Speech is fluent; comprehension is good but difficulty in repeating words.
Due to lesion in the fibers of arcuate fasciculus connecting the Wernicke and broca area.
Anomic aphasia: No difficulty in speech but trouble to understand written language or pictures.
Due to lesion in angular gyrus.
Techniques for studying language function in brain:
1) Correlating language deficits with postmortem analysis of brain damage;
2) Electrical brain stimulation (Penfield noted that stimulation at certain locations in
cortex affected speech):
--area corresponding to Brocas area,
--posterior parietal lobe near the Sylvian fissure (in the vicinity of the arcuate
fasciculus),
--the temporal lobe (near the Wernickes area).
3) PET(positron emission tomography) imaging
Neglect Syndrome: a syndrome in which a person appears to ignore objects, people, and
sometimes their own body to one side of their center of gaze. Due to lesion in posterior parietal
cortex in right hemisphere.
fMRI studies revealed in humans that the brain activity in the occipital cortex is increased when
attention is focused on the location shift.
PET studies in humans revealed: Ventromedial occipital cortex was affected by attention in color
and shape discrimination task; Areas in parietal cortex were influenced by attention to the motion
task

Neural mechanism controlling attention
Pulvinar nucleus of the thalamus plays a possible role in guiding attention.
--Anatomical evidence: pulvinar has reciprocal connections with most visual
cortical areas of the occipital, parietal and temporal lobes;
--Pathological evidence: pulvinar lesion reduces the ability to focus the attention;
--Pharmacological evidence: Injection of GABA produces difficulty in attention.
Superior colliculus and posterior parietal cortex may also be involved in controlling
attention
What evidence indicates that declarative and nondeclarative memory use separate circuits?
- Electrical Stimulation in the temporal lobes cause memory flashback
- In a person with bilateral medial temporal lobectomy, he have retrograde amnesia
and extreme anterograde amnesia, but he can still learn a new task (that is to create
new procedural memories (nondeclarative memories))
- Person with Huntington Disease have problem learning task in which a motor
response is associated with stimulus. Striatum are important for procedural
memories.
What evidence indicates that long-term memories are stored in neocortex?
Delayed non-match to sample experiment (DNMS). In this experiment a monkey faces a
table with one object on it covering a well. The monkey is trained to displace the object
so that it can get a food reward in the well. After the monkey gets the food a curtain is
placed for some period. When the curtain is raised, the monkey is able to see the table
again, but now with 2 objects. The monkeys task is to displace the new object to get
another food reward. Normal monkey are able to do this even if the closing period reach
10 minutes. However monkey with bilateral medial temporal lesion are not able to do
this, as they displaced the same object again if the period is more than 15 seconds. This
proves that long term memories are stored in neocortex.

Declarative memories: Memory for facts and events. They are available for conscious recollection,
easy to form and easy to forget.
Nondeclarative memories: Memory for skills, habits, and behaviors. The task and reflexes we
learned operate smoothly but without conscious recollection, they are hard to form as it requires
repetition and longtime but less likely to be forgotten.
Memories are stored in short term memory and gradually converted into permanent long-term
memory via a process called memory consolidation.
Anterograde amnesia: the inability to create new memories following brain trauma.
Retrograde amnesia: memory loss for events prior to the brain trauma.
Engram or memory trace is the physical representation or location of a memory.
Role of hippocampus in working memories:
In 8-arm radial arm maze, a trained mouse will only enter each arm once. However rat
with damaged hippocampus will enter the arm more than once. In other experiment, not
all of the arms contain food. All the rats are trained and they are able to remember which
arms contain food and which one do not. Rat with damaged hippocampus can also
remember which arms doesnt contain food but they still enter the arm that they have
entered. The empty arms are the same at each test but the entered arms are different
each time. So hippocampus are important in creation of working memory.
Many neurons in the hippocampus selectively respond when a rat or human is in a particular
location in its environment. These neurons are called place cells which are specialized for location
memory.
Striatum are important for procedural memory. In a radial arm maze, the arms that contained
food are lit by lights. The rat will only enter the lighted arm. But when there is lesion in striatum,
the rat has impaired performance.






What property of NMDA receptor makes it well suited to detect coincident presynaptic and
postsynaptic activity? How may Ca2+ entering through NMDA receptor possibly trigger both LTP
and LTD in CA1 and neocortex?
NMDA receptor in the postsynaptic membrane can only be open if and only if the
postsynaptic membrane is depolarized. Depolarization occurs when there is activation of
the AMPA receptor. As such activation of NMDA means there are activities in the
presynaptic and postsynaptic membrane.
The key is in the postsynaptic depolarization. When it is weakly depolarized, only a small
amount of Ca2+ can enter as most of the receptors are blocked by Mg2+. Weak amount
of Ca2+ activate protein phosphatase which pluck the Phosphate group from AMPA
receptors thereby inhibiting them. In strong depolarization, all of the NMDA receptors
are open making pathway for high amount of calcium. High concentration of Ca2+ will
activate protein kinase C and calcium-calmodulin dependent protein kinase II or CaMKII
that will activate more and increase the number of AMPA receptors.
In H.M and R.B, destruction of the hippocampus appears to have impaired the mechanism that
fixes new memories in neocortex. Propose a mechanism involving CREB explaining why this may
be true.
Protein synthesis is required in the formation of long term memory that is they have
important role in the memory consolidation. This protein will facilitate the formation of
new synapses. The process of gene expression is regulated by the transcription factor
cAMP response element binding protein (CREB). CREB bind to the cAMP response
element (CRE) upstream from the genes. There are 2 forms of CREB: CREB-2 and CREB-1.
Normally CREB-2 binds to CRE and represses the gene expression. When phosphorylated,
CREB-1 displaces the CREB-2 and activates the transcription.

Long term depression: a long-lasting decrease in the effectiveness of synaptic transmission that
follows certain types of conditioning stimulation.
LTD in the cerebellar cortex can be induced to the Purkinje cells by the stimulation of both parallel
fibers and climbing fibers at the same time. Activation of the climbing fibers is so strong that it
causes influx of Ca2+ into Purkinje cells. Parallel fibers use glutamate as their neurotransmitter.
Glutamate binds to the AMPA receptors and cause influx of Na+, they also activate metabotropic
glutamate receptors which are G-protein coupled receptors. Activation of metabotropic glutamate
receptors causes the activation of phospholipase C that cleaves PIP2 into DAG. DAG will activate
Protein Kinase C. influx of Ca2+, influx of Na+ and activation of PKC at the same time cause LTD.
Long term Potentiation: a long lasting enhancement of the effectiveness of synaptic transmission
that follows certain types of conditioning stimuli.
LTP may occur in the Schaffer collateral synapse on the CA1 pyramidal neurons. It is the result of
continuous stimulation (tetanus) of high-frequency stimulation. Other way include the activation
of more than 2 neurons to the same postsynaptic neurons and cause significant spatial summation.
Schaffer collateral-CA1 pyramidal neuron synapse uses glutamate as neurotransmitter. However
they use AMPA and NMDA receptors. NMDA receptors are more permeable to Ca2+ than Na+.
Influx of Ca2+ will cause the activation of Protein Kinase C and CaMKII. They will activate more and
add the number of AMPA receptors.
LTD in CA1
Evidence of LTP and LTD in memory is in the experiment of Morris Water Maze. The rat is placed in
a pool filled with milky water. Submerged at one location is a small platform that will allow the rat
to escape. Normal rats quickly learn where the platform is. Rats with lateral hippocampal damage
will never remember where the platform is. NMDA blocker injection into rats will also produce
the same result. Genetic deletion of NMDA receptor only in CA1 region shows a striking deficit in
LTP, LTD and water maze performance.
Molecular basis of long term memory:
Persistently Active Protein Kinase:
CaMKII and LTP. CaMKII is divided into two subunit connected by a hinge. One
subunit is the catalytic region and the other is regulatory region. Without 2
nd

messenger, regulatory region cover the catalytic region. At the presence of
calcium-calmodulin, the hinge open. After LTP, however, CaMKII remain active.
This is because CaMKII phosphorylate the neighboring enzyme causing persistent
activation.
Protein Synthesis. When protein synthesis inhibitor are injected to animals, there are
deficits in learning and memories. CREB