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Nervous System

3. NERVOUS SYSTEM
3.1 Types of nervous systems (Refer Figure. 48.2,
Pg. 1012)

1.No nerves
 Sponges - multicellular
animals that lack nerves.

2 Nerve Net:
 Cnidarians : ex. Hydra
Simplest nervous system/simplest animal with
nervous system.
 Posses a network of neurons/ nerve nets.
 All neurons are similar, linked to one another
in a web/net.
 No central brain/ central control organ
/coordinated activity/ definite neural
pathway.
 Responses involve large parts of the body.
 Respond effectively from any direction of
body.

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3. Radial nervous system


 Echinoderms: Sea star
 Modified nerve net.
 Each arm contains a nerve net, nerve net are
connected to radial nerve and radial nerves
are connected to central nerve ring.
 Enables a more complex movement
compared to hydra.

4. Bilateral nervous system


 In bilaterally symmetrical animals.
 Simplest central nervous system/CNS.
 Trends in the evolution of bilateral nervous
system:

(i)Increased number of nerve cells.


(ii) Concentration of nerve cell forming ganglia
(two nerve cords) and brain /primitive
brain/CNS at front end of body.
(iii) Specialization of function (afferent nerves,
efferent nerves)
(iv) Increased number of association neurons/
interneurons and more complex synaptic
contacts.
(v) Cephalization- formation of a head with a
brain.

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 Advantages of cephalization:

(i) Coordinates forward /change of direction


of movement.
(ii) Sense organs concentrated at front end of
body.
(iii) Animal able to detect enemy escape
quickly// see/sense food and capture it.
(iv) More rapid responses: shorter pathway
from sense organ to nerves.

 Example:
Phylum Plathyhelminthes :
e.g. Flatworm/Planaria
 Two peripheral nerves extend outward to
the muscles of the body.
 Two major longitudinal nerve cords.
 Masses of nerve cells in the head region
form cerebral ganglia = primitive brain
(have some control on the rest of nervous
system).

5.Centralization:
 Exist in more complex invertebrates e.g.
Annelids and Arthropods
 clusters of neurons = ganglia
 nerves that connect CNS (brain/nerve cord)
to rest of animal’s body are called peripheral
nervous system/PNS.
 E.g. Arthropods : Grasshopper.

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The central coordination of complex


response localized in the front end of
the nerve cord.-cephalisation.

 Cephalopods mollusks: e.g. squids and


octopuses
 Most sophisticated /complex nervous
system in invertebrates.
 Large brain, large image forming
eyes, rapid signaling along nerves.
 Suitable to their active, predatory
life.

 Sessile/slow moving mollusks: e.g. clams


and chitons
 Little or no cephalization, simple
sense organs.

 Vertebrate nervous system:


(i) CNS: brain & spinal cord
(ii) PNS: nerves & ganglia

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3.2 Organization of the nervous system in humans

 More complex.
 Two main divisions:
 CNS : brainspinal cord
 central control, integrate incoming
information, determine appropriate
response
 PNS : sensory receptorsnerves
 Connect CNS to rest of body and vice
versa

 Information processing
 Three stages (Refer Figure. 48.3, pg. 1013)

(i)SENSORY INPUT
Internal/external
stimulisensorssensory
neuronsCNS

(ii)INTEGRATION
Interneurons integrate/analyze &
interpret input from sensory
Type of response initiated

(iii)MOTOR OUTPUT
 Information for response/motor output
leaves CNS motor neuronseffector
cells

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 (Refer Figure. 39.1, pg. 745, Solomon, 7th Ed.)

External Internal Stimulus


Stimulus (e.g., change in blood
(e.g., vibration, pH or blood pressure)
movement,
light, odor) RECEPTION

Detection by Detection by
external internal
sense organs sense organs

TRANSMISSION

Sensory (afferent) neurons


transmit information

Figure 39-1(1)
Page 745
Slide 2

INTEGRATION

Central Nervous System


(brain and spinal cord)

Information interpreted and


response initiated

TRANSMISSION

Motor (efferent) neurons


transmit impulses

Action by effectors
(muscles and glands)

e.g., animal e.g., respiration


runs away 6 rate increases; Figure 39-1(2)
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Page 745 IIUM
blood pressure
rises Slide 3
Nervous System

 Neuron Structure (Refer Figure. 48.5 & 48.6, pg.


1014)
Q: Give the function of each neuron part.

Neuron part Function


Cell body Contains nucleus, most of
cytoplasm, organelles –
integrates incoming signals
Dendrites Cellular extentions
specialized to receive
stimuli// send signals to cell
body
Axon Cellular extentions
specialized to conduct
nerve impulse away from
cell body towards another
neuron /target cell/effector
Synaptic terminals Release neurotransmitters
Myelin sheath Insulating covering of axon
outside CNS-inhibit transfer
of impulse
Nodes of Ranvier Non insulated regions of
axon – allows impulse to
jump/transfer more
efficiently from node to
node

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Q: Describe the function neurons?


(A neuron - nerve cell,) specialized to receive
and send information by producing and
transmitting rapid electrical signals.

Q: State the functions of:

(i) sensory neurons:


 transmit information to CNS/
interneurons in CNS.

(ii) interneurons :
 integrate input and output of information/
interpreting incoming sensory
information/determining appropriate
response.

(iii) motor neurons:


 transmit information away from CNS to
effectors/muscles/glands

Q: What is a glial cell?

Also known as neuroglia


they support and protect neurons
90% of CNS

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Q: Briefly discuss function of each glial cell:

Type of glial cell Function


1 Microglia  phagocytotic/ removes
cell debris/ mediate
response to injury
/disease
2 Astrocytes  provide glucose/ oxygen
to neurons
 regulate composition of
extracellular fluid (ions
and neurotransmitters) in
CNS
 induce formation of tight
junctions between cells
that line capillaries and
CNS/to form blood brain
barrier during
development
3 Oligodendrocytes  form electrical insulating
sheaths/myelin around
axons of CNS
Schwann cells  form electrical insulating
sheaths/myelin around
axons of PNS

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 The Division of the vertebrate nervous


system

Nervous system

CNS PNS

Brain Spinal Sensory Motor


cord pathway pathway

Somatic Autonomic
(voluntary) (involuntary)

Sympathetic Parasympathetic

Mobilization of energy Conservation of


energy

 somatic motor neuron.: stimulate contraction


of skeletal muscles/voluntary control

 autonomic motor neuron.: regulate


contraction of smooth muscle, cardiac
muscle, glands/involuntary control

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.
3.3 Generation, characteristic and transmission of
impulse

 Characteristics of nervous impulse:

i. Impulse will be produced when there is a


strong enough stimulus.~ the `all or none
law/phenomenon’.

ii. Impulse are electrochemical changes


along a neuron
 An electrical signal that relies on ion flow
across a membrane
 Begins when changes in the electrical
gradient across the membrane occur.

 Resting Membrane Potential (Refer pg. 1016)

 In resting neuron (neurons not producing


impulses/signals), the plasma membrane is
polarized:
 The inside of membrane  negative
 The outside of membrane  positive
 The resting membrane potential (electrical
/ voltage/ energy difference across their
plasma membrane) is between –60 to –80
mV (more commonly –70 mV)

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Q: Why the minus sign?


Inside of the cell is negative with respect to
the outside

 Voltage: force that causes charged particles to


flow between two points

(Method to measure membrane potential of cells:


Refer Figure. 48.9, pg. 1016)

Q: How is the resting potential developed?


Different concentration of ions inside and
outside membrane or unequal distribution of
electrical charges across membranes

(Refer Figure. 48.10, pg. 1016)


Outside membrane : Inside membrane
[Na+]  [K+]  [Cl- ] [A-]  : [Na+]  [K+]  [Cl- ] [A-]

[Na+] is 10x higher outside than inside.


[K+] is 10 x to 30x higher inside than outside
[Cl-] is 10 x to 12x higher outside than inside
[A-] is higher inside than outside

Q: Why is there an imbalance of ions across the


membrane?

i. The action of the sodium-potassium pumps.


 Actively pumps 3 Na+ out of cells and 2 K+ into
cells

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 Its action determines resting potential

ii. The presence of fixed anions (negatively


charged proteins and organic phosphates)
 Too big to diffuse out, contribute a constant
internal negative charge.
 Attract cations from the extracellular
environment.

iii. The different degrees of permeability of the


plasma membrane to different ions.
 Plasma membrane much more permeable to K+
than to Na+.
 Plasma membrane has many open / leak K+
channels but fewer open / leak Na+ channels.
 Na+ pumped out cannot easily pass back into
cell but K+ pumped into cell can easily
diffuse out .
 As a result, resting membrane potential is
closer to the equilibrium potential for K+.
 Membrane potential can change from resting
value when membrane’s permeability to ions
changes.

 Neurons have 3 types of ion channels: (Refer


pg. 1017)

Q: List down the three types of ion channels found


within the cell membrane of neurons.
(i) Passive/ ungated/ leak ion channels .

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(ii) Voltage activated/ gated ion channels.


(iii) Chemically/ ligand activated/ gated ion
channels.

 Passive ion channels:


 not gated / always open.
 specific for particular ions (Na+/K+/ Cl-/Ca2+).
 K+ passive ion channels are most
abundant/membrane more permeable to K+
than other ions.

 Voltage activated/gated ion channels:


 Open or close in response to a changes in
membrane potential.
 Found in axons/dendrites/cell body of
neurons.
 Specific for particular ions.
 Involved in the generating of signals/impulse
of the nervous system.

 Chemical/ligand
activated/gated ion channels:
 Open or close in response to a chemical
stimulus / neurotransmitter binding to the
channel.
 Found at synapses.
 Specific for particular ions.

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 Generation of action potential (Refer Figure


48.12, pg. 1018)
 Neuron – highly excitable cells.
 Have ability to convert stimulus to neural
impulses.
 Membrane potential can change in response
to appropriate stimulation.
 Process of depolarization: Stimulus 
Sodium channels open sodium diffuses
into axon membrane potential/the inside
of the membrane becomes less negative
closer to transmitting impulse =
excitatory effect

 Process of hyperpolarization: Stimulus


Pottasium channels open pottasium
diffuses out of axonmembrane
potential/inside of the membrane more
negative  more difficult to transmit
impulse = inhibitory effect

 Slighty stimulated /weak stimulus local


response only /graded potential. Fades and
dies within a few mm from the point of
stimulus.

 Sufficiently strong stimulus membrane


potential increases above threshold/ 15 –
20 mV more positive than resting potential

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 transmission of neural impulse/action


potential occurs.

Action potential & activity of voltage gated ion


channels
 If membrane potential depolarises above
threshold value (~>55mV) a response called
action potential occurs.
 All or none phenomenon: a standard
magnitude/size of action potential will be
produced, which is independent of strength of
stimulus.
 Each action potential lasts ~ 1 – 2 milliseconds
 Involves both Na+ and K+ voltage gated
channels.
 Na+ channels open before K+ channels.
(activation gates for K+ channels open slowly
in response to depolarization).

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Stages in action potential: (Refer Figure Figure. 48.13,


pg. 1019)

(1) Resting state

(2) Depolarisation

(3) Rapid depolarization

(4) Repolarisation

(5) Undershoot/hyperpolarisation
 Undershoot: (notes for Lecturer only)
 Membrane temporary become more
negative than the resting potential/shift
from –70mV to –85mV)
 Occurs before the membrane returns to its
resting potential / -70mV.
 At the lowest level of the undershoot, all
K+channels are completely closed.

 The Refractory Period: (Lecturer ‘s notes)


 After opening, Na+ channels spontaneously and
rapidly enter the inactivation state
 At the peak of the action potential, all Na+
channels become inactivated., they cannot be
immediately opened again
 The period from the initiation of the action
potential to immediately after the peak is
referred to as the absolute refractory period
(ARP)

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 This is the time during which another


stimulus given to the neuron (no matter how
strong) will not lead to a second action
potential.
 The absolute refractory period takes about 1-2 ms.
After this period, Na+ channels begin to
recover from inactivation and if strong
enough stimuli are given to the neuron, it
may respond again by generating action
potentials. However, during this time, the
stimuli given must be stronger than was
originally needed when the neuron was at rest.
This situation will continue until all Na+ channels
have come out of inactivation.
 The period during which a stronger than
normal stimulus is needed in order to elicit
an action potential is referred to as the
relative refractory period (RRP). During the
relative refractory period, since pK remains above
its resting value (Fig. 6-8), continued K+ flow out of
the cell would tend to oppose any depolarization
caused by opening of Na+ channels that have
recovered from inactivation.
 In summary, inactivation of Na+ channels is solely
responsible for the absolute refractory period.
 Both Na+ channel inactivation and the greater
than resting pK value are responsible for the
relative refractory period.
 The absolute refractory period is responsible for
setting the upper limit on the maximum number of
action potentials that can be generated during any
given time period.

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 Reestablishing resting condition


 Refractory period provides the recovery time
(for repolarization) needed between one
impulse and the next.
 Resting potential is not yet established
because [Na+]  inside, [K+]  outside during
refractory period.
 the sodium-potassium pump are active again
during the relative refractory period to restore
resting membrane potential of -70mV
 Most neurons can transmit several impulses
per second.

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Conduction /transmission of action potentials


(Refer Figure.48.14, pg. 1020)

Conduction along an unmyelinated


axon/continuous conduction
 Action potential in one region can depolarize
the next region to threshold  next region
produces action potential.
 Na + entering cell depolarizes the next
neighbouring region above threshold producing
new action potential in forward direction.
 Action potential at one point cannot induce
action potential at the previous region/behind.
 Because previous region will undergo
repolarization followed by a refractory period.
 Action potential is regenerated along an axon /
wave of depolarization occurs.

Q: List out the reasons why an action potential


cannot travel backwards towards the cell
body:

1. previous depolarized region is undergoing


repolarisation
2. Na+ channels are closed by inactivation
gates during repolarisation / not reset/
cannot respond to depolarization stimulus

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Saltatory Conduction (Refer Fig. 48.15, pg. 1021)

 Impulse transmission within myelinated


neuronsSaltatory conduction.
 Myelin: effective electrical insulator.
 No action potential at myelinated regions.
 Voltage gated Na+ & K+ channels concentrated
only at nodes of Ranvier.
 Extracellular fluid is in contact with axon
membrane only at nodes.
 Therefore, ion movement across membrane
only occur at nodes.
 action potential/impulse jumps from one node
of Ranvier to another.
 Ions will diffuse along axon to depolarize next
node.
 Myelinated axon :
 conducts impulse 50X faster than fastest
unmyelinated axon.
 require less energy/ATP.
 Speed of impulse by saltatory conduction :
120m/sec.
 Action potential conduction without
decrement.

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Q: List out factors that affect the speed of action


potential conduction? (Refer Pg. 1020 )

(1) Diameter of axon: the larger the diameter, the


faster the speed of transmission/ conduction.
Resistance to flow of electrical current is
inversely proportional to the cross-sectional
area of conductor.

(2) Myelinated axons: Action potential jumps from


node to node. Myelinated axon conduct
impulse more rapidly than non-myelinated
axons//causes depolarizing current to spread
farther along axon.

3.4. Synapses
Structure and function

 Junction between two neurons or between


neuron and muscle cell/gland cell.
 Presynaptic neuron : axon transmitting
action potential to the synapse.
 Postsynaptic neuron: cell receiving signal
on other side synapse.

 Two types of synapses:


1. Electrical synapses
2. Chemical synapses

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Electrical synapses

 Pre synaptic and postsynaptic membranes are


close together, with pores made of protein
linking the cytoplasm of two cellsgap
junctions.
 Junctions enables electrical signals to jump
relatively unchanged from pre to the
postsynaptic cell.
 Transmission very fast- no intervening
chemicals involved.
 Found where responses have to be very fast.
 eg. : Escape responses in some animal (giant
axons of lobsters and other crustaceans, in
brain of fish rapid flapping of tail to escape
predators).
 Mammals: nerve pathway which control rapid
eye control/ synapse between cardiac muscle.

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Chemical synapses: (Refer Figure 48.17, pg. 1022 to


explain)

Q: What are the properties of a chemical synapse?

1. Most common type of nerve pathway.


2. Communication between cells using
neurotransmitters /chemical messengers.
3. Presynaptic and postsynaptic neurons are
separated by narrow space = synaptic cleft
(20nm).
4. Action potential that reaches the end of an
axon cannot jump gap/space.
5. Electrical signal must be converted to
chemical signal.

Q: What are the advantages of impulse


transmission through chemical synapse?

1. Enables integration of information from


different parts of the nervous system.
2. Ensures that nerve impulses are one way
/from presynaptic membranes to the
postsynaptic membranes only.
3. Synapses may act as switches. Nerve
impulse can pass along one of several
discrete pathways.

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4. A presynaptic action potential can be


transmitted as an inhibitory signal (or an
excitatory signal).
5. A small presynaptic nerve terminal may
cause a large depolarization in the
postsynaptic cell (amplification).

 Mechanism of synaptic transmission across a


chemical synapse

Impulse arrive at the synaptic terminal /


Depolarization

Voltage-gated Ca++ channel open

Influx of Ca++/ Ca++ passes into synaptic knob

[Ca++] stimulates synaptic vesicles to fuse


with presynaptic membrane

Neurotransmitter released into synaptic


cleft (by exocytosis)

Neurotransmitters diffuse rapidly to the


other side.
Bind to receptor protein in the postsynaptic
membrane

Creates post synaptic potential.

EPSP
IPSP
25 depolarization
hyperpolarization HMM/SCM 1424,CFS, IIUM
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Neurotransmitter and their function


 Different neurons release different types of
neurotransmitter.
 Effect of neurotransmitters depends on the
type of postsynaptic receptor with which it
combines .
 Some n.t. bind to channel  opens channel
ions diffuse across postsynaptic membrane =
direct synaptic transmission / creates
postsynaptic potential.

(a) Excitatory neurotransmitter :

 Binding of n.t. with receptor causes


depolarization of postsynaptic
membrane/excitatory postsynaptic potentials
(EPSPs)
 E.g.Acetylcholine (Ach)
 It is an excitatory n.t at synapses
connecting motor neurons with skeletal
muscle/neuromuscular junctions

Q: Describe the activity of acetylcholine released


at neuromuscular junctions?
 Receptor activation causes Na+ channels at
postsynaptic membrane to open.
 Postsynaptic membrane more permeable to Na +,
producing a graded potential

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 If enough ACh is released, graded potential


may become large enough to generate an
action potential.
 Stimulate muscle contraction.
 e.g. Serotonin: uses second messenger
system, closes K+ channels, depolarizes cell.

(b) Inhibitory neurotransmitter:

 Neurotransmitter-receptor combination causes


hyperpolarisation of the postsynaptic
membrane/inhibitory postsynaptic potentials
(IPSPs).
 Postsynaptic membrane more negative than
normal/hyperpolarized.(-80mV)

 e.g. GABA
 GABA binds to GABAB receptors
 K+ channels opens, K+ diffuses out, neuron
becomes more negative/farther away from
threshold.

 GABA binds to GABAA receptors


 Cl- channels open, Cl- enter cell, neuron
becomes more negative/farther away from
threshold.

Q: Different types of action for some major


neurotransmittesr (Refer Table 48.1, pg. 1024)

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Q: What are the various mechanisms that may end


the effect of neurotransmitters on
postsynaptic cells?
(i) The neurotransmitter may simply diffuse
out of the synaptic cleft.
(ii) The neurotransmitter may be taken up by
the presynaptic neuron through active
transport and repackaged into synaptic
vesicles.
(iii) Glia actively take up the neurotransmitter
at some synapses and metabolize it as
fuel//neurotransmitter degraded by
enzyme.

 The neurotransmitter acetylcholine is


degraded by acetylcholinesterase, an enzyme
in the synaptic cleft.

Acetylcholine choline + esterase


Acetylcholinesterase

 The products from the degradation diffuses


back into presynaptic knob.
 Resynthesis of ACh will occur in
synaptic knob using the energy from
ATP.

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3.4 Autonomic nervous system


3.4.1The Peripheral Nervous System

 Component of nervous system apart from the


CNS.
 Consists of:
 cranial nerves (originate from the brain)
 spinal nerves (originate in pairs along the
spinal cord and emerge from between
vertebrae).

 Transmits information to and from CNS.


 Regulates vertebrate’s movement and internal
environment.
 Divided into two functional components:
 somatic nervous system
 autonomic nervous system

 Somatic nervous system:


 carries info. to and from skeletal muscles .
 mainly in response to external stimuli.
 often voluntary (conscious control).
 Sometimes controlled by reflexes (spinal
cord or brainstem).

 Autonomic nervous system:


 regulates the internal environment.

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 controlling smooth & cardiac muscles,


organs of digestive, cardiovascular,
excretory, and endocrine systems.
 Generally involuntary.
 Made up of three divisions:
i. Sympathetic
ii. Parasympathetic
iii. Enteric

 The medulla oblongata coordinates the


autonomic system.

 The sympathetic and parasympathetic systems


 work together : opposing action /antagonistic
reaction.
 ensures the activity level is appropriate to the
particular situation.

Sympathetic:
o arousal and energy generation/fight or
flight response.
o Have adrenergic nerve ending (use
noradrenaline as n.t).

Parasympathetic:
o calming and returning to self-
maintenance.
o Usually have cholinergic nerve ending (use
ACth as n.t.).

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Enteric:
o network of neurons in digestive tract,
pancreas, and gallbladder (secretions and
peristalsis).
o regulated by sympathetic and
parasympathetic divisions.

Q: Make comparisons between the somatic and


autonomic nervous systems
Refer to notes above:

 An autonomic reflex:
 Involve two motor neuron in the efferent
pathway. (Refer Figure 48.22, pg. 1027)

Preganglionic neuron
 Cell body in the CNS and send an axon to an
autonomic ganglion.
 Release Ach at its synapse.

Postganglionic neuron
 Cell body in the autonomic ganglion and sends
its axon to synapse with a smooth muscle,
cardiac muscle or gland cell.

 Parasympathetic Syst: Synapse of PostGN –


target cell releases Ach
 Sympathetic Syst: Synapse of PostGN – target
cell releases norepinephrine

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3.6 Drug abuse


Cocaine

 Stimulant drug .
 Effect nerves in the brain’s pleasure pathway
(Limbic system) .
 These cells transmit pleasure message using
the neurotransmitter dopamine (excitatory
drug).
 Cocaine stimulate a massive release of
dopamine at brain limbic system and prevents
reabsorption of dopamine.

How does cocaine alters events at the synapse?

 (Without cocaine) Normal synapse: after


dopamine has acted, it will be removed from
postsynaptic cell and reabsorbed to
presynaptic cell using transporter proteins.
 (Presence of cocaine) Cocaine will bind to the
dopamine transporter reabsorption of
dopamine is blocked.
 Effect : Dopamines stay in the synaptic cleft
longer and continue to stimulate the
postsynaptic membrane.
 The increased amount of n. t. (dopamine) in
the synapse cause overstimulation of
postsynaptic membrane.

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Nervous System

Cocaine thus acts to intensify pleasurable


sensations (feeling of self confidence and self
power).

Cocaine may act as a neuromodulator. (Refer to


Raven 8th Ed. Pg. 882-883)

 The central nervous system adjusts to the


increased firing/overstimulation by producing
fewer receptors in the postsynaptic
membrane.
 This results in addiction in which physiological
changes take place.
 With so few receptors, the user needs the drug
to maintain even normal levels of limbic
activity.
 When the drug is removed (when the drug
addict stops taking drugs) normal absorption
of dopamine resumes .
 But the decreased number of receptor creates
a less-sensitive pathway.
 User will suffer physical illness and
characteristic withdrawal effects–
anxiousness, depression, weak memory,
fatigue, violent behavior and suicidal.
 Physiologically, the only way an addicted
person can maintain normal functioning is by
continuing to take the drug.
 However, if drug is removed permanently, the
nervous system will eventually adjust to
restore the original amount of receptor

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HMM/SCM 1424,CFS, IIUM
Nervous System

3.7 Diseases and disorders of the nervous


system
 Unlike the PNS, the mammalian CNS does not
have the ability to repair itself when damaged
or injured by disease.
 Surviving neurons in the brain can make new
connections and sometimes compensate for
damage.
 Generally speaking, brain and spinal cord
injuries, strokes, and diseases that destroy
CNS neurons have devastating effects.

SCHIZOPHRENIA
 Sufferers : ~ 1% of the world’s population
 severe mental disturbance characterized by
psychotic episodes.
 Symptoms: hallucinations and delusions.
 The cause is unknown, although the disease
has a strong genetic component, (Multiple
genes must be involved because inheritance
does not follow a simple Mendelian pattern.)
 Evidences suggest that excessive stimulation
of dopamine pathways or blockage to
glutamate pathways may be involved.

DEPRESSION

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HMM/SCM 1424,CFS, IIUM
Nervous System

 Symptoms: Depressed mood/abnormalities in


sleep/appetite/energy level
 Major depressive disorder-long periods of
depression.
 affects 1 in every 7 adults, women
affected twice more often.
 Bipolar disorder- involves swings in mood from
high to low and affects about 1% of the world’s
population.
 Both diseases may have genetic and
environmental causes.

ALZHEIMER’S
 mental deterioration or dementia : confusion,
memory loss, and a variety of other symptoms.
 Its incidence is age related, rising from 10% at
age 65 to 35% at age 85.
 disease is progressive, with patients losing the
ability to live alone and take care of
themselves. May fail to recognize people.
 There are also personality changes, almost
always for the worse.
 It is difficult to diagnose Alzheimer’s disease
while the patient is still alive.
 However, it results in characteristic brain
pathology.
 Neurons die in huge areas of the brain
(hippocampus & cerebral cortex), often leading
to shrinkage of brain tissue.

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HMM/SCM 1424,CFS, IIUM
Nervous System

 The diagnostic features are postmortem


findings of neurofibrillary tangles and
senile/amyloid plaques in the remaining brain
tissue.
 Currently there is no cure.

PARKINGSON’S DISEASE
 ~ 1 million people in the United States are
afflicted with this diseases
 Symptoms: a motor disease characterized by
difficulty in initiating movement, slowness of
movement, and rigidity.
 Incidence: 1% at age of 65, 5% at age of 85
 Like Alzheimer’s disease, Parkinson’s disease
results from death of neurons in a midbrain
nucleus called the substantia nigra which
normally releases dopamine at synapses.
 The consensus among scientists is that it
results from a combination of environmental
and genetic factors.
 No cure. To manage symptoms, brain surgery
(implant dopamine secreting neurons) /brain
stimulation/L-dopa treatment may be done.

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HMM/SCM 1424,CFS, IIUM

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