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by: Putra Santoso-Bio FMIPA UA
Physiology of Nervous System
By: Putra Santoso
Biology Department Andalas University
2017

A tragedy on September 13, 1848, Vermount, USA
After tragedy: childish, putative loss memory, agressive, profane (rude)
Brain damage (frontal cortex) induces alteration in behavior

Deja vu or not ??

Memory-related phenomenon
• Déjà vu: having the strong sensation that an event or
experience currently being experienced, has already
been experienced in the past, whether it has actually
happened or not (frequently occurs in younger age 15-
25 y.o).
• Presque vu: almost, but not quite, remembering
something (tip of the tongue).
• Jamais vu: unfamiliar impression of seeing the actually
well-known situation/event (may be associated with
aphasia, amnesia, and epilepsy).

 Medial temporal lobe is involved in our
conscious memory.
 Within the medial temporal lobe are
the parahippocampal gyrus, the rhinal
cortex and the amygdala.
 Hippocampus enables us to consciously recall
events.
 Parahippocampal gyrus enables us to
determine what's familiar and what isn't (and
without actually retrieving a specific memory
to do it).
Previous hypothesis:
Involving hippocampus (center of memory)

Mechanism of Deja Vu
Experimental study (2016):
• Frontal regions of the brain are probably checking through our
memories, and sending signals if there’s some kind of memory
error – a conflict between what we’ve actually experienced and
what we think we’ve experienced.
• Some conflict resolutions going on in the brain during déjà vu.
• Déjà vu is a sign that your brain’s memory checking system is
working well, and that you’re less likely to misremember events.
• Never experience deja vu : may also indicate the lack/less of
error in the brain

Blood-brain barrier (BBB)?

MSG as the exitoxic substance

Int J Clin Exp Med (2009) 2, 329-336
www.ijcem.com /IJCEM910003
Deciphering the MSG controversy
Robert S. Dow Neurobiology Laboratories, Legacy Clinical Research Center, USA.

Vitamin C and low-
dose preexposure to
MSG prevent cells
death caused by
higher dose of MSG

Yulyaningsih et al., 2017, Cell Reports 19, 2257–2271
http://dx.doi.org/10.1016/j.celrep.2017.05.060

Topics of Discussion
1. Neuron and neurotransmitters
2. Electric synapses and chemical synapses
3. Electric charge of neuron (intra and extracelluar) and
ion channels in neurons
4. Resting potential and action potential
5. Measurement of neuronal activity, patch clamp and
optogenetic technique
6. Memory formation, storage, recall in the brain
7. Neural mechanism of taste and vision
8. Alzheimer & parkinson disease: mechanism and
therapy

neurotransmitters

A- (negatively charge
protein molecules)
At rest, there are
relatively more
sodium ions outside
the neuron and
more potassium ions
inside that neuron.

Ion channels in neuronal plasma membranes
Each type of channel protein has a specific function in the electrical activity of
neurons. (a) Resting K+ channels are responsible for generating the resting
potential across the membrane. (b) Voltage- gated channels are responsible for
propagating action potentials along the axonal membrane. (c, d) Two types of
ion channels in dendrites and cell bodies are responsible for generating electric
signals in postsynaptic cells.

by: Putra Santoso-Bio FMIPA UANature 525, 333-338: 2015/09/09 (Japan time), doi: 10.1038/nature15257

 Short-term memory lets you remember a name or phone number long enough to
enter it. It's brother...
 Medium-term memory lets you remember what you had for breakfast yesterday
that didn't agree with you today.
 Working memory (the first to go) lets you keep a lot of data in mind while you sort
through it to save what is important to you.
 Primitive memory systems are similar to those of a reptile. They tell your human
heart to pump blood to your cheeks when you are embarrassed or breath faster
when your boss's secretary calls to say he wants to see you in his office.
 Motor memory lets you steer a bike or soap up in the shower while you are
thinking of something else.
 Explicit memory clicks in when you rehearse something a lot until it comes
naturally,
because your system thinks it must be important to your survival. Teacher time.
 Implicit memory already knows what just happened is so important for your
survival it acts on your body before you know it. You cannot control it but it can
control you. (Example: "If an acquaintance betrays me I can't remember her phone
number any more.")

7. Memory formation, storage, recall in the brain
Centers of memory

8. Alzheimer and parkinson disease: mechanism and therapy

 Plaques are deposits of a protein fragment called beta-amyloid that
build up in the spaces between nerve cells.
 Tangles are twisted fibers of another protein called tau (rhymes with
“wow”) that build up inside cells.
 Though autopsy studies show that most people develop some plaques
and tangles as they age, those with Alzheimer’s tend to develop far
more and in a predictable pattern, beginning in the areas important
for memory before spreading to other regions.
 plaques and tangles play a critical role in blocking communication
among nerve cells and disrupting processes that cells need to survive.

II. Tangles:II. Tangles: Many AD patients also have “tangles” in neurons
Microtubules are long string-like structures that transport
things from the cell body to the end of the axon and dendrites
In AD, these microtubules break apart andIn AD, these microtubules break apart and
collapse into a tangles mess and neurons don’t function normally,collapse into a tangles mess and neurons don’t function normally,
so they dieso they die--off.off.
Tau proteins (like rungs of a ladder)

Physiology of nervous system (Bahan Diskusi Kelas Fisiologi Hewan)

Meso-Striatal Dopamine system
components of this system
1. Substantia Nigra- in midbrain
- send fibers to Basal Ganglia
- releases dopamine = movement
2. Basal Ganglia (part of striatum)-
-sends fibers to motor cortex
-receives fibers from sensory
cortex and substantia Nigra
In Parkinson’s Disease
Substantia Nigra neurons die =
reduced excitatory input into basal
ganglia
The two parts of the basal ganglia
(Caudate and Putamen) also die

Symptoms of parkinson disease
 Difficulty initiating movementDifficulty initiating movement
 Shuffling gaitShuffling gait
 “Cogwheel” rigidity“Cogwheel” rigidity
 Tremor at restTremor at rest
 Advanced stages may includeAdvanced stages may include
psychiatric complicationspsychiatric complications::
 depressiondepression
 hallucinationshallucinations
 ParanoiaParanoia
 Cognitive declineCognitive decline

Postmortem AnalysisPostmortem Analysis
brain photographs courtesy of thebrain photographs courtesy of the
University of Utah Medical SchoolUniversity of Utah Medical School
Roberta J.Roberta J. SeidmanSeidman,, M.D.,M.D., SUNYSUNY
ShrunkenShrunken SubstantiaSubstantia NigraNigra

Loss of cellular activity in the Basal GangliaLoss of cellular activity in the Basal Ganglia
PET ScanPET Scan

Treatment of parkinson:
• Levodopa (L-dopa) therapy (L-dopa is a dopamine precursor)
• Direct-acting dopamine receptor agonists
• Experimental brain surgery & stimulation:
– lesions of nuclei that inhibit basal ganglia
– remove inhibition of dying neurons, they may be more
active = motor control
– neural tissue implants (e.g., fetal dopamine cells)
– Deep brain stimulation : indwelling electrodes implanted
in some of the dying neurons. Patients can stimulate
electrodes , provides a brief pulse to these neurons,
which rapidly restores some control of motor activity
– Intracranial magnetic stimultaion, focused ultrasound
stimulation.

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Physiology of nervous system (Bahan Diskusi Kelas Fisiologi Hewan)

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