REFLEX DAN

NEUROMUSCULAR
JUNCTION

REFLEX

Definisi

Reflex adalah rangkaian gerakan yang

dilakukan secara cepat, involunter dan
tidak direncanakan sebagai respon
terhadap suatu stimulus
Merupakan fungsi integratif
Lengkung reflex (reflex arc) adalah jalur
yang dilewati oleh impuls saraf untuk
menghasilkan reflex

Jenis reflex

Reflex spinal
Reflex cranial
Reflex otonom

Komponen lengkung
refleks

Reseptor sensorik
Saraf sensorik (neuron afferen)
Pusat refleks (Batang otak, medula
spinalis)
Saraf motorik (Neuron efferen)
Efektor (otot, kelenjar)

Refleks regang
Reflex

Monosinaptik
Refleks regang menyebabkan kontraksi otot
rangka sebagai respon terhadap
peregangan otot
Mekanisme umpan balik untuk mengontrol
panjang otot dengan menimbulkan kontraksi
Dapat terjadi dengan mengetuk tendon otot
Contoh : refleks biseps, triseps, patella,
achilles

Refleks Fleksor dan Ekstensor

Refleks Polisinaptik
Respon terhadap rangsangan nyeri

REFLEX FLEXOR
= Reflex nociceptif
= Reflex penarikan diri (withdrawn reflex)
Stimulus : rangsangan nyeri
Mekanisme neuronal :
1. Sirkuit divergen
2. Sirkuit inhibisi timbal balik
3. After discharge
REFLEX EKSTENSOR MENYILANG

0,2-0,5 detik sesudah timbul reflex flexor

Terjadi ekstensi pada ekstremitas yang berlawanan
Mekanisme neuronal : sinyal sensoris menyeberang ke
kontralateral

Refleks fisiologis

Refleks yang normal ditemukan pada

orang sehat
Contoh : refleks regang

Refleks patologis

Refleks yang ditemukan pada orang yang

mengalami gangguan pada sistem
sarafnya
Contoh : refleks Babinsky, kecuali jika
ditemukan pada bayi
Babinsky group :
Refleks chaddock
Refleks schaffer
Refleks gordon
Refleks Oppenheim

NEUROMUSCULAR
JUNCTION

Neuromuscular junction
(example of chemical synapse)

Neuromuscular junction : the synapse

between motor neuron and muscle fiber

Motor neurons : are the nerves that

innervate muscle fibers

Motor unit : single motor neuron and the

muscle fibers it innervate

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Penyebaran potensial aksi

ke serat syaraf berikutnya

Melalui sinaps
Neuro-transmitter
- Asetilkolin

16

Neuromuscular Junction

Motor Endplate
- Serat otot disyarafi syaraf
bermielin
- 1 junction per 1 serat otot
- Ujung syaraf invaginasi ke
dalam serat otot, tapi berada
di luar membran serat otot
- Ditutupi oleh sel Schwan
insulasi dari cairan intersisial
- Akson terminal mengandung
banyak mitokondria untuk
sintesis neurotransmiter
- Neurotransmiter disimpan di
dalam vesikel sinaptik

Axon terminal
didalam lekukan
sinaptik

Vesikel
sinaptik
Celah
sinapti
k

Celah subneural

1. An action potential arrives at the

presynaptic terminal causing voltage
gated Ca2+ channels to open,
increasing the Ca2+ permeability of
the presynaptic terminal.
2. Ca2+ enters the presynaptic terminal
and initiates the release of a
neurotransmitter, acetylcholine (ACh),
from synaptic vesicles in the
presynaptic terminal.
3. Diffusion of ACh across the synaptic
cleft and binding of ACh to ACh
receptors on the postsynaptic muscle
fiber membrane causes an increase in
the permeability of ligand-gated Na+
channels.
4. The increase in Na+ permeability
results in depolarization of the
postsynaptic membrane; once
threshold has been reached a
postsynaptic action potential results.

Action
Ca2+
Presynaptic potential
channel terminal

Ca2+

Presynaptic
terminal

ACh
Acetic
acid

Synaptic
vesicle

Synaptic cleft

Choline
2

ACh

Na+
ACh
3

Synaptic
cleft ACh

5
4

Action
potential

Na+

Receptor
molecule

5. Once ACh is released into the synaptic cleft it binds to the receptors for
ACh on the postsynaptic membrane and causes Na+ channels to open.
6. ACh is rapidly broken down in the synaptic cleft by
etylcholinesterase to acetic acid and choline.
7. The choline is reabsorbed by the presynaptic terminal and combined
with acetic acid to form more ACh, which enters synaptic vesicles.
Acetic acid is taken up by many cell types.

Choline

Acetic
acid
6

receptor
site

Action
potential
Postsynaptic
membrane Acetylcholinesterase
Na+

Action
Ca
Presynaptic potential
channel terminal
2+

Ca2+

An action potential arrives at the presynaptic terminal causing voltage

gated Ca2+ channels to open, increasing the Ca2+ permeability of
the presynaptic terminal.

Ca2+

Presynaptic
Ca2+
channel terminal

ACh

Ca2+ enters the presynaptic terminal and initiates the release of a

neurotransmitter, acetylcholine (ACh), from synaptic vesicles in the
presynaptic terminal.

Synaptic cleft

Na+

Na+

ACh

Receptor
molecule

Diffusion of ACh across the synaptic cleft and binding of ACh to ACh
receptors on the postsynaptic muscle fiber membrane causes an
increase in the permeability of ligand-gated Na+ channels.

Na+

Action
potential

Na+

Action
potential

The increase in Na+ permeability results in depolarization of the

postsynaptic membrane; once threshold has been reached a
postsynaptic action potential results.

ACh
Synaptic ACh
receptor
cleft
site

Postsynaptic
membrane
Na+

Once ACh is released into the synaptic cleft it binds to the receptors for
ACh on the postsynaptic membrane and causes Na+ channels to open.

ACh

Choline Acetic
acid
ACh
receptor
site

Acetylcholinesterase

ACh is rapidly broken down in the synaptic cleft by

acetylcholinesterase to acetic acid and choline.

Presynaptic
terminal

ACh
Acetic
acid

Synaptic
vesicle

ACh

Choline

Choline

The choline is reabsorbed by the presynaptic terminal and combined

with acetic acid to form more ACh, which enters synaptic vesicles.

Choline Acetic
acid

Acetic acid is taken up by many cell types.

Agents &disease that alters the

function of N.M junction

Black widow spider venom: the venom

of black widow spider exerts its effect by
triggering explosive release of Ach from
the storage vesicles, not only at N.M
junction but all cholinergic sites. all
cholinergic sites undergoes prolong
depolarization.

The most harmful result is respiratory

failure
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Botulinum toxin:
botulinum toxin exerts its lethal effect
by blocking the release of Ach .

Clostridium botulinum poisoning most

frequently result from improperly canned
food contaminated with clostridia bacteria

Death is due to reparatory failure caused

by inability to contract diaphragm .

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Curare : curare competitively binds to

Ach receptor sites on motor end plate ,so
Ach can not combine with these sites to
open ion channels .and muscles paralysis
ensues .

In sever poisoning person dies of

respiratory failure

In past it was used as deadly arrowhead

poison.
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Myasthenia gravis

A disease involving N.M junction is characterized by the

extreme muscular weakness (myasthenia=muscular &
gravis=severe)

It is an auto immune condition (auto immune means

immunity against self) in which the body erroneously
produces antibodies against its own motor end plate ach
receptors.

Thus not all Ach molecules can find functioning receptors

site with which to bind.

As a results ,AchE destroys much of Ach before it ever has

a chance to interact with receptor site & contribute to EPP.
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Terima kasih