Anatomi hepar

Hepar terbagi menjadi 2 lobus yaitu lobus hepatis dextra dan lobus hepatis sinistra oleh incisura
umbilikalis, ligamentum falciforme hepatis, dan fossa sagittalis sinistra.
Pada lobus hepatis dextra, terdapat fossa sagittalis sinistra, fossa sagittalis dextra, dan porta
hepatis. Fossa sagittalis sinistra hepatis terdiri dari fossa ductus venosi dan fossa venae
umbilicalis. Fossa sagittalis dextra terdiri dari fossa vesicae fellea dan fossa venae cavae. Porta
hepatis membentuk lobus quadratus hepatis dan lobus caudatus hepatis.

Lobus Quadratus Hepatis memiliki batas

anterior pada margo anterior hepatis, batas dorsal pada porta hepatis, batas dextra pada fossa
vesicae fellea, dan batas sinistra pada venae umbilicalis. Pada lobus quadratus hepatis ini,
terdapat cekungan yang disebut impressio duodeni lobi quadrati.
Lobus Caudatus Hepatis (Spigeli) memiliki batas ventro-caudal pada porta hepatis, batas dextra
pada fossa venae cavae, dan batas sinistra pada fossa ductus venosi. Pada lobus caudatus hepatis
ini terdapat tonjolan yaitu processus caudatus dan processus papillaris.
Lobus Hepatis Sinistra adalah lobus hepar yang berada di sebelah kiri ligamentum falciforme
hepatis. Lobus ini lebih kecil dan pipih jika dibandingkan dengan lobus hepatis dextra. Letaknya
adalah di regio epigastrium dan sedikit pada regio hyochondrium sinistra. Pada lobus ini,
terdapat impressio gastrica, tuber omentale, dan appendix fibrosa hepatis.
Sekarang, kita akan membahas sedikit tentang facies hepatis. Facies hepatis terdiri dari facies
diaphragmatica dan facies visceralis hepatis. Facies diaphragmatica (sisi yang berhadapan
dengan diaphragma) pada facies anteriornya (sisi depan facies diaphragmatica) terdiri dari margo
anterior hepatis dan perlekatan ligamentum falciforme hepatis, sedangkan pada facies
superiornya (sisi atas facies diaphragmatica) terdapat impressio cardiaca dan pars affixa hepatis
(bare area).
Facies visceralis hepatis (sisi yang menghadap organ intraperitoneal) memiliki facies posterior
yang pada facies itu terdapat pars affixa hepatis, fossa vena cavae, impressio suprarenalis,
ligamentum hepatogastricum, impressio oesophagea. Pada facies inferiornya terdapat impressio
colica, impressio renalis, impressio duodenalis, fossa vesicae felleae, dan fossa venae
umbilicalis.

Porta hepatis terdiri dari vena porta, ductus

cysticus, ductus hepaticus, dan ductus choledochus, arteri hepatica propria dextra dan arteri
hepatica sinistra, serta nervus dan pembuluh lymphe.
Ligamenta hepatis terdiri dari:

1. Ligamentum falciforme hepatis

2. Omentum minus
3. Ligamentum coronarium hepatis
4. Ligamentum triangulare hepatis
5. Ligamentum teres hepatis
6. Ligamentum venosum Arantii
7. Ligamentum hepatorenale
8. Ligamentum hepatocolicum
Ligamentum falciforme hepatis merupakan reflexi peritoneum parietale yang terdiri dari 2
lembaran (lamina dextra dan lamina sinistra) serta membentuk lamina anterior ligamentum
coronarii hepatis sinistrum dan dextrum. Pada tepi inferior ligamentum ini terdapat ligamentum
teres hepatis dan vena para umbilicalis.
Omentum minus membentang dari curvatura ventriculi minor dan pars superior duodeni menuju
ke fossa ductus venosi dan porta hepatis. Ligamentum gastrohepatica dan ligamentum
hepatoduodenale merupakan bagian dari omentum minus ini.
Fiksasi hepar dilakukan oleh vena hepatica, desakan negatif (tarikan) cavum thoracis, desakan
positif (dorongan) cavum abdominis, dan oleh ligamenta yang telah disebutkan sebelumnya,
diantaranya:

1. Lig.falciforme hepatis
2. Omentum minus
3. Lig.Triangulare hepatis
4. Lig.coronarium hepatis
5. Lig.Teres hepatis
6. Lig.venosum Arantii

Vascularisasi hepar oleh:

1. Circulasi portal
2. A. Hepatica communis
3. Vena portae hepatis
4. Vena hepatica

Arteri hepatica communis berasal dari a.coeliaca. Arteri ini melewati lig. hepatoduodenale
(bersama ductus choledochus, v.portae, pembuluh lymphe dan serabut saraf) dan bercabang
menjadi a. hepatica propria dextra dan a.hepatica propria sinistra.
Vena portae hepatis dibentuk oleh v. mesenterica superior dan v.lienalis. Vena ini berjalan
melewati lig. hepatoduodenale, bercabang menjadi ramus dexter dan ramus sinister.
Innervasi hepar oleh:

1. Nn. Splanchnici (simpatis)

2. N. Vagus dexter et sinister (chorda anterior dan chorda posterior), dan
3. N. Phrenicus dexter (viscero-afferent)

Apparatus excretorius hepatis (oleh karena hepar sebenarnya adalah suatu kelenjar raksasa)
adalah:

1. Vessica fellea
2. Ductus cysticus
3. Ductus hepaticus, dan
 4. Ductus choledochus

----*

Histologi Hepar
Secara mikroskopik terdiri dari Capsula Glisson dan lobulus hepar. Lobulus hepar dibagi-bagi
menjadi:

Lobulus klasik
Lobulus portal
Asinus hepar

Lobulus-lobulus itu terdiri dari Sel hepatosit dan sinusoid. Sinusoid memiliki sel endotelial yang
terdiri dari sel endotelial, sel kupffer, dan sel fat storing.
Mari kita bahas satu per satu:
Lobulus hepar:
Lobulus klasik:

Berbentuk prisma dengan 6 sudut.

Dibentuk oleh sel hepar yang tersusun radier disertai sinusoid.
Pusat lobulus ini adalah v.Sentralis
Sudut lobulus ini adalah portal area (segitiga kiernann), yang pada segitiga/trigonum
kiernan ini ditemukan:
o Cabang a. hepatica
o Cabang v. porta
o Cabang duktus biliaris
 o Kapiler lymphe

Lobulus portal:

Diusulkan oleh Mall cs (lobulus ini disebut juga lobulus Mall cs)
Berbentuk segitiga
Pusat lobulus ini adalah trigonum Kiernann
Sudut lobulus ini adalah v. sentralis

Asinus hepar:

Diusulkan oleh Rappaport cs (lobulus ini disebut juga lobulus rappaport cs)
Berbentuk rhomboid
Terbagi menjadi 3 area
Pusat lobulus ini adalah sepanjang portal area
Sudut lobulus ini adalah v. sentralis

Ilustrasinya:
Sekarang kita bahas tentang sel hepatosit dan sinusoid:
Mikroskopi sel hepatosit:

Berbentuk kuboid
Tersusun radier
Inti sel bulat dan letaknya sentral
Sitoplasma:
o Mengandung eosinofil
o Mitokondria banyak
 o Retikulum Endoplasma kasar dan banyak
o Apparatus Golgi bertumpuk-tumpuk
Batas sel hepatosit :
o Berbatasan dengan kanalikuli bilaris
o Berbatasan dengan ruang sinusoid
o Berbatasan antara sel hepatosit lainnya

Mikroskopi sinusoid:

Ruangan yang berbentuk irregular

Ukurannya lebih besar dari kapiler
Mempunyai dinding seluler yaitu kapiler yang diskontinu
Dinding sinusoid dibentuk oleh sel hepatosit dan sel endotelial
Ruang Disse (perivascular space) merupakan ruangan antara dinding sinusoid dengan sel
parenkim hati, yang fungsinya sebagai tempat aliran lymphe

Sekarang kita bahas tentang sel endothelial pada sinusoid:

Sel endothelial:
o Berbentuk gepeng
o Paling banyak
o Sifat fagositosisnya tidak jelas
o Letaknya tersebar
Sel Kupffer:
o Berbentuk bintang (sel stellata)
o Inti sel lebih menonjol
o Terletak pada bagian dalam sinusoid
o Bersifat makrofag
o Tergolong pada RES (reticuloendothelial system)
o Sitoplasma Lisozim banyak dan apparatus golgi berkembang baik
Sel Fat Storing:
o Disebut juga Sel Intertitiel oleh Satsuki
o Disebut juga Liposit oleh Bronfenmeyer
o Disebut juga Sel Stelata oleh Wake
o Terletak perisinusoid
o Mampu menyimpan lemak
o Fungsinya tidak diketahui

Sistem duktuli hati (sistem saluran empedu), terdiri dari:

kanalikuli biliaris
o cabang terkecil sistem duktus intrahepatik
o letak intralobuler diantara sel hepatosit
 o dibentuk oleh sel hepatosit
o pada permukaan sel terdapat mikrovili pendek
kanal hering

Termasuk apparatus excretorius hepatis: Vesica fellea:

Gambaran mikroskopisnya:

Tunica mucosa-nya terdiri dari epitel selapis kolumnair tinggi

o Lamina propria-nya memiliki banyak pembuluh darah, kelenjar mukosanya
tersebar, dan jaringan ikat jarang
o Tidak ada muscularis mucosa
Tunica muscularis terdiri dari lapisan otot polos tipis
Tunica serosa:
o merupakan jaringan ikat berisi pembuluh darah dan lymphe
o permukaan luar dilapisi peritoneum

sinus rockitansky aschoff

Merupakan sinus yang terbentuk karena invaginasi epitel permukaan yang menembus ke lapisan
otot dan sampai ke lapisan jaringan ikat perimuskuler.

Fisiologi Hepar :
1. Pembentukan dan ekskresi empedu (metabolisme garam empedu dan pigmen empedu)
Garam empedu penting untuk pencernaan dan absorbs lemak serta vitaminlarut lemak dalam
usus, bilirubin (pigemen mpempedu utama) merupakanhasil akhir metabolism pemecahan
eritrocyt yang sudah tua, proseskonjugasi berlangsung dalam hati dan diekskresi kedalam
empedu2.
2. Metabolidme karbohidrat (glikogenesis glikogenolisis, glukoneogenesis)dan metabolism
protein, serta sintesis protein, hati berperan penting dalam mengatur kadar glukosa darah normal
menyediakan energy untuk tubuh. Karbohidrat disimpan dalam hati dalam bentuk glikogen.
Protein serumyang disentesis oleh hati adalah albumin serta globulin alfa dan beta(gamma
globulin tidak). Faktor pembekuan darah yang disentesis oleh hatiadalah fibrinogen (1),
protrombin (II), dan factor V, VII, IX, dan X,sedangkan vitamin k merupakan kofaktor yang
penting dalam sintesissemua factor ini kecuali factor V3.

3. Pembentkan urea, penyimpanan protein (asam amino), metabolism lemak,ketogenesis,

sintesis kolesterol,dan penimbunan lemak. Urea dibentuk semata-mata dalam hati dari
amoniak (NH3

) yang kemudian diekskresidalam feses , NH3 dibentuk dari deaminasi asam amino dan kerja
bakteriusus terhadap asam amino. Hidrolisisi trigleserida, kolesterol,fosfolipid,dan lipoprotein
(diabsorbsi dari usus) menjadi asam lemak dan gliserol,hati memgang peranan utama dalam
sintesis kolesterol, sebagian besar diekskresi dalam empedu sebagai kolesterol dan asam kolat4.

4. Penimbunan vitamin dan mineral. Vitamin larut lemak A D E K disimpandalam hati juga
vitamin B 12 tembaga dan besi5.

5. Metabolism steroid. Hati menginaktifkan dan menyekresi aldosteronglukokortikoid,

ekstrogen, progresteron dan testoteron.6.

6. Detoksifikasi, hati bertanggung jawab atas biotransformasi zat-zat berbahaya (obat) menjadi
zat-zat yang tidak berbahaya yang kemidiandiekskresi oelh ginjal7.

7. Gudang darah dan filtrasi. Sinusoid hati merupakan depot darah yangnmengalir kermbali
dari vena cava (gagal jantung kanan ), kerja fagositik sel kuffer membuangn bakteri dan debris
dari darah.
Morphology of Alcoholic Liver Disease
July 26, 2011 | 9:37 am | Pathology | One Comment

Alcoholic Liver Disease (ALD) is a term used to describe the spectrum of liver injury associated
with acute andchronic alcoholism.

The 3 stages of Alcoholic Liver Disease are:

1. Hepatic steatosis (fatty change)

2. Alcoholic hepatitis
3. Alcoholic cirrhosis

Interrelationships among stages of Alcoholic Liver Disease:

Gross appearance of Normal Liver:

Weighing 1200-1600 grams

Reddish brown in color

Soft in consistency

Smooth surface

Microscopic examination of Normal Liver and Hepatocytes:

Hepatic Steatosis:

Steatosis is a condition characterized by abnormal accumulations of triglycerides within

parenchymal cells. Hepatic steatosis (fatty change) is reversible even when extensive.

Gross appearance:

No gross change occurs with mild steatosis. Later, the liver is:

1. Soft
2. Yellow
3. Greasy
4. Large (up to 4 to 6 kg)

Microscopic examination:

1. Moderate alcohol intake: small (microvesicular) lipid droplets acculmulate in hepatocytes that
doesnt compress and displace nucleus to periphery
2. Chronic alcohol intake: large (macrovesicular) globules, compressing and displacing the nucleus
to the periphery of hepatocytes
3. Initially, cell damage produces centrilobular fat depositions.
4. But in severe cases entire lobule may be involved.
5. Little or no perivenular fibrosis
Alcoholic Hepatitis

Alcoholic hepatitis develops acutely, usually following a bout of heavy drinking. In 10% to 35%
of heavy drinkers, alcoholic hepatitis is superimposed on pre-existing hepatic steatosis increasing
the risk of cirrhosis.

Gross appearance:

The liver is:

1. Mottled red with bile stained areas

2. Of normal or increased size
3. Often contains visible nodules and fibrosis

Microscopic examination:

1. Hepatocyte swelling (ballooning): due to accumulation of fat, water and protein.

2. Hepatocyte necrosis (ballooning degeneration) which attracts neutrophils
3. Mallory bodies (Cytokeratin aggresomes): Eosinophilic cytoplasmic inclusions in degenerating
hepatocytes
4. Neutrophilic reaction: Neutrophils surround the mallory bodies like jackals around a campfire
5. Fibrosis: Chicken wire fibrosis surrounds the hepatocytes (sinusoidal, perivenular and
ocassionaly periportal)

Alcoholic Cirrhosis:

Alcoholic cirrhosis is the final and irreversible form of alcoholic liver disease which usually
evolves slowly and insidiously. Cirrhosis is a diffuse process (affecting whole liver)
characterized by fibrosis and conversion of the liver architecture into nodules.
Gross appearance:

At Beginning: Micronodular (nodules <3cm in diameter), Yellow, Fatty, Enlarged (>2 kg)

After years: Macronodular (nodules >3cm in diameter), Brown, Non-fatty, Shrunken (<1 kg)

Microscopic examination:

1. Lobular architecture: No normal lobular architecture can be identified and central veins are hard
to find.
 2. Fibrous septa: The fibrous septa that divide the hepatic parenchyma into modules are initially
delicate and extend through sinusoids from:
o Central vein to portal regions and
o Portal tract to portal tract
3. Hepatic parenchyma:
o Hepatocyte regeneration generates micronodules (parenchyma shows extensive fatty
change) .
o As fibrous septa widens and surround nodules, liver becomes more fibrotic, loses fat
and shrinks progressively in size.
o Mixed micronodular and macronodular pattern seen
o Laennec cirrhosis: Ischemic necrosis and fibrous obliteration of nodules create broad
expanses of tough, pale, scar tissue.
4. Inflammation: Sparse infiltrate of mononuclear cells in the fibrous septa
5. Bile stasis

References:

1. Robins and Cotran Pathological Basis of Disease 7th edition

2. Robins Basic Pathology 8th edition
3. Textbook of Pathology by Harsh Mohan
4. Riede / Werner Color Atlas of Pathology Thieme
5. Pathology Illustrated 6th Edition by Robin Reid and Fiona Roberts
6. Library.med.utah.edu
Prepared for Correlation Seminar for Gastrointestinal System in KIST Medical College by:

Srijana Shakya (Roll no.79)

Sulabh Shrestha (Roll no.80)

Tags: alcoholic cirrhosis, Alcoholic hepatitis, Alcoholic Liver Disease, Hepatic steatosis

Read more Morphology of Alcoholic Liver Disease | Medchrome

Miscellaneous Lesions of the Mouse Liver

The Digitized Atlas of Mouse Liver Lesions

Extramedullary Hematopoiesis (EMH) - Click on thumbnails to view larger images

Extramedullary hematopoiesis (EMH) can occur in the liver, especially when there is long-standing
anemia. Typical morphological features consist of small aggregates of cells with intensely basophilic
nuclei (erythroid) or small collections of immature and mature myelocytic cells (myelopoiesis) located in
the sinusoids and, in severe cases, in portal areas.

Extramedullary hematopoiesis characterized by small aggregates of immature erythroid cells.

Multiple aggregates of neutrophilic band cells and erythroid precursor cells are present in the sinusoids
with a large aggregate in a portal area.

Hepatocellular Hypertrophy/Cytomegaly - Click on thumbnails to view larger images

Hepatocellular hypertrophy is frequently seen in the liver following exposure to agents that cause
hepatic enzyme induction. The hypertrophy typically starts in the centrilobular area and extends
to the mid-lobular and eventually periportal areas provided there is sufficient stimulus over time.
In situations of prolonged exposure to some agents, the hypertrophic hepatocytes are seen to
have enlarged polyploid nuclei. With some treatment regimens, hepatocytes may actually
become cytomegalic. Cytomegalic hepatocytes typically have single polyploid and/or multiple
nuclei.

Minimal centrilobular hepatocyte hypertrophy is present and most dramatically involves

enlargement of hepatocytes immediately adjacent to the central vein. The periportal hepatocytes
(right side of image) are not affected.

Generalized hepatocyte hypertrophy involving all portions of the hepatic lobule. Higher magnification
shows a cytomegalic hepatocyte in the lower right. It has an enlarged nucleus with multiple nucleoli.

Hypertrophic and cytomegalic hepatocytes are present in the centrilobular and midlobular areas in
these images from a mouse treated with chlordane for several months. Some cytomegalic hepatocytes
have several nuclei.

Intrahepatocyte Erythrocytes and Pigment - Click on thumbnails to view larger images.

The presence of erythrocytes within hepatocytes is seen on rare occasions. It is not known for
sure why or how intact erythrocytes come to be located within individual hepatocytes. Perhaps it
is by erythrophagocytosis, but that is only supposition. The affected hepatocytes often become
very large and, presumably, ultimately die and become phagocytosized by Kupffer cells along
with their contents. Exacerbation of this change by chronic treatment may occur. We have seen it
in three of approximately 500 NTP two-year studies. The cause and significance of this change is
not known.

Low magnification of a liver in which multiple small collections of erythrocytes that resemble
peliosis can be seen. These actually represent individual enlarged hepatocytes containing
numerous erythrocytes.

Several hepatocytes contain erythrocytes. The nucleus is of normal size while the cytoplasmic mass is
markedly enlarged with margination of the cytoplasm. The nucleus in these cells is often localized at the
cell margin.

Intrahepatocytic erythrocytes.

In this example, the intrahepatocytic erythrocytes have become partially lysed.

In addition to an hepatocytes filled with erythrocytes, there is accumulation of pigment within Kupffer
cells (macrophages).

Kupffer cells throughout the liver are filled with golden brown pigment which is believed to represent
breakdown of hemoglobin.
 Polyploidy - Click on thumbnails to view larger images.

The normal mouse liver contains hepatocytes that are diploid, tetraploid, and octaploid with
increase ploidy occurring as the animal ages. A tetraploid hepatocyte may have twice the
complement of DNA either by having two diploid nuclei (binucleated hepatocyte) or a single
nucleus which contains twice the diploid amount of DNA. A variety of treatment regimens cause
alterations in ploidy with single hepatocytes sometimes having several diploid nuclei
(multinucleated hepatocytes). The hepatocyte regeneration that follows partial hepatectomy is
the result of proliferation of diploid cells. Polyploidy develops once the liver has completed
regeneration.

Normal mouse liver showing a mixture of diploid, binucleate, and tetraploid hepatocytes.

Extreme polyploidy consisting of cytomegalic hepatocytes with very large nuclei as well as cytomegalic
hepatocytes with several diploid nuclei is seen in these images from a mouse treated with chlordane for
18 months.

Multinucleated Hepatocytes - Click on thumbnails to view larger images

Adult mouse liver with scattered multinucleated hepatocytes.

A mouse treated chronically with chlordane, showing enlarged hepatocytes with multiple nuclei.
Multinucleated hepatocytes in a B6C3F1 male mouse.

National Toxicology Program (NTP) Data and Reports Website

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Surface righting First day and time in seconds for pups placed

in a supine position to return to the prone

position with all four paws on the ground

Rooting First day that the head turns toward the side

of the face being stroked with the tip of a

cotton swab

Cliff aversion First day and time in seconds for pups positioned

with forepaws and snout over the

edge of a shelf to turn and begin to crawl

away from the edge

Negative geotaxis First day and time in seconds for pups placed

head down on a 45 degree incline to turn

180 degrees and begin to crawl up the slope

Ear twitch First day that the ear twitches after stimulation

with the tip of a cotton swab

Forelimb grasping First day pups could remain suspended for at

least 1 sec after grasping a thin rod with

their forepaws

Auditory startle First day that pups respond with a quick involuntary

jump after a small metal object is

dropped on a lab bench 25 cm from the pup

Air righting First day that pups released upside-down from

a height of approximately 60 cm turn rightside-

up and land on all four paws on a bed

of shavings

Eye opening First day that both eyes are open

Pinna detachment First day that both ears are open

Meluruskan Hari pertama dan waktu dalam detik untuk anjing Permukaan ditempatkan
dalam posisi telentang untuk kembali ke rawan
posisi dengan keempat kaki di tanah
Rooting Hari pertama bahwa kepala berbalik ke arah samping
wajah yang membelai dengan ujung
kapas
Keengganan Cliff Hari pertama dan waktu dalam detik untuk anjing diposisikan
dengan kaki depannya dan moncong atas
tepi rak untuk berbalik dan mulai merangkak
jauh dari tepi
Geotaxis Negatif Hari pertama dan waktu dalam detik untuk anjing ditempatkan
kepala ke bawah di lereng 45 derajat untuk mengubah
180 derajat dan mulai merangkak naik lereng
Telinga berkedut Hari pertama bahwa berkedut telinga setelah stimulasi
dengan ujung kapas
Tungkai depan menggenggam pups Hari pertama bisa tetap ditangguhkan selama
Setidaknya 1 detik setelah menggenggam batang tipis dengan
kaki depannya mereka
Mengagetkan Auditory Hari pertama yang anjing merespon dengan cepat involunter
melompat setelah benda logam kecil
dijatuhkan di bangku lab 25 cm dari anak anjing
Air meluruskan Hari pertama yang dirilis anjing terbalik dari
ketinggian sekitar 60 cm berubah rightside-
dan tanah di keempat kaki di tempat tidur
serutan
Membuka mata Hari pertama bahwa kedua mata terbuka
Pinna detasemen Hari pertama bahwa kedua telinga terbuka

2.3. Early Postnatal Development

From P2 to P21, pups were assessed for the ability to reach critical developmental milestones evaluating the
appearance of age-appropriate motor skills such as bal- ance, motor coordination, strength and reflexes, follow-
ing Hill and colleagues [40]. Tests were performed at the same time each day until the pup was able to perform the
task in the prescribed amount of time for two consecutive days [41]. The tests used included surface righting,
nega- tive geotaxis, cliff aversion, forelimb grasp, auditory star- tle, ear twitch, open field traversal, air righting and
eye opening. Pups from T3 (P4 and P7) underwent develop- mental milestone testing beginning at 9:30 am,
followed by injections at 12:00 pm.

Developmental and behavioral milestones (Gandhi, et al., 2012)

Eye opening (PND 11-16), The dam was first removed from the home cage and the individual test within each
testing category proceeded in the following order :

i. Reflex development-raghting reflex

ii. Motor coordination the negative geotaxis test
iii. Muscle strength test
iv. Open field activity
v. Spontaneuos or non bahavioural tests.
The days of appearance of each melistone werw recorded using previous criteria.

Reflex development
For the righting reflex, the pup was placed in its back (dorsal position) and the time required for the animal to turn
ventrally itself within 60 sec was recorded. Each pup received five trials per day from PND 1-5. Other reflexes were
assessed such as palmer grasps (PND11), negative geotaxis (PND 9-11), rotarod (PND 20), cliff avoidance (PND 1-4),
auditory startle (PND 7) as described. Forelimb placing (PND 4-5), hind limb placing (PND 6), surface righting (PND
9-11), ear witch (PND 18).
Motor and coordination capacity was examined using the negative geotaxis test as described on PND 9-11. On day
20 the animals ability to hang, the length of time it does hang, and its activity while hanging were observed.

Perkembangan Awal Postnatal

Dimulai dari PND 2 - PND 21, anak mencit dinilai untuk kemampuan mencapai tahap perkembangan
kritis motorik sesuai usia seperti motorik, kekuatan dan refleks. Pengujian dilakukan pada waktu yang
sama setiap hari sampai anak mencit tersebut mampu melakukan serangkaian test tingkah laku dalam
jumlah dan waktu yang ditentukan selama dua hari berturut-turut.
Tahap perkembangan dan perilaku (Gandhi, et al., 2012)
pengujian berlangsung dalam urutan sebagai berikut:
1. kemampuan refleks
2. Test geotaxis negatif
3. Uji kekuatan otot
Setiap anak mencit menerima lima uji coba per hari dari PND 1-5. Refleks lain dinilai seperti, geotaxis
negatif (PND 9-11), menghindari jurang (PND 1-4), pendengaran (PND 7), dan membuka mata (PND 11-
16)