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Conjugate movements (yoked movements) of the eyeballs are when both eyeballs move on one side. In a normal person only these eye ball movements are seen. The side may be right, left upwards or downwards. They are of four types.

 

TYPES OF CONJUGATE MOVEMENTS:

 

A. searching movements: When light from the retina falls on the visual cortex, axons are sent to the frontal eyefields ipsilaterally. Axons from the frontal eyefields move up and medially downwards to cross and synapse with the PONTINE UNIT (Parapontine reticular formation and 6^th nerve nucleus). The right frontal eyefield synapse with the left pontine unit and vice versa. The right pontine unit is connected to the left 3^rd nerve nucleus via the left medial longitudinal fasiculus (MLF) and vice versa.

The 3^rd nerve nuclei are connected to both medial rectus muscles while the 6^th nerve nucleus are connected to the lateral medial rectus muscles such that the frontal eyefields act as PUSH BUTTONS (when the right frontal eyefield fire, the eyeballs move towards the left and vice versa) for FAST SEARCHING MOVEMENTS.   

Note: When person watches straight both right and left frontal eyefields are firing.

 

B. Tracking movements: the occipital eyefields (located in the secondary visual cortex) are also connected with the pontine unit. The right occipital eyefield is connected with the left pontine unit and vice versa. They too act as PUSH BUTTONS, but for GRADUAL TRACKING MOVEMENTS. {When your eyes follow something slowly}.

 

REMEMBER: both searching and tracking movement are movements of the eye horizontally. THE RECTUS MUSCLES CONTRACT TO PULL EYE TOWARDS THEIR SIDE. THE PONTINE UNITS ACT AS PULL BUTTONS; THEY FIRE TO PULL EYE TOWARDS THEIR SIDE. THE EYEFIELDS ACT AS PUSH BUTTONS; THEY FIRE TO PUSH EYE TOWARDS THE OPPOSITE SIDE.

 

LESIONS:

1. If one MLF damaged due to some reason like multiple sclerosis (eg: right).

The right eye can not move left.

2. Both MLF damaged.

Right eye cannot move left and left eye cannot move right.

3. One and a half syndrome: both MLF damaged and one pontine unit damaged (eg: right).

Right eye cannot move left and left eye cannot move right. Since each pontine unit act as a pull button, the right cannot move right.

OPTHALMOPLEGIA:

Defined as the paralysis of muscles involved in eye movements.

Types:

External opthalmoplegia: paralysis of external extra-occular muscles.

Internucleaur opthalmoplegia: paralysis of medial rectus muscles due to damage to both MLF.

Internal opthalmoplegia: paralysis of the internal extra-occular muscles (dilator pupillae, constrictor papillae and ciliary muscle). Cycloplegia is a type of internal opthalmoplegia concerning ciliary muscle paralysis.

 

IF THE EYEFIELDS GET IRRITATED (overstimulation due to epilepsy or tumour), EYEBALLS MOVE AWAY FROM THE SITE OF LESION. IF THE EYEFIELDS EVENTUALLY GET DAMAGED, EYEBALLS MOVE TOWARDS THE SITE OF LESION.

Overstimulation of eyefields result in NYSTAGMUS: involuntary eyeball movements.

 

 

http://media-2.web.britannica.com/eb-media/47/63347-004-610F94B5.gif -open the link to view relevant diagram. 

Of these external eye muscles, the rectus muscles contract to pull the eye towards itself. The lateral rectus moves it in the lateral direction, the medial rectus in the medial direction, the superior rectus move it upwards while the inferior rectus moves it downwards. The oblique muscles however contract to push the eye towards the opposite. The superior oblique moves the eye downwards and the inferior oblique upwards. The levator palpebrae superioris muscle contracts to pull the eyelid upwards.

Now remember: occulomoter nerve (3^rd) is connected to the medial rectus muscles, the superior and inferior rectus muscles, the inferior oblique muscle (pushes the eye upwards) and the levator palpebrae superioris. It is thus responsibe for moving the eye medially upwards, downwards and also responsible for elevating the eyelid.

Abducent nerve (6^th) is only connected to the lateral rectus muscles. It is responsibe for moving the eyes laterally.

Trochlear nerve (4^th) is only connected to the remaining superior oblique, that pushes the eye downwards.

 

VERTICAL GAZE: the movement of eye up and down along the vertical axis.

 

At the posterior side of the brainstem the vestibular, 3^rd 4^th and 6^th nerve nuclei are connected to eachother via the right and left MLFs. The two MLFs move upwards and join with the posterior commisure (joining the pre-tectal nuclei). At the point of junction, the nucleus of Cajal (rostral or interstitial nucleus of MLF/posterior commisure) is present. Axons from the nucleus of cajal move up to synapse with the 3^rd nerve nucleus and down to synapse with the 4^th nerve nucleus. These nuclei are then connected to the respected external muscles of eye that move the eye upwards and downwards.  

 

  

 

 

Parinaud’s syndrome: Tumour in the pineal gland (located above the nucleus of Cajal) may damage the nucleus of cajal, affecting vertical gaze and the 3^rd nerve nucleus and edhinger westphal nucleus, affecting convergence.

 

Marcus Gunn Pupil test: it is a test to determine whether optic neuritis or multiple sclerosis affecting an optic nerve is completely recovered or no.

If it is not recovered, it will be weak.

E.g the right optic nerve: it light is shone on the right eye, both eye pupils constrict slightly since light stimulus cannot penetrate the optic nerve properly. However if light is shone on the left eye, both pupils constrict.

If light source is made to swing from left to right eye, it is observed that the pupils constrict and dilate. The pupils don’t actually dilate but when they constrict lightly from constricting completely, it seems they dilate.

 

3. Vestibular movements: when the head or body is moving but the eyes are fixed at one point.   

 

4. Convergence movements.

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VISUAL REFLEXES

LIGHT REFLEX:

In a normal human, exposure of light on to one eye will cause the constriction of both eye pupils. For example: if light is made to fall on the left eye and left eye pupil constricts, we say the DIRECT LIGHT REFLEX for left eye is POSITIVE. The right eye pupil will also constrict, even though the left eye is stimulated, we say the INDIRECT OR CONSENSUAL LIGHT REFLEX for the left eye is also positive.  Same is true if the right eye is stimulated.

 

The red line indicates the 10% fibers from the optic tract entering the midbrain. They terminate at the pretectal nucleus (anterior to the superior colliculus). When light stimulation from one eye is accepted by that eyes retina. Fibers from the retina move via the optic chiasma to both right and left optic tracts. 10% of these tracts enter the midbrain and synapse at the pretactal nucleus. The pretactal nucleus gives axons to the rostral (upper) part of the EDINGER WESTIPHAL NUCLEUS: (cranial nucleus for parasympathetic system) of the same side. Also both right and left pretactal nucleus are connected with eachother by the POSTERIOR COMMISURE, via which some fibers go to the opposite pretactal nucleus.  On the medial sides of the edinger westiphal nucleus lies the right and left occulomoter nerve nucleus. From the

 

 

 

occulomoter nerve nucleus the occulomoter the nerve arises. THE AXONS FROM THE WESTIPHAL NUCLEUS ALSO JOINS THE AXONS FROM THE OCCULOMOTER NERVE NUCLEUS TO FORM THE OCCULOMOTER NERVE. The occulomoter nerve synapses at the ciliary ganglion. From the ciliary ganglion short ciliary nerves arise, penetrate the sclera, move between the sclera and choroid, and pierce the cilliary muscle to reach the sphinter pupillae (circular smooth muscles that contracts pupil).

 

ACH is released at the ciliary ganglion as well as the sphinter pupillae. {on the sphinter pupillae there are M3 receptors which when stimulated by ACH, inturn stimulate Gq protein, which in turn stimulates phospholipase C. Phospholipase C breaks  phosphatidyl-inositol  diphosphate in the cell membrane to IP3 and diacylglycerol. IP3 acts on endoplasmic reticulum and pumps out Ca from it. Presence of Ca brings about contraction}

 

ACCOMODATION REFLEX:

 

Accommodation reflex is performed by the eye when a far object is brought near. It includes changes in lens, and constriction of the pupil. The pupil is constricted and the lens are made more rounded and converging by the contraction of the ciliary muscle {receive short ciliary fibers from the ciliary body. The whole pathway mentioned earlier}

Additional to this the medial rectus muscles also contracts to reduce ocular axis. When the neurons in the optic radiation terminate at the calcarine sulcus, some next order neurons move backwards from the medial side of cerebral hemisphere to its lateral side and terminates in the frontal eye fields situated in the middle frontal gyrus anterior to the precentral gyrus.

Axons from the frontal eyefields move upwards and downwards medially to synapse with the edhinger westphal nucleus and the occulomoter nerve nucleus, which again give axons that move along the occulomoter nerve. These fibers leave the occulomoter nerve to synapse with the the medial rectus muscles.

{The ciliary muscle innervates the zonules that innervate the lens, while the sphinter pupillae innervates the anterior pupil. When the sphinter pupilae contracts the pupil constricts and when the ciliary muscle contracts, the zonules contract and the lens becomes rounded.}  

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The axons of the second order neurons originating from the lateral geniculate bodies form upper and lower optic radiations on each side. The upper optic radiations contain fibers from the upper hemi retina while the lower optic radiation contains fibers from the lower hemi retina. These tracts pass through the retrolenticular limb of the internal capsule (the posterior limb continues as the retrolenticular limb) and terminate in the upper and lower lip of the calcarine sulcus {the parieto occipital sulcus on the medial side gives rise to a posterio-inferior sulcus-the calcarine sulcus. Above and below the calcarine sulcus each there is an inner band of primary visual area and an outer band of secondary visual area-Snells 290 fig 8-4 B}.    

            
            http://wdict.net/img/optic+radiation.jpg  -open this link to view relevant diagram.

 

Note: the lateral geniculate body has 6 layers. The fibers in an optic tract from the ipsilateral eye go to layer 2,3 & 5 while the fibers from the contralateral eye go to the remaining layers.

 

Look at FIG 1 for the 5 lesions and the visual fields affected on right. The grey side indicates the side of visual field affected.

1.   TOTAL BLINDNESS OF ONE EYE: when there is lesion completely across the optic nerve.

2.   NASAL HEMI-ANOPIA: when there is a lesion across the lateral fibers of the optic nerve. These lateral fibers have come from the temporal hemi retina which in turn has come from the right side of the left visual field and left side of the right visual field. Anopia means blindness.

3.   BITEMPORAL HEMI-ANOPIA: when there is a lesion across the central part of chiasma, the contralateral fibers are affected only. The right side of the right visual field is and the left side of the left visual field is affected. The pituitary gland moves anteriorly towards the chiasma. Pituitary adenoma (tumour) may cause lesion in chiasma.

4.   CONTRALATERAL HOMONYMOUS HEMI-ANOPIA: any lesion after the optic chiasma, i.e. in the optic tract or optic radiation causes blindness in the right sides of both right and left visual field, if the left tract or radiation is affected. Blindness in the left sides of both right and left visual field occurs if the right tract or radiation is affected.

 

                   PUPILLARY SKIN REFLEX:

When your skin is pricked, afferents from the skin synapse with cell-bodies in the lateral grey horn at the thoracic level. From the lateral grey horn, the second order neurons rise up the sympathetic trunk to synapse with the ganglion in the sympathetic trunk at the cervical level. From the sympathetic trunk the third order neurons originate and synapse with the dilator pupillae, to dilate the pupil.

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OPTIC NERVE

 

It is SPECIAL SOMATIC AFFERENT. Soma meaning body part refers to the eye since it carries visual stimulus from the eye, afferent means it is sensory, named special because it carries the special sensation of vision.

 

It forms as an out pouching of the diencephalon to form an optic vesicle. The optic vesicle gets detached from the diencephalon and a lens invaginates the optic vesicle anteriorly to form the optic cup. The inner wall of the cup develops into the retina while the outer wall develops into the choroid.

 

OPTIC NERVE IS NOT A PEREPHERAL NERVE.

 

·       Myelinated by oligodendrocytes which cause myelination in the CNS, and are affected by multiple sclerosis, a demyelination disease of the CNS.

·       The peripheral nerves can regenerate while nerves of CNS can’t. The optic nerve can’t regenerate either.

·       Out pouching of the diencephalon.

·       The peripheral nerves are surrounded by epineurium (collagen covering) while the optic nerve is surrounded by the three meninges of the brain.

 

VISUAL PATHWAY:

 

FIG 1.

Each retina has a temporal part, towards the temporal lobes on lateral side and a nasal part, towards the nose on medial side and each visual field has a left A part and right B part.

On the right visual cortex, vision forms from the left sides (A part) of both right and left visual fields (follow the red color) and vice versa (follow the blue color). For example with your right eye you see a dog (RIGHT VISUAL FIELD) while with your left eye you see a cat (LEFT VISUAL FIELD). The right visual field has a RIGHT A AND LEFT B SIDE.

The left visual field has a RIGHT A AND LEFT B SIDE.

 

                                       

  

On the right visual cortex, images of both A sides will form, while on the left visual cortex images of both B sides will form. Furthermore A (left) of cat will be sensed by nasal hemi retina of left eye, while B (right) of cat will be sensed by temporal hemi retina of left eye. Same is true for the right side of the eye.

 

Image in the form of light on hitting the retina from the inner side penetrates the various layers of retina to be received by the dendrites of rod and cone cells. The stimulus produce graded (local) potentials inside rod and cone cells {that allow only few Na channels to open. This causes little Na influx that is not enough to reach threshold potential (-70 to -55 mV) and generate an action potential}. This graded potential is transmitted to the bipolar cells and then the ganglionic cells via neurotransmitter glutamine at both synapses.

 

The bundles of axons of the ganglionic cells form the optic nerve. The right optic nerve consists of all the fibers from the right eye and all the vision seen by the right eye. Same is true for the left eye.

 

Fibers from both eye’s temporal hemi retina DONOT CROSS at the optic chiasma and move in their side’s optic tract while fibers from both eye’s nasal hemi retina CROSS and move in the opposite optic tracts. THE RIGHT OPTIC TRACT WILL HAVE FIBERS FROM THE LEFT SIDES OF BOTH RIGHT AND LEFT VISUAL FIELDS WHILE THE LEFT OPTIC TRACT WILL HAVE FIBERS FROM THE RIGHT SIDES OF BOTH RIGHT AND LEFT VISUAL FIELD.

Note: the optic nerve leaves the orbital cavity (cavity of cranium containing the eye) through the optic canal (a small opening). After coming out of the optic canal it joins the optic nerve from the other eye to form the optic chiasma.

 

90% fibers from optic tracts terminate at their side’s lateral geniculate nucleus while 10% go to the midbrain.

PAGE 1

BASIC CONCEPTS RELATING THE EYE AND RETINA.

 

 

The retina from outer to inner side has 8 layers.

 

1.   The pigmented epithelium over which lie the choroidal capillaries which in turn are supplied by major choroidal vessels.

2.   The rod and cone layer collectively called the photoreceptors on which light hits after crossing the inner layers of retina. It has an outer limiting membrane, indicated by the green line in diagram, across the dendrites of the rod and cone cells, and an outer nucleur layer, indicated by the red line that connects the cell bodies of the rod and cone cells.

3.   The outer plexiform layer, indicated by the green bracket. It includes the synapsing junctions between the rod and cone cell layer and the bipolar cells. It is named plexiform because the axons synapse with the dendrites to form a network. THE ABOVE 3 LAYERS ARE PROVIDED NUTRITION BY SIMPLE DIFFUSION FROM THE CHORIO CAPILLARIES.

4.   The bipolar cell layer that contains an inner nuclear layer, across is cell bodies indicated by the black line.

5.   The inner plexiform layer at the synapse between bipolar cells and ganglion cells, indicated by the red bracket.

6.   The ganglion cell layer.

7.   The optic nerve fiber layer.

8.   The inner limiting membrane indicated by the blue line. THE ABOVE 5 LAYERS ARE PROVIDED DIRECTLY BY THE RETINAL ARTERIES.

 

 

The diagram also shows inhibititory gabaergic horizontal cells and amacrine cells. The horizontal cells connect adjacents synapses between rod/cone cells and bipolar cells, while the latter connect adjacent axons and dendrites of ganglion cells and rod/cone cells. In addition to this oligodendrocytes give axonal extensions to the optic nerve fibers and myelinate them while radial (molar) glial cells are large cells that extend from the outer limiting membrane to the inner limiting membrane.

 

The diagram shows rod receptor on the left and cone receptor on the right. The many folds on their membranes are so that they can absorb maximum light. They contain different pigments due to which rods are sensitive to dim light (roDim) or rhodopic vision while cones are sensitive to bright light or photopic vision.

 

THE RODS, CONES, BIPOLAR AND GANGLIONIC CELLS ARE ALL GLUTAMINERGIC.

TRANSTENTORIAL OR UNCINATE HERNIATION:

 

 

The tentorium cerebelli is an inward fold of the dura matter that separates the cerebrum with the cerebellum from the lateral sides.

Increased cranial pressure in the supra-tentorium (above the tentorium cerebelli) puts pressure on the the insula (between the frontal and temporal lobe) and the insula moves downwards in the notch between the midbrain and tentoriom cerebelli. In the midbrain it damages the following structures from lateral to medial.

The posterior cerebellar artery, the optic tract causing contralateral homonymous hemianopia and the parasympathetic fibers, overstimulates the 3^rd nerve nucleus causing pupillo-constriction. It also pushes the midbrain towards the opposite side, damaging the cortico-spinal fibers of the other side resulting in hemiplegia (paralysis of muscles of the limbs and trunk of one side of the body). The hemiplegia is on the same side as the herniation, although the opposite cortico-spinal tracts are affected because the cortico-spinal tracts of one side innervate the other side of the body. In severe cases the third nerve nucleus may get damaged and there is no innervation to the medial rectus muscle. Thus! The eyeball of the eye on the side of the herniation can not move on the side of herniation.

Kernohans notch is a notch formed in the continuous cerebral peduncle due to damage to some fibers of the peduncle.

In the midline region and paramedian regions of the midbrain arteries and veins rupture causing DURET HEMORAGES.

PAPILLEDEMA:

It is edema in the optic disc in which the optic disc shows a blurred circumference. Due to high intracranial pressure in the subarachnoid space both retinal arteries and veins {that enter across the optic nerve penetrating the dura, arachnoid and pia matter to enter the inside of the eye via the optic disc.} get compressed. When arteries get compressed blood is pushed faster (since blood is moving under high pressure) while when veins are compressed, blood is not allowed to pass through it (since blood is moving under low pressure). Since blood moves faster into the eye through the arteries and cannot be drained by the veins edema or accumulation of fluid takes place in the optic disc. Papilledema may also be caused due to infection.

PTOSIS:
Of the extraoccular muscles of the eye, the superior rectus & superior oblique (collectively called superior tarsal muscles) and the levator palpebrae superioris control the opening and closing of the eyelids.

These muscles are innervated by axons from the 3^rd nerve nuclei and the sympathetic fibers. If these muscles get paralysed due to various reasons, drooping of the eyelids take place, a condition called ptosis.

Disruption of the sympathetic fibers (HORNERS SYNDROME) leads to occulo-sympathetic ptosis.

Disruption of the 3^rd nerve nucleus fibers leads to occulo-sympathetic ptosis.

Neuro-muscular junction disorders such as myasthenia gravis {auto-immune antibodies are produced against the ACH receptors on the post synaptic membrane, blocking them} can also paralyze these muscles leading to occulo-myasthemic ptosis.

DIFFERENCE BETWEEN THE SYMPATHETIC (THORACO-LUMBER OUTFLOW) AND THE PARASYMPATHETIC (CRANIO-SACCRAL OUTFLOW)

 

1.  The sympathetic PREGANGLIONIC CELLBODIES are located in the intermedio-lateral grey horn of the spinal cord at level T1-L2. The parasympathetic PREGANGLIONIC CELLBODIES are located in the cranial nerve nucleus (grey matter of brain) 3, 7, 9, and 10 AND the intermediate grey horn of the spinal cord at level S2-S4. Some may also be seen in the splanchnic nerves.

2.  The sympathetic PREGANGLIONIC AXONS are found in spinal nerves T1-L2 and can also be seen crossing the sympathetic (paravertibral) trunk without synapsing.  The parasympathetic PREGANGLIONIC AXONS are found in cranial nerves 3, 7, 9 and 10 AND sacral nerves of spinal cord S2-S4. They leave their anterior ramus to form PELVIC SPLANCHNIC NERVES. All preganglionic axons are myelinated forming bundles of axons called white rami comunicantes.

3.  The sympathetic POSTGANGLIONIC CELLBODIES are found in either the sympathetic (paravertibral) trunk or the prevertibral plexus (adjacent to the aorta). The parasympathetic POSTGANGLIONIC CELLBODIES are found in the ganglions in the head and neck, cranial nerve autonomic ganglions, and the hypogastric plexus. The pelvic splanchnic nerves innervate the hypogastric plexus.

4.  The POSTGANGLIONIC AXONS of both sympathetic and parasympathetic go to different viscera of the body. Note: the hair follicles are only innervated by the sympathetic postganglionic axons, since they are only contracted, as part of sympathetic response. Bundles of postganglionic axons form the grey rami comunicantes because these axons are non-myelinated.

5.  The primary neurotransmitters released by both sympathetic and parasympathetic preganglionic axons are acetylcholine. The primary neurotransmitter released by postganglionic parasympathetic is also acetylcholine but the ones released by postganglionic sympathetic is NOREPINEPHRINE to all target organs except for the sweat glands to which acetylcholine is released.

Note: acetylcholine released in the synaptic cleft after used is hydrolyzed to acetic acid and choline by enzyme ACETYLCHOLINESTERASE.

6. The sympathetic preganglionic to postganglionic are in the ratio 1:10 while parasympathetic preganglionic to postganglionic are in the ratio of 1:3.

7. The sympathetic postganglionic fibers are longer than the parasympathetic postganglionic because the latter originate from plexus and ganglia around the viscera

 

Note: the preganglionic axons are myelinated, longer and slow conducting B fibers while the post ganglionic fibers are unmyelinated, shorter and slower conducting C fibers.

CLEARING CONCEPTS OF CONUS MEDULARIS, FILUM TERMINALIS AND CAUDA EQUINA.

 

 

In infants the spinal cord extends from the base of the medulla oblongata and terminates between vertibra L4 and L5 of vertebral coloumn. The curved caudal terminal part of the spinal cord is the conus medularis. The pia matter around the conus medularis connects the conus medularis to the innerside of the coccygeal vertibra. In adults the spinal cord ascends in the vertebral column and the conus medularis comes to lie between L2 and L3 vertibra. The pia matter connecting the conus medularis with the coccygeal vertibra now elongates forming the filum terminalis.

Cauda eqina is a collective term given to anterior and posterior roots of the thoracic sacral and lumber nerves.

PHARMACOLOGY OF AUTONOMIC NERVOUS SYSTEM. ALL YOU NEED TO KNOW FROM SNELL NEUROANATOMY.

 

·      Ganglion stimulating agents: bind with nicotinic receptors on post synapting membrane initiating fast EPSP to cause sympathetic or parasympathetic response. Eg: nicotine, lobeline and dimethyl-pipera-zinium.

·      Ganglion inhibiting agents: hexa-methonium and tetra-ethyl-ammonium bind with nicotinic receptors and do not let ACH bind with it. Nicotine in high concentrations bind with nicotinic receptors causing depolarization and maintaining it (depolarization is not followed by repolarization and action potential is not generated). Muscurinic receptors on post synaptic membrane can be blocked by atropine.

·       Stimulation at neuroeffector junction: PHENY-EPHIRINE: alpha receptor stimulator. ALBUTEROL & METAPROTERENOL: beta 2 receptor stimulator causing bonchodilation.

·      Inhibition at neuroeffector junction: alpha receptors can be blocked by phenoxybenzamine while beta receptors can be blocked by propranolol. Reserpin is a drug that does not allow synthesis of norepinephrine inside the postganglionic axon and thus it is not released in the neuroeffector synaptic cleft. {acetylcholine is formed from dopamine inside the postganglionic axon, but dopamine before converting into ACH has to be preserved in a vesicle or else it would be destroyed by monoamine-oxidase (MAO), an enzyme present freely in the cytoplasm of the axon. Reserpin binds with the vesicle and does not allow dopamine uptake and dopamine is destroyed by MAO}. Muscurinic receptors on target organs can be blocked by atropine.

ACETYLCHOLINE AND NOREPINEPHRINE SENSITIVE RECEPTORS ON POSTSYNAPTIC MEMBRANE OF THE PREGANGLIONIC AND POSTGANGLIONIC JUNCTION AND TARGET ORGANS.

 

 

1. On all postsynaptic membranes of the preganglionic and postganglionic junction, cholinergic (acetylcholine sensitive) receptors are present since all preganglionic axons release acetylcholine to the postganglionic axons. There are two types of cholinergic receptors: nicotinic and muscurinic. The nicotinic cause fast action potential while the latter causes slow. The acetylcholine released binds predominantly with the nicotinic receptors on the postganglionic axons causing fast action potential also called fast EXCITORY POST SYNAPTIC POTENTIAL (EPSP). After the fast EPSP has been fired, the acetylcholine may bind with muscurinic receptors on the post synaptic membrane to cause slow EPSP or slow INHIBITORY POST SYNAPTIC POTENTIAL (IPSP).

During EPSP, when ACH (acetylcholine) binds with cholinergic receptors, the Na and Ca channels open causing their influx generating an action potential. During IPSP when ACH binds to muscurinic cholinergic receptors, k channels open causing their efflux resulting in hyperpolarization.

              

2.The target organs posses both adrenergic (noradrenaline sensitive receptors) for the sympathetic response and cholinergic MUSCURINIC receptors for the parasympathetic response. An exception is the receptors on the sweat glands and blood vessels of skeletal muscles which posses cholinergic MUSCURINIC receptors and respond to ACH for SYMPATHETIC response.

 

Note: the muscurinic receptors are found on postsynaptic membrane of the postganglionic axon and the target organs while nicotinic are only found on post synaptic membrane of the post ganglionic axons.

 

Atropine can competitively inhibit muscurinic receptor sensitivity to ACH. 

 

Similarly the axons that release ACH are called cholinergic fibers and those that release Noradrenaline are called adrenergic fibers.

 

There are also 4 types of adrenergic receptors a1 a2, b1 and b2 and are only present on target organs for sympathetic response. A1 is also present on the presynaptic membrane of the neuroeffector junction.

 

All respond to norepinephrine. A1 and a2 on target organs when stimulated cause excitory functions while b1 and b2 cause inhibitory functions. The a1 present on presynaptic membrane is stimulated when there is too much norepinephrine in the synaptic cleft. It inhibits the production of more norepinephrine into the synaptic cleft.

 

All beta receptors cause inhibitory effects (e.g. B2 receptors present on lungs cause bronchodilation) except for the b1 receptors present on myocardium that cause excitory effects.

Note: norepinephrine has a greater effect on alpha receptors than beta receptors.

AUTONOMIC NERVOUS SYSTEM: INTRODUCTION.

AUTONOMIC NERVOUS SYSTEM: INTRODUCTION.

 

The cell bodies of the preganglionic sympathetic axons lie in the intermediolateral grey horn at the level T1-L2 of the spinal cord while the cell bodies of the preganglionic SACRAL parasympathetic axons lie in the intermediate grey horn at the level S2-S4 of the spinal cord.

 

The sympathetic and parasympathetic SACRAL efferents travel in the anterior root of spinal cord, the trunk and the anterior rami. From here it takes different courses.

 

SYMPATHETIC MOTOR PATHWAY

 

1. Each sympathetic efferent leave the anterior ramus and innervate in the sympathetic trunk (paravertibral trunk) at which the preganglionic axons terminate and postganglionic axons begin. The postganglionic axons again enter the same anterior ramus, from where they also go to the posterior ramus to provide both the anterior and posterior body parts. Note that the sympathetic trunks are two, on either side of the spinal cord and lie anterior to the anterior rami of spinal cord so the preganglionic axons from an anterior ramus moves anteriorly innervates the cell body of the postganglionic axon in the sympathetic trunk and then the postganglionic axon again moves posteriorly to join the same anterior ramus (Students Grays. Pg: 44 Fig: 1.45). The sympathetic efferent preganglionic axon may ascend or descend along the sympathetic trunk to innervate a postganglionic cell body at a different level. This postganglionic axon moves posteriorly from the sympathetic trunk to enter the anterior ramus of its own level. The axons also go to the posterior ramus.

2.Some sympathetic efferents after leaving the anterior ramus pass the sympathetic trunk without synapsing and synapse at the prevertibral plexus   (adjacent to the aorta and anterior to the vertebral column, hence the name PRE vertebral), the renal plexus or the adrenal medulla instead. One of the sub divisions of the prevertibral plexus is the celiac plexus. The bundles of preganglionic axons penetrate the diaphragm to synapse at the above mentioned plexus. There are three.

 

·GREATER SPLANCHNIC NERVE: that synapse at the renal plexus, celiac plexus and suprarenal medulla (the suprarenal medulla is a collection of ganglia which release norepinephrine and epinephrine).

 

·LESSER SPLANCHNIC NERVE: that synapse only at the

Renal plexus.

 

·LEAST SPLANCHNIC NERVE: that synapse only at the celiac plexus.

 

The plexus contain a connective tissue capsule, satellite cells, postganglionic cell bodies, efferent and afferent axons (both sympathetic and parasympathetic).

 

The postganglionic axons leaving the renal plexus provide the kidneys and leaving the celiac plexus provides the celiac artery.

 

Note: Each sympathetic trunk has 3 cervical ganglia, 12 thoracic ganglia, 5 lumber and 5 sacral ganglia.

 

PARASYMPATHETIC MOTOR PATHWAY

 

1.The sacral parasympathetic preganglionic efferents after leaving the anterior rami of sacral nerves S2-S4 form the pelvic splanchnic nerves that synapse at the hypogastric plexus from where postganglionic axons innervate the gastro intestinal tract.

2.The cranial parasympathetic preganglionic efferents initiate from the grey matter of the brain stem at level cranial 3, 7, 9 and 10 to form the corresponding cranial nerves. The cranial nerves synapse either at ganglions  in the head and neck or the cranial autonomic nuclei from where postganglionic axons emerge and innervate parts of the head and neck.

 

All efferent preganglioinc axons release acetylcholine.

The parasympathetic postganglionic axons also release acetylcholine but the sympathetic postganglionic mainly release norepinephrine except that to the sweat glands and blood vessels of skeletal muscles, it releases acetylcholine.

 

The parasympathetic and sympathetic postganglionic axons are also seen to release neuropeptide Y, substance P and ATP. These have an inductive effect on the primary neurotransmitters.

 

Apart from the preganglionic and postganglionc neurons, there may be interneurons called small intensely fluorescent cells-SIFs (since they contain catecholamine and shine under light). The SIFs release dopamine.