Posts Tagged ‘ glutamate ’

Surviving Anoxia

Introduction

Oxygen comprises a large proportion of our atmosphere (21%) and has become a vital gas for many organisms on Earth. Without it our ability to produce energy (as ATP) via aerobic respiration fails. Oxidative phosphorylation, the primary method of aerobic ATP production, produces large amounts of ATP (from our glycogen stores) just as long as we are able to continually supply O2. Without oxygen we resort to anaerobic respiration, where the primary method of ATP production is glycolysis. In comparison to oxidative phosphorylation, the amount of ATP produced is minimal.

Whilst we take oxygen for granted in our environment, there is a large variety of situations where oxygen levels are limited, or where oxygen is completely absent. Typically, such conditions arise in aquatic environments where the ability of oxygen to diffuse is greatly reduced and oxygen levels depend heavily on the ability of organisms to photosynthesise. Yet many respiring organisms are able to live in these environments due to adaptations to low oxygen/ zero oxygen situations.

When referring to the content of oxygen in an environment, we usually state its partial pressure i.e. the proportion of the total gas which comprises oxygen. At sea level, the total pressure of the gases in the environment is 101kPa (or 1 atmosphere), as oxygen makes up 21% of these gases, the partial pressure of oxygen at sea level is 21kPa.

From this we can define four terms:

Hyperoxia (>21kPa)  – When oxygen levels are greater than normal

Normaxia (21kPa)      – When oxygen levels are normal

Hypoxia (<21kPa)      – When oxygen levels are below normal

Anoxia (0kPa)              – When oxygen is completely absent

Why We Require Oxygen

Aerobic Respiration

The major role of oxygen is to provide the body with metabolic energy in the form of ATP. This is done during aerobic respiration via a process known as oxidative phosphorylation which occurs within the inner mitochondrial membranes. The role of oxygen in this process is to act as a terminal electron acceptor. The transfer of electrons to oxygen provides enough energy to phosphorylate ADP to ATP.

However, for oxygen to form ATP in this manner, there are a number of prerequisites. Glucose (a 6-carbon molecule) must be readily available, if it is not it must be mobilised from the body’s glycogen stores. There are 3 major steps which occur before oxidative phosphorylation:

Glycolysis – Glucose is metabolised into 2 molecules of pyruvate (a 3-carbon molecule). This provides a small amount of ATP as well (2 per glucose molecule).

Pyruvate is metabolised into 2 molecules of Acetyl CoA (a 2-carbon molecule). One molecule of carbon is lost as CO2.

The Krebs cycle – Each molecule of acetyl CoA undergoes a number of enzyme-catalysed reactions producing a number of highly energised electrons. These electrons are used in the electron transport chain to produce vast amounts of ATP.

Anaerobic respiration

However, oxygen isn’t always available. In this situation, respiration may continue but it can go no further than glycolysis. As a result, the ATP yield per molecule of glucose alters dramatically:

Glycolysis Krebs Cycle Oxidative Phosphorylation
Aerobic 2 2 34
Anaerobic 2 0 0

Anaerobic Glycolysis

The efficiency of ATP production drops to around 5% during anaerobic reproduction. One way the body can cope with this is to increase the glycolytic rate (the rate of glycolysis). Increasing the glycolytic rate by about 20x returns the level of ATP production to that seen in aerobic respiration. This is known as the Pasteur Effect.

There are of course negative effects as a result of this:

Increasing the glycolytic rate causes a rapid drop in the body’s store of glycogen. Without glycogen, the body will be unable to perform any form or respiration – anaerobic or not, which will inevitably lead to death.

The Krebs cycle stops soon after oxygen becomes absent. This means there is no demand for acetyl CoA. The result of this is excess production of pyruvate. Lactate dehydrogenase converts the excess pyruvate to lactate (and also recycles NADH + H+ to NAD+ allowing glycolysis to continue). A build up of lactate is also undesirable however as it immediately dissociates into lactic acid. The low pH of lactic acid will begin to reduce cellular pH and denature sensitive enzymes.

Decreasing Cellular pH

As a result of decreased pH and ATP, maintaining the membrane potential becomes very difficult. The Na/K ATPase pump which actively removes N+ from the cell and uptakes K+ in order to maintain the correct (-70mV) membrane gradient, stops functioning when ATP production diminishes. The maintained -70mV gradient begins to equilibrate at 0mV, causing a breakdown of the transmembrane gradient within a matter of minutes.

This has dire consequences on the mammalian brain in particular; the change in the membrane potential allows calcium ions to enter the cell. Intracellular calcium causes cell damage and hastens enzyme breakdown. The breakdown of these important brain cells causes permanent brain damage and if not supplied with oxygen quickly enough, will lead to death.

Strategies to Survive Anoxia

To survive anoxic conditions, an organism must be able to deal with the problems associated with anaerobic respiration; keeping up ATP levels (particularly in the brain) and avoiding acidification and associated cellular damage. Two organisms which are highly adapted to surviving anoxic conditions are; the crucian carp and the painted turtle. Both have different strategies for maintaining the body without oxygen, but both do so by combating the associated problems with anaerobic respiration.

Glycogen Stores in the Crucian Carp

One of the problems with anaerobic respiration is that, after a short time in anoxia, glycogen levels decrease rapidly. The Pasteur effect (where glycolytic rate increases for a short period to accommodate the lack of ATP production from oxidative phosphorylation) is only temporary. All body stores of glycogen are quickly depleted and the body is no longer able to survive.

The crucian carp (and to a smaller extent the painted turtle) has an unusually large glycogen reserve in the liver (30% of the total liver mass). Such large stores of glycogen allow the crucian carp to survive in anoxia by glycolysis alone for a much longer period of time.

The crucian carp will typically only face anoxic conditions during the winter months, when a thick layer of ice forms over the water sources they inhabit. Because of this, the crucian carp has adapted to build up glycogen stores throughout the year so that come winter, the glycogen stores are as great as possible. To do this, during the warmer summer months, instead of using carbohydrates for energy (i.e. Glucose / glycogen) lipids are used, allowing the crucian carp to build glycogen stores.

Metabolic Depression in the Crucian Carp

Although increased glycogen stores length the period of time the crucian carp is able to survive in anoxic conditions, it is not the only factor which prolongs this survival period. Metabolic depression means slowing down the rate at which the body consumes ATP, so combining reduced ATP requirements with greater stores of glycogen to produce ATP ensures a near maximum survival time in anoxia.

To reduce metabolic rate, locomotion is reduced during anoxia this means muscles use as little energy as possible. Also, some sensory functions are suppressed, these include vision and hearing. During the winter months when anoxic conditions arise, the thick layer of ice above reduces light levels to a minimum so vision is not a necessity.

Crucian carp will also induce voluntary hypothermia during anoxia. This is actually beneficial to the carp because at lower temperatures, metabolic rate decreases. Therefore when anoxic conditions arise, the crucian carp will swim to cooler waters to reduce their metabolism.

Avoiding Acidification in the Crucian Carp

The problem with glycolysis is the production of lactate and hence lactic acid, causing a decrease in cellular pH and thus acidification. If the crucian carp is producing ATP from glycolysis alone then cellular concentrations of lactic acid would normally quickly rise and pose a major threat for the carp. However, instead of producing lactate as the end product of glycolysis, the crucian carp has adapted to produce ethanol.

By producing ethanol instead of lactate, the crucial carp benefits in a number of ways. Primarily ethanol is non-acidic and thus will not decrease intracellular pH (therefore avoiding the associated damage to the cell as a result of acidification). Ethanol is also lipid soluble meaning it will not build up in the body as it is easily excreted across the gills.

Normally, during glycolysis, pyruvate is metabolised to acetyl CoA by pyruvate dehydrogenase – producing lactate as the end product. Yet a mutation in the pyruvate dehydrogenase enzyme of the crucian carp means that instead of acetyl CoA, acetaldehyde is produced. Acetaldehyde is then metabolised by alcohol dehydrogenase to produce ethanol.

However, the brain is unable to produce ethanol in this manner, only skeletal muscle can. Any glycolysis occurring in the brain will therefore produce lactate as the end product. This lactate however, is transported via the blood, to the skeletal muscle. Here, the lactate is turned into pyruvate where glycolysis will metabolise it into ethanol, it is subsequently excreted across the gills.

Avoiding Acidification in the Painted Turtle

The painted turtle deals with anoxia in a different way to the crucian carp. Whereas the crucian carp has very large glycogen stores and avoids acidification by producing ethanol, the painted turtle favours metabolic depression. Although the crucian carp also depresses its metabolism, it is on a much smaller scale. The crucian carp is still aware and the brain functions as normal. The painted turtle on the other hand becomes almost ‘comatose’ as many more body systems are shut down.

The painted turtle must too deal with the excess of lactate produced during glycolysis to avoid acidification. The painted turtle produced lactate as the end product of glycolysis and does not have the ability to form ethanol from pyruvate. To avoid acidification, it must therefore buffer the low pH of the lactic acid.

To buffer the lactic acid, the painted turtle uses bicarbonate and carbonate. The turtle has large stores of these in its shell (which has a rich blood and nerve supply). The carbonates are able to ‘mop up’ excess H ions (which make the blood acidic) and through a number of reactions, the carbonate and H ions and turned into carbon dioxide and water.

The shell is also a rich store of calcium ions. These calcium ions are able to bind with lactate and the resulting molecule becomes stored in the shell until it is possible to excrete the lactate during aerobic respiration.

This method of avoiding acidification is arguably not as efficient as the crucian carp (producing non-acidic ethanol) but it does help the turtle to avoid acidification for a much longer period of time than would normally be possible.

Metabolic Depression in the Painted Turtle

The painted turtle is able to survive anoxia for such extended periods of time due to the amazing amount at which it is able to decrease its metabolic rate by (90-95%). All non-essential systems are shut down which causes the turtle to become ‘comatose’ as the brain becomes quiescent. Even essential systems such as protein synthesis cut their ATP demand drastically. However on system reduces its ATP demand as little as possible -the Na/ K ATPase pump.

As we know, if the Na/ K ATPase pump stops functioning, then the transmembrane gradient breaks down due to the leakage of Na & K ions across the membrane. This allows calcium ions to enter the cell and cause fatal destruction if normoxic conditions are not resumed. However, the painted turtle is not able to maintain 100% efficiency of this pump during anoxia due to the large demand of ATP it requires. Its efficiency is essential cut down to 25%.

To combat the reduction in the ATPase pump’s efficiency a phenomenon known as ‘Channel Arrest’ occurs. This allows the retention of the transmembrane gradient. Normally Na & K are able to leak into and out of a cell via transmembrane ion channels, down their respective concentration gradients. However during channel arrest these ion channels are forced to close greatly decreasing the amount of ion leakage into and out of the cell. This essentially counteracts the 4-fold reduction in the ATPase pump’s efficiency and allows for the preservation of the transmembrane gradient – thus preventing cell damage.

Another phenomenon of the painted turtle which allows for further depression of the metabolic rate is ‘Spike arrest’. This inactivates Na & K ion channels normally associated with producing action potentials. However as these channels are inactivated the action potential threshold becomes greatly elevated – thus forcing the brain into a quiescent state and preventing responses to stimuli.

The Role of Neurotransmitters and Metabolites

Certain molecules are involved with mediating the transition to an anoxic state. The main ones are the neurotransmitters; glutamate and GABA as well as the metabolite adenosine.

Adenosine release is associated with low levels of oxygen. When low blood oxygen is detected, adenosine is released shortly after. The immediate result is an increase of cerebral blood flow. This decreases soon after in the painted turtle as the metabolic rate is lowered – however as the crucian carp remains ‘active’ during anoxia, cerebral blood flow does not reduce.

Adenosine is basically responsible for ensuring ATP production is able to meet demand as it is responsible for a number of factors contributing to the metabolic depression associated with anoxia. It blocks the production of glutamate (an excitatory neurotransmitter) and has been found to suppress protein synthesis and down-regulate NDMA receptor activity.

The NDMA receptor is highly permeable to Ca2+ ions, which are responsible for cell damage in anoxic conditions of unspecialized organisms. Normally in anoxic conditions excessive glutamate over-stimulates this receptor and causes a massive influx of calcium ions into the cell. Therefore the ability of adenosine to down regulate this receptor is highly beneficial during anoxia.

GABA and glutamate are highly related neurotransmitters; GABA is an inhibitory neurotransmitter and glutamate an excitatory neurotransmitter. During anoxia, we see a steady rise in GABA and a steady decline in glutamate. An initial steep rise of GABA in the painted turtle is due to increased levels of adenosine (released at low blood oxygen levels). Because GABA is an inhibitory neurotransmitter it is able to effectively reduce the amount of ATP the body requires, as the painted turtle reduces its metabolism by 90-95% we see very large amounts of GABA released. Release of GABA is seen in the crucian carp too, but as the carp remains active, GABA levels observed are much more modest.

Conclusion

Effectively we see two different strategies for combating anoxic conditions. The painted turtle, although it has larger glycogen stores than other animals, chooses to reduce its metabolism by such a large amount that it becomes almost comatose. This is achieved by Spike arrest, channel arrest, nearly a total suppression of nervous activity and a huge increase in extracellular inhibitory neurotransmitter, GABA. The limiting factor of how long the painted turtle can remain in anoxia is therefore the build-up of lactate. Although it is steadily removed and stored in the shell, it eventually builds up enough to reduce cellular pH to fatal levels if normoxic conditions are not returned.

The crucian carp on the other hand has glycogen stores so large it is able to survive on glycolysis alone at a metabolic rate not too far below normal. In terms of metabolic depression the crucian carp only moderately suppresses nervous activity, coupled with moderate release of GABA and suppression of locomotor activity (as well as voluntary hypothermia to decrease metabolic rate further). The key strategy for survival is the production of the non-acidic glycolytic end product – ethanol, thus preventing cellular pH from falling to fatal levels. Because of this, the limiting factor of anoxia survival in crucian carp is therefore the amount of glycogen stored in the liver.

Summary

Crucian Carp Painted Turtle
Activity level during anoxia Slightly reduced Comatose, quiescent brain
Production of ATP from glycolysis Great Above average
Glycogen storage Great Above average
End product of glycolysis Ethanol Lactate (Lactic acid)
Blood pH and cellular pH Stable (ethanol is non-acidic) Slowly rises when uptake of lactate decreases
Overall metabolic depression 70% 90-95%
ATP levels and membrane potential of the brain Maintained at normoxic levels – Brain function is preserved Maintained at normoxic levels – Brain function is preserved
Suppression of neuronal activity Above average Great
Channel & Spike Arrest No Yes

Special Senses – Vision

Introduction

The eye is the organ of vision. The main cells responsible for beginning the process of converting light (of varying wavelengths) into an interpreted image we can ‘see’ are photoreceptors. These cells respond to the stimulus of light and are located in the innermost layer of the eye – the retina.

The eyeball itself can be split into three layers:

  1. The sclera – The protective, fibrous outer coating of the eye which also helps to maintain the eyeball’s globe shape. The sclera layer also includes the cornea, which helps to focus light onto the retina.
  2. The uvea – A vascular and pigmented layer consisting of the following:
    1. Choroid – Darkly pigmented to prevent light escaping the eye, it contains blood vessels which supply all the internal structures of the eyeball.
    2. Tapetum Lucidum – A triangular area containing light reflecting cells found behind the retina in some species (e.g. cats); it helps to reflect light back to the retina, especially useful in low light situations.
    3. Ciliary body – Contains the smooth ciliary muscles which control lens thickness and shape.
    4. Suspensory ligament – Supports the perimeter of the lens.
    5. Iris – Contains radial and circular smooth muscles which control the opening of the pupil to regulate the amount of light entering the eye and to prevent damage.
  3. The retina – The lens focuses light onto the photoreceptor cell of this innermost layer of the eye. The information which the photoreceptors receive is transmitted to the brain via the optic nerve (II). The image arrives at the photoreceptor cells inverted due to the way the lens focuses the light, however the brain processes the image so we see it the correct way up. The retina also consist of several layers:
    1. Pigmented layer – Prevents light leaking out from the eye, synergising with choroid of the uvea to produce a greater effect.
    2. Photoreceptors – There are two types of photoreceptors, both with different shapes and functions, these are:
      1. i.      Rods – Sensitive even in low light conditions but they only provide black and white vision. This makes them useful for night vision. High sensitivity, low acuity.
      2. ii.      Cones – Only sensitive in well light conditions, but they are able to provide colour vision. Low sensitivity, high acuity.
    3. Bipolar neurones – Receive the raw information from the rods and cones and transmit this to the ganglion cells. One neurone can serve multiple rods/cones.
    4. Horizontal/ Amacrine cells – Located between the rods/ cones and the ganglion cells, they are situated amongst the bipolar neurones. Their role is to integrate the visual information received from the rods/ cones before it is sent to the brain.
    5. Ganglion cells – Each bipolar neurone synapses with a ganglion cell. When an action potential is generated from rod/cones stimulation, it is transmitted down the axons of the ganglion cells.

Light enters the eye through the cornea, pupil and then lens. The lens focuses the image onto the retina. Photoreceptor cells of the retina are stimulated by the light sending nerve impulses from the rods/cones through bipolar neurones to the ganglion cells. The axons of the ganglion cells travel across the surface of the retina towards the optic disc at the centre of the retina. The nerves from all the ganglion cells bundle together at the optic disc to form the optic nerve (II). There are no rods or cones located on the optic disc. From the optic nerve (II) information is carried to the primary visual cortex of the cerebral hemispheres located at the rear of the brain. This is where the light information is finally interpreted as an image.

Species Differences

There are certain differences which are observed between different species, a few of these are listed below:

  1. Pecten – Birds contain an organ within their vitreous humour (the jelly-like substance which fills the eye cavity). It is thought that the pecten both nourishes the retina and controls the pH of the vitreous body. It is present in all birds and some reptiles.
  2. Shape – The actual shape of the eyeball itself may vary between species. For example humans have a globe shaped eyeball, whereas horses have a non-spherical, almost cuboidal eyeball. This allows for more than one fovea (the area of the retina which provides maximum acuity).
  3. Fovea – As above, the size, shape and number of fovea may differ between species.
  4. Pupils – The shape and size of pupils also differs between species. Humans have round pupils, whereas cats for example have pupils shaped as vertical slits.

Diseases of the Retina

There are a many diseases which can affect the retina. Some common examples found in animals are:

  • Collie eye anomaly (CEA) – a congenital, inherited, bilateral eye disease of dogs involving the retina, choroid, and sclera. It can be a mild disease or cause blindness. CEA is caused by a simple autosomal recessive gene defect. There is no treatment.
  • Progressive retinal atrophy (PRA) – a group of genetic diseases seen in certain breeds of dogs and more rarely, cats. It is characterised by the bilateral degeneration of the retina, causing progressive vision loss culminating in blindness. The condition in nearly all breeds is inherited as an autosomal recessive trait. PRA can be considered similar to retinitis pigmentosa in humans.
  • Retinopathy – a general term that refers to some form of non-inflammatory damage to the retina of the eye. Cats experience ‘Taurine Deficient Retinopathy,’ a lack of taurine in the diet of the cat leads to the degeneration of the photoreceptors. Cat food is therefore supplemented with taurine.

Photoreceptor Cells

As mention earlier, the photo receptor cells are rods and cones. Cones are associated with colour vision but are not sensitive in low light, whilst rods are – but they have low acuity and provide only black and white vision.

The initial steps for photoreceptors in perceiving light requires the use of a chemical called rhodopsin, found in rod cells it can be broken down into the protein opsin and a small molecule retinal (Derived from retinol – vitamin A). Rhodopsin is extremely sensitive to light, enabling vision in low-light conditions. When exposed to light, the pigment immediately photobleaches breaking down into opsin and retinal. The breakdown of rhodopsin causes a secondary messenger cascade (phototransduction) eventually resulting in the information reaching the visual cortex.

Similar to rod cells, cone cells contain a rhodopsin like pigment called iodopsin or photopsin. Just like rhodopsin, photopsin contains opsin and retinal except the opsin component varies slightly by a few amino acids. These slight changes allow them to absorb different wavelengths of light. In humans there are three extra opsins each tuned to different wavelengths:

  • Opsin S – Blue, wavelengths 400-500nm
  • Opsin M – Green, wavelengths 450-630nm
  • Opsin L – Red, wavelengths 500-700nm

The three colour photopsins work together in bright light, to give colour vision. Species which utilise:

  • Only one photopsin are called monochromats
  • Two – dichromats
  • Three – trichromats
  • Four – tetrachromats (Opsin R – its range overlaps with all the opsins)

In summary the differences between the two types of photoreceptor are:

  • Rods – Black & white (night) vision, high sensitivity, low acuity, uses rhodopsin = opsin + retinal
  • Cones – Colour vision, low sensitivity, high acuity, uses photopsin/iodopsin = retinal + opsin S (blue) OR opsin M (green) OR opsin L (red) (OR opsin R – Tetrachromats)

Phototransduction

Phototransduction covers the process of how the photoreceptors send information to the brain. The process is as follows:

  • Photoreceptors in the absence of light release the neurotransmitter glutamate. When light falls on the photoreceptors they stop releasing glutamate.
  • cGMP is bound to sodium channels in the plasma membrane of the rods. It keeps the sodium channels open and maintains a membrane potential of around -40mV
  • Opsin is a G-Coupled Protein Receptor which spans the membrane of discs located just inside of the rods.
  • When light reaches rhodopsin, it causes opsin to isomerise (change from a cis to trans shape).
  • The now active form of rhodopsin activates a G protein called transducin.
  • Transducin in turn activates the enzyme phosphodiesterase
  • The active enzyme phosphodiesterase hydrolyses cGMP to CMP, causing it to detach from the sodium channel, thus the sodium channel closes.
  • As sodium can no longer enter into the rod, the membrane potential decreases to -70mV causing the rod to hyperpolarise. Glutamate is no longer released.
  • Bipolar cells which synapse with the rods may generate an action potential when glutamate is no longer being released across the synaptic cleft.

Glutamate may act as either an excitatory or inhibitory molecule to the bipolar neurone which synapses with the rod. This gives rise to ‘on’ and ‘off’ bipolar cells.

The ‘on’ bipolar cells are activated by light – therefore glutamate was acting as an inhibitor as glutamates inhibition (caused by light hitting the rod) activates the bipolar cell.

The ‘off’ bipolar cells are deactivated by light – glutamate was therefore acting as an excitatory molecule. Light prevents glutamate being released which was stimulating the bipolar cell.

Receptive Fields and Lateral Inhibition

Ganglion cells only detect light from a region known as its receptive field. The receptive field is split into the field centre and the field surround. Basically forming two concentric circles, these circles representing regions at which light is detected.

Some ganglion cells will only generate action potentials when the centre field is lit. (On centre cells) Whilst the others only generate an action potential if the surround field is lit. (Off-centre cells)

With receptive fields alone, images would appear blurry. The process of lateral inhibition aids this process to form sharp images. Lateral inhibition is the ability of a neuron to reduce the activity of its neighbours. In terms of vision this means ganglion cells receiving a moderate or low amount of light (yet still enough to generate an action potential) which contribute to blurry images, can be inhibited by neighbouring neurons which are receiving greater light stimulus. The brain is able to perceive sharper images from this information.

It is believed the horizontal and amacrine cells discussed earlier are involved in this process. Horizontal cells being involved in sustained lateral inhibition and amacrine cells believed to be involved with transient lateral inhibition.

The Visual Pathway

As you know, light enters through the lens and is focused on the retina. From there it is detected by photoreceptor cells which synapse with bipolar cells. These bipolar cells synapse with ganglion cells. The axons of the ganglion cells group together at the centre of the retina to form the optic disc. This goes on to form the optic nerve (II).

From the optic nerve (II) the majority of axons are directed to the lateral geniculate nucleus (via the optic chiasm and the optic tract) in the thalamus. The lateral geniculate nucleus (LGN) acts as the primary processing centre for visual information received by the retina. The neurones of the LGN send their axons through the optic radiation to the primary visual cortex.

There is a visual cortex for each hemisphere of the brain, both located at the very back of the brain. The left hemisphere visual cortex receives signals from the right visual field and the right visual cortex from the left visual field. Within the visual cortex, groups of ‘simple cells’ (receptive areas) join to form ‘complex cells’ which are able to detect particular shapes.

From the visual cortex, information is sent to the cortex in the temporal lobe; here it is connected to a response i.e. recognising a face, performing a task etc.

Development of Vision

Studies have been conducted on animals to determine how they cope with monocular deprivation:

“It was confirmed that suturing the lids of one eye (monocular deprivation), until only 5 weeks of age, leaves virtually every neurone in the kitten’s visual cortex entirely dominated by the other eye. On the other hand, deprivation of both eyes causes no change in the normal ocular dominance of cortical neurones, most cells being clearly binocularly driven.

Kittens were monocularly deprived until various ages, from 5 to 14 weeks, at which time reverse suturing was performed: the initially deprived right eye was opened and the left eye closed for a further 9 weeks before recording from the visual cortex.

Reverse suturing at 5 weeks caused a complete switch in ocular dominance: every cell was dominated by the initially deprived right eye. Reverse suturing at 14 weeks, however, had almost no further effect on ocular dominance: most cells were still driven solely by the left eye. Animals reverse sutured at intermediate ages had cortical neurones strongly dominated by one eye or the other, and they were organized into clear columnar groups according to ocular dominance.

Thus, between 5 weeks and 4 months of age, there is a period of declining sensitivity to both the effects of an initial period of monocular deprivation and the reversal of those effects by reverse suturing.” Blakemore, C., Van Sluyters, R.C. Reversal of the physiological effects of monocular deprivation in kittens: Further evidence for a sensitive period (1974) Journal of Physiology, 237 (1), pp. 195-216.

As it states, this shows how important early development of the visual system is. Other experiments have also been conducted, where animals have been brought up in closed environments, which for example contain only vertical lines. After development, when the animal is released from this environment it is not able to process horizontal lines. It is therefore unable to perceive these lines.