Neurons & Neurotransmission

We have all experienced the reflex reaction when we accidentally touch something hot. But did you know how fast the nerve impulse that conducts this response is? It is estimated that the speed of a neural impulse can reach up to 120 meters/second or 268 miles/hour! That is much faster than the top speed of any of our cars, unless one of us is lucky enough to own a supercar like the one below. Impressive isn’t it?


Records of studying the nervous system dates back to Egyptian manuscripts from 1700 BC. However, major breakthrough discoveries were made in the field of Neuroscience in the late 19th century, and finally in 1906, Golgi and Ramón y Cajal shared the Nobel Prize in Physiology or Medicine in recognition of their work on the structure of the nervous system. A neuron, or a nerve cell, is one of the two main components of the central nervous system (glial cells are the other type).

Unlike other cells in the body, a neuron is a specialized cell (with great powers!) that is capable of conducting electrical and chemical signals in a process known as neurotransmission. A typical neuron is divided into three parts: the soma or cell body, dendrites and axon. While there are as many as 10,000 different types of neurons in the human brain, they can be broadly classified into three types: motor neurons (for conveying motor information), sensory neurons (for transmitting sensory information), and interneurons (which convey information between different types of neurons).



Synapses are the junctions where neurons pass signals to other neurons, muscle cells, or gland cells. Synaptic signals from other neurons can be received either by the soma, dendrite or axon, whereas signals to other neurons are transmitted only by the axon. The typical synaptic cleft (cell-to-cell distance) can vary between 3.5 nm to 40 nm (compare that to the thickness of your hair which is more than 250 times wider!). Thus the nervous system is wired by numerous neurons interconnected by synapses in a super-complicated neuronal circuit. It is estimated that the human brain alone contains around one hundred billion neurons and one hundred trillion synapses!
There are two main types of synapses, chemical and electrical. Electrical synapse is an electrical connection between neurons through structures known as gap junctions. Gap junctions are intercellular channels that allow ions and small molecules to pass directly from one cell to the other. On the other hand, in a chemical synapse, signals are transmitted via release of neurotransmitters (that are packed in synaptic vesicles in the presynaptic neuron) into the synaptic cleft. Binding of the neurotransmitters to receptors in the postsynaptic membrane causes activation of this cell through the post synaptic density (a protein dense signaling apparatus). Depending on the type of effect the neurotransmitter has on the postsynaptic cell, a chemical synapse can either be excitatory or inhibitory.

The fundamental process that triggers the release of neurotransmitters is the action potential, which is an electrochemical wave that travels along the axon of a neuron when there is a change in the membrane potential. Neurons maintain a steady resting voltage gradient (typically from –70 to –80 millivolts) across their membranes via ion channels and ion pumps.

In response to an external stimulus, when enough voltage-dependent positive ion channels such as sodium or calcium channels are activated, they allow a net inward sodium or calcium current which depolarizes the cell to a threshold potential above the resting potential and this triggers the neuron to fire. Eventually, the sodium/calcium channels inactivate and the potassium/chloride channels are activated which results in an outward current of positively charged potassium ions/inward current of negatively charged chloride ions causing the neuron to repolarize and hyperpolarize and ultimately return to the resting state.

Neuron Fun Fact

Neurons are cells within the nervous system that transfer info to other nerve cells, muscle, or gland cells. Most neurons have a cell body, an axon, and dendrites. The cell body includes the nucleus and cytoplasm. The axon extends from the cell body and often gives rise to many smaller branches before ending at nerve terminals. Dendrites extend from the neuron cell body and receive messages from other neurons. Synapses are the contact points where one neuron communicates with another. The dendrites are covered with synapses formed by the ends of axons from other neurons.

Read : Sensory Neuron

The brain is what it is because of the structural and functional properties of interconnected neurons. The mammalian brain consists of between 100 million and 100 billion neurons, depending on the species. Each mammalian neuron contains a cell body, dendrites, and an axon.

The cell body contains the nucleus and cytoplasm. The axon extends from the cell body and often gives rise to many smaller branches before ending at nerve terminals.

Dendrites extend from the neuron cell body and receive messages from other neurons. Synapses are the contact points where one neuron conveys with another. The dendrites are covered with synapses formed by the ends of axons from other neurons.


When neurons receive or send messages, they transmit electrical impulses along their axons, which can range in length from a tiny fraction of an inch (or centimeter) to three feet (about one meter) or more. Many axons are covered with a layered myelin sheath, which accelerates the transmission of electrical signals along the axon. This sheath is made by specialized cells called glia. In the brain, the glia that make the sheath are called oligodendrocytes, and in the peripheral nervous system, they are known as Schwann cells.

The brain consists of at least ten times more glia than neurons. Glia perform many jobs. Researchers have known for a while that glia transport nutrients to neurons, clean up brain debris, digest parts of dead neurons, and help hold neurons in place. Current research is uncovering important new roles for glia in brain function.

Sensory Neuron

Sensory neurons, also known as afferent neurons, are neurons in the nervous system, that convert a specific type of stimulus, via their receptors, into action potentials or graded potentials. This process is called sensory transduction. The cell bodies of the sensory neurons are located in the dorsal ganglia of the spinal cord.

The sensory information travels along afferent nerve fibers in a sensory nerve, to the brain via the spinal cord. The stimulus can come from exteroreceptors outside the body, for example those that detect light and sound, or from interoreceptors inside the body, for example those that are responsive to blood pressure or the sense of body position.

Centra nervous syatem

Types and Function

Different types of sensory neurons have different sensory receptors that respond to different kinds of stimuli. There are at least six external and two internal sensory receptors:

  1. External receptors 

External receptors that respond to stimuli from outside the body are called exteroreceptors. Exteroreceptors include olfactory receptors (smell), taste receptorsphotoreceptors (vision), hair cells (hearing), thermoreceptors (temperature), and a number of different mechanoreceptors (stretch, distortion).


The sensory neurons involved in smell are called olfactory sensory neurons. These neurons contain receptors, called olfactory receptors, that are activated by odor molecules in the air. The molecules in the air are detected by enlarged cilia and microvilli.

These sensory neurons produce action potentials. Their axons form the olfactory nerve, and they synapse directly onto neurons in the cerebral cortex (olfactory bulb). They do not use the same route as other sensory systems, bypassing the brain stem and the thalamus. The neurons in the olfactory bulb that receive direct sensory nerve input, have connections to other parts of the olfactory system and many parts of the limbic system.


Similarly to olfactory receptorstaste receptors (gustatory receptors) in taste buds interact with chemicals in food to produce an action potential.


Photoreceptor cells are capable of phototransduction, a process which converts light (electromagnetic radiation) into electrical signals. These signals are refined and controlled by the interactions with other types of neurons in the retina. The five basic classes of neurons within the retina are photoreceptor cellsbipolar cellsganglion cellshorizontal cells, and amacrine cells.

The basic circuitry of the retina incorporates a three-neuron chain consisting of the photoreceptor (either a rod or cone), bipolar cell, and the ganglion cell. The first action potential occurs in the retinal ganglion cell. This pathway is the most direct way for transmitting visual information to the brain. There are three primary types of photoreceptors: Cones are photoreceptors that respond significantly to color. In humans the three different types of cones correspond with a primary response to short wavelength (blue), medium wavelength (green), and long wavelength (yellow/red). Rods are photoreceptors that are very sensitive to the intensity of light, allowing for vision in dim lighting.

The concentrations and ratio of rods to cones is strongly correlated with whether an animal is diurnal or nocturnal. In humans, rods outnumber cones by approximately 20:1, while in nocturnal animals, such as the tawny owl, the ratio is closer to 1000:1.  Retinal ganglion cells are involved in the sympathetic response. Of the ~1.3 million ganglion cells present in the retina, 1-2% are believed to be photosensitive.

Different kinds of neurons. structure of a typical neuron

Problems and decay of sensory neurons associated with vision lead to disorders such as:

  • Macular degeneration – degeneration of the central visual field due to either cellular debris or blood vessels accumulating between the retina and the choroid, thereby disturbing and/or destroying the complex interplay of neurons that are present there.
  • Glaucoma – loss of retinal ganglion cells which causes some loss of vision to blindness.
  • Diabetic retinopathy – poor blood sugar control due to diabetes damages the tiny blood vessels in the retina.


The auditory system is responsible for converting pressure waves generated by vibrating air molecules or sound into signals that can be interpreted by the brain.

This mechanoelectrical transduction is mediated with hair cells within the ear. Depending on the movement, the hair cell can either hyperpolarize or depolarize. When the movement is towards the tallest stereocilia, the Na+ cation channels open allowing Na+ to flow into cell and the resulting depolarization causes the Ca++ channels to open, thus releasing its neurotransmitter into the afferent auditory nerve. There are two types of hair cells: inner and outer. The inner hair cells are the sensory receptors .

Problems with sensory neurons associated with the auditory system leads to disorders such as:

  • Auditory processing disorder – Auditory information in the brain is processed in an abnormal way. Patients with auditory processing disorder can usually gain the information normally, but their brain cannot process it properly, leading to hearing disability.
  • Auditory verbal agnosia – Comprehension of speech is lost but hearing, speaking, reading, and writing ability is retained. This is caused by damage to the posterior superior temporal lobes, again not allowing the brain to process auditory input correctly.


Thermoreceptors are sensory receptors, which respond to varying [temperature]s. While the mechanisms through which these receptors operate is unclear, recent discoveries have shown that mammals have at least two distinct types of thermoreceptors. The bulboid corpuscle, is a cutaneous receptor a cold-sensitive receptor, that detects cold temperatures. The other type is a warmth-sensitive receptor.

Read; Neuron Fun Fact


Mechanoreceptors are sensory receptors which respond to mechanical forces, such as pressure or distortion.

Specialized sensory receptor cells called mechanoreceptors often encapsulate afferent fibers to help tune the afferent fibers to the different types of somatic stimulation. Mechanoreceptors also help lower thresholds for action potential generation in afferent fibers and thus make them more likely to fire in the presence of sensory stimulation.

Some types of mechanoreceptors fire action potentials when their membranes are physically stretched.

Proprioceptors are another type of mechanoreceptors which literally means “receptors for self”. These receptors provide spatial information about limbs and other body parts.

Nociceptors are responsible for processing pain and temperature changes. The burning pain and irritation experienced after eating a chili pepper (due to its main ingredient, capsaicin), the cold sensation experienced after ingesting a chemical such as menthol or icillin, as well as the common sensation of pain are all a result of neurons with these receptors.

Problems with mechanoreceptors lead to disorders such as:

  • Neuropathic pain – a severe pain condition resulting from a damaged sensory nerve 
  • Hyperalgesia – an increased sensitivity to pain caused by sensory ion channel, TRPM8, which is typically responds to temperatures between 23 and 26 degrees, and provides the cooling sensation associated with menthol and icillin.
  • Phantom limb syndrome – a sensory system disorder where pain or movement is experienced in a limb that does not exist.2. Internal receptorsInternal receptors that respond to changes inside the body are known as interoceptors.
  • Blood

    The aortic bodies and carotid bodies contain clusters of glomus cells – peripheral chemoreceptors that detect changes in chemical properties in the blood such as oxygen concentration. These receptors are polymodal responding to a number of different stimuli.


    Nociceptors respond to potentially damaging stimuli by sending signals to the spinal cord and brain. This process, called nociception, usually causes the perception of pain. They are found in internal organs as well as on the surface of the body to “detect and protect”. Nociceptors detect different kinds of noxious stimuli indicating potential for damage, then initiate neural responses to withdraw from the stimulus.

    • Thermal nociceptors are activated by noxious heat or cold at various temperatures.
    • Mechanical nociceptors respond to excess pressure or mechanical deformation, such as a pinch.
    • Chemical nociceptors respond to a wide variety of chemicals, some of which signal a response. They are involved in the detection of some spices in food, such as the pungent ingredients in Brassica and Allium plants, which target the sensory neural receptor to produce acute pain and subsequent pain hypersensitivity.

    Connection with the central nervous system

    Information coming from the sensory neurons in the head enters the central nervous system (CNS) through cranial nerves. Information from the sensory neurons below the head enters the spinal cord and passes towards the brain through the 31 spinal nerves. The sensory information traveling through the spinal cord follows well-defined pathways. The nervous system codes the differences among the sensations in terms of which cells are active.

Cholinergic Basal Forebrain Neurons

The integrity of cholinergic basal forebrain neurons depends on expression of Nkx2-1  categories:

The transcription factor Nkx2-1 belongs to the homeobox-encoding family of proteins that have essential functions in prenatal brain development. Nkx2-1 is required for the specification of cortical interneurons and several neuronal subtypes of the ventral forebrain. Moreover, this transcription factor is involved in migratory processes by regulating the expression of guidance molecules. Interestingly, Nkx2-1 expression was recently detected in the mouse brain at postnatal stages.

Using two transgenic mouse lines that allow prenatal or postnatal cell type-specific deletion of Nkx2-1, we show that continuous expression of the transcription factor is essential for the maturation and maintenance of cholinergic basal forebrain neurons in mice. Notably, prenatal deletion of Nkx2-1 in GAD67-expressing neurons leads to a nearly complete loss of cholinergic neurons and parvalbumin-containing GABAergic neurons in the basal forebrain.

We also show that postnatal mutation of Nkx2-1 in choline acetyltransferase-expressing cells causes a striking reduction in their number. These degenerative changes are accompanied by partial denervation of their target structures and results in a discrete impairment of spatial memory.

Article by: Lorenza Magno, Oliver Kretz, Bettina Bert, Sara Ersözlü, Johannes Vogt, Heidrun Fink, Shioko Kimura, Angelika Vogt, Hannah Monyer, Robert Nitsch and Thomas Naumann.

Read the full article on Wiley Online Library.

Tips for Immunohistochemistry

educationImmunohistochemistry is like cooking. There are many recipes out there, but some of them do not work out well. However, when they do, they are great! You need the right ingredients, a dose of experience, a few tricks from old cooks, and a grain of common sense. Read more to learn about traps to avoid, and important information to report when you publish your findings.

The problem

The validity of scientific results depends to a large extent on the use of appropriate methods providing the required precision and sensitivity, as well as controlled specificity of reagents and procedures. This statement is particularly valid for immunohistochemistry, where sensitivity and specificity of the antibodies, as well as technical procedure are crucial to avoid false-positive and false-negative results.

When using immunohistochemistry, several factors can cause false-negative or false-positive results and all should be verified as much as possible in each experimental set-up used. In particular, primary antibodies can fail to detect their target antigen even if the antigen is present in the tissue for many reasons, including conformation changes induced by fixation/embedding, steric hindrance by interacting proteins/post-translational modifications, low affinity of the antibody for the target, or failure of the antibody to penetrate into the tissue. Conversely, antibodies can bind non-specifically to other targets or tissue components. This observation holds true for both primary and secondary antibodies.

The problem is further confounded by the vast literature describing various procedures – such as the use of distinct “blocking” reagents and antigen-retrieval – to minimize these pitfalls and ensure high-fidelity binding of antibodies. This makes it difficult to choose the adequate method, and testing alternatives can be laborious. However, blindly following an established protocol might prove insufficient. It requires considerable experience, rational thinking and evidence from other methods to determine whether a given staining pattern obtained by immunohistochemistry is likely specific or non-specific. For instance, antibodies directed against a synaptic protein should produce no staining of the cell nucleus (unless this protein plays an additional, previously not described role in this compartment). In such case of wrong labeling, either the antibody or the staining protocol may be unsuitable.

Read: Sensory Neuron

The solutions

Here, we provide a practical guide of what should be tested and what should be reported in order to provide convincing evidence for the validity of immunohistochemical experiments. This includes dealing with the three main steps that can lead to false negative and false positive results:

Detection of the antigen of interest by the primary antibody
Detection of the primary antibody by secondary antibodies
Tissue preparation

1) Primary antibody specificity

The most stringent specificity test is performed in tissue devoid of the antigen of interest (knockout mouse). When not feasible, the best alternative is to show that two antibodies raised against different epitopes of the antigen of interest yield the same staining pattern. A third control includes inactivation of the antibody by incubation with its antigen prior to use for immunohistochemistry. This control does not exclude, however, that several targets sharing a common epitope are detected by this antibody. If doubts remain, additional information about the expression and localization of the antigen of interest should be provided by alternative methods.

As a consequence of the requirement by the Journal of Comparative Neurology to provide detailed characterization of primary antibodies, there is now a large collection of commercially-available antibodies that fulfill these criteria. To avoid unnecessary duplication, the Journal of Comparative Neurology has published an Antibody database listing all these products, which can be considered as being well characterized. Keep in mind, however, that polyclonal antibodies can vary considerably in their affinity and specificity from batch to batch, even when sold under the same catalog number. Every new batch ought to be tested to avoid bad surprises.

2) Secondary antibody specificity

Secondary antibodies are raised against immunoglobulins (typically IgGs) of the species in which primary antibodies were raised. As they are used in fairly high concentration, the likelihood that they bind non-specifically to tissue components (extracellular matrix proteins, blood vessels, etc) is higher than for primary antibodies. Further, they might cross-react with IgGs from other species, which is particularly relevant in multiple-labeling experiments. To minimize cross-reactivity, whenever available, it is best to use highly cross-adsorbed secondary antibodies.

Influence of immunoglobulins in lesioned tissue. Immunoperoxidase staining with secondary antibody binding to IgGs potentiated by tissue lesion. Sections were stained for a marker of microglia in the mouse hippocampus following injection of kainic acid. Left: section from wild-type mouse; Right: section from mouse devoid of IgGs (Zattoni et al., 2011)

To test for specificity, secondary antibodies should be applied in the absence of primary antibodies: all residual staining can be considered as being non-specific. In immunofluorescence experiments, beware of possible autofluorescent molecules that may be contained in tissues, their presence can be detected best in the absence of secondary antibodies. Note, however, that non-specific binding to tissue components depends both on the antibody and the tissue type. Embryonic/neonatal brain tissue has much more non-specific binding than adult tissue, and lesions, which cause damage to the blood-brain-barrier and leakage of serum proteins into brain parenchyma, also increase non-specific binding of secondary antibodies. The same can be said for weak tissue fixation over extended time (e.g., poor perfusion-fixation, fixation by immersion, etc.).

3) Influence of tissue preparation

Relative to antibody specificity, this issue is more versatile and complex and it can result in both, false-positive and false-negative results, even when using highly specific and well-characterized antibodies. As noted above, these effects arise mainly from epitope masking due to fixation-induced conformational changes and failure of the antibody to penetrate the tissue, as well as from non-specific binding of secondary antibodies, which can mask the specific signals. Furthermore, it needs to be emphasized that when antibodies do not recognize or do not have access to their epitope, they will typically bind non-specifically to other tissue components, and therefore produce false-positive results. Finally, it is important to realize that control tests performed with knockout tissue only provide information about false-positive results, but not false-negatives.

There are a number of published examples of pitfalls resulting from the influence of tissue preparation, notably fixation and the need in some cases, to use stringent methods for unmasking epitopes, in particular for postsynaptic proteins (Fritschy et al., 1998; Watanabe et al., 1998; Lorincz & Nusser, 2008).

The following aspects should be considered, when aiming at improving immunohistochemistry procedures because of apparent false-negative or false-positive results produced by an antibody. Typically, a compromise between preservation of the (ultra)-structure and staining sensitivity should be sought.

Reduce (or enhance) tissue fixation: type of fixative, pH, concentration, duration of the fixation (and postfixation), use of additives (e.g. picric acid). These effects are age-dependent (neonatal, but not adult, brain tissue benefits from a longer postfixation) and related to the nature of the antigen (soluble proteins tend to diffuse away in weakly fixed tissue).
When fixation has deleterious effects, consider using weak fixation by brief immersion of tissue slices or tissue sections, as described in detail in (Schneider Gasser et al., 2006).
Antigen-retrieval methods (e.g., heating/boiling tissue in acidic buffer; enzymatic digestion).
Use of detergent or repeated freeze/thaw to enhance penetration of the antibodies into the tissue.
Use of blocking solutions before and during primary antibody incubation. Note that in perfusion-fixed tissue, good results can be obtained without any pre-blocking step (see Fritschy & Mohler, 1995).
Temperature and duration of incubation in primary antibody and secondary antibody solution, as well as duration of the rinsing steps between antibody solutions. Here, an increase in signal-to-noise ratio can be achieved, sometimes with striking reduction of non-specific binding to tissue components.
Standard perfusion-fixation for detection of neurochemical markers. Double immunofluorescence staining for calbindin (green), a cytoplasmic marker of Purkinje cells and vesicular glutamate transporter type 2 (red), a marker of climbing fiber terminals. Staining was performed on perfusion-fixed, free-floating tissue sections (Fritschy et al., 2006).
High sensitivity detection of postsynaptic markers by antigen-retrieval (pepsin treatment). Double-immunofluorescence staining for postsynaptic markers (green; left, PSD-95; right, gephyrin) and presynaptic markers (red; left, vesicular glutamate transporter type 1; right, vesicular GABA transporter) in the hippocampus. Staining was performed using pepsin-mediated antigen retrieval. See Tyagarajan et al., 2011 for details.
Combined detection of soluble cytoplasmic protein (eGFP) and postsynaptic markers in weakly fixed tissue. Triple-immunofluorescence staining showing the presence of GABAergic postsynaptic proteins – GABAA receptor a2 subunit (red) and gephyrin (blue) – in relation to newborn granule cells in the olfactory bulb, selectively expressing eGFP (green) upon transduction with a lentivirus. The combination of eGFP and gephyrin immunofluorescence was achieved by preparing live tissue slices that were briefly fixed by immersion in a paraformaldehyde solution; see Panzanelli et al., 2009 for details.

Submitting to EJN

In the Author guidelines, EJN emphasizes the need to provide enough information in the Materials and Methods section to enable proper evaluation of the results and reproduction of the data. With regards to immunohistochemistry, detailed information about the antibodies used and about control experiments validating their specificity and the sensitivity of the method is mandatory. Authors should indicated which exact antibody was used (catalog and batch number, species of origin, immunogen information) and should provide information on the characterization of the antibody (description -or reference to experiments previously reported- performed to test its specificity, see EJN author guidelines). These requirements are in line with the policy of the Journal of Comparative Neurology, which refuses publication of articles that do not provide detailed characterization of antibodies used for immunohistochemistry. EJN encourages its contributors to consult the antibody database of the Journal of Comparative Neurology when selecting antibodies for experiments and when reporting their use in their manuscripts.

Despite these pitfalls of immunohistochemistry, only a minority of articles submitted to EJN fulfills these explicit requirements of the author guidelines. In 2008, in order to improve this situation, EJN published a technical spotlight emphasizing the necessity to check whether negative findings (failure to detect the antigen of interest in the sample analyzed) might be due to the method – in particular, tissue fixation – used for analysis (Fritschy, 2008).

We hope this article will help you to prepare and analyze your immunohistochemistry experiments. Please feel free to ask questions!

Useful resources:

The antibody database of the Journal of Comparative Neurology

Is my antibody staining specific? (Fritschy and Sarter, 2008)


Fritschy, J.M. (2008) Is my antibody-staining specific? How to deal with pitfalls of immunohistochemistry. Eur. J. Neurosci., 28, 2365-2370.

Fritschy, J.M. & Mohler, H. (1995) GABAA-receptor heterogeneity in the adult rat brain: differential regional and cellular distribution of seven major subunits. J. Comp. Neurol., 359, 154-194.

Fritschy, J.M., Panzanelli, P., Kralic, J.E., Vogt, K.E. & Sassoè-Pognetto, M. (2006) Differential dependence of axo-dendritic and axo-somatic GABAergic synapses on GABAA receptors containing the a1 subunit in Purkinje cells. J. Neurosci., 26, 3245-3255.

Fritschy, J.M., Weinmann, O., Wenzel, A. & Benke, D. (1998) Synapse-specific localization of NMDA- and GABAA-receptor subunits revealed by antigen-retrieval immunohistochemistry. J. Comp. Neurol., 390, 194-210.

Lorincz, A. & Nusser, Z. (2008) Specificity of immunoreactions: the importance of testing specificity in each method. J. Neurosci., 28, 9083-9086.

Panzanelli, P., Bardy, C., Nissant, A., Pallotto, M., Sassoè-Pognetto, M., Lledo, P.M. & Fritschy, J.M. (2009) Early synapse formation in developing interneurons of the adult olfactory bulb. J. Neurosci., 29, 15039-15052.

Schneider Gasser, E.M., Straub, C.J., Panzanelli, P., Weinmann, O., Sassoè-Pognetto, M. & Fritschy, J.M. (2006) Immunofluorescence in brain sections: simultaneous detection of presynaptic and postsynaptic proteins in identified neurons. Nature Protocols, 1, 1887-1897.

Tyagarajan, S.K., Ghosh, H., Yevenes, G.E., Nikonenko, I., Ebeling, C., Schwerdel, C., Sidler, C., Zeilhofer, H.U., Gerrits, B., Muller, D. & Fritschy, J.M. (2011) Regulation of GABAergic synapse formation and plasticity by GSK3beta-dependent phosphorylation of gephyrin. Proc. Natl. Acad. Sci. USA, 108, 379-384.

Watanabe, M., Fukaya, M., Sakimura, K., Manabe, T., Mishina, M. & Inoue, Y. (1998) Selective scarcity of NMDA receptor channel subunits in the stratum lucidum (mossy fibre-recipient layer) of the mouse hippocampal CA3 subfield. Eur. J. Neurosci., 10, 478-487.

Zattoni, M., Mura, M.L., Deprez, F., Schwendener, R., Engelhardt, B., Frei, K. & Fritschy, J.M. (2011) Brain infiltration of leukocytes contributes to the pathophysiology of temporal lobe epilepsy. J. Neurosci., 31, 4037-4050.