Tag Archives: Neuroscience

Animal Models in Neuroscience

Invertebrate Models 

The squid giant axon is pretty well renowned for his its applications neuroscience research. J Z Young discovered the giant squid axon and giant squid synapse and was the first to apply it neurophysiological research. The giant squid (loligo pealii) was and is still considered to extrodinarly vital to neuroscience research because of the sheer size of its axon (<1mm). It’s size makes it easy to dissect and support. External and internal perfusion with varying saline levels allowed scientists to determine ion flows in action potential.  Using the giant squid axon, Alan Lloyd Hodgkin and Andrew Huxley won the Nobel Prize in Physiology or Medicine in 1963 for developing Hodgkin–Huxley model mathematical model that describes how action potentials in neurons are initiated and propagated.


In electrophysiology, worms are used as a model for cellular death (apoptosis) and development and are also studied because of their relatively large axon. The C.elegans a nematoda (roundworm) is often studied because its genome, nervous system and genetic regulation of behaviour has been fully mapped. Specifically, these roundworms are an ideal model for apoptosis.

Fruit flies or drosophilia melangosaster have probably come up a fair few times if you have ever taken biology. Fruit flies are used in neuroscience for the identification of genes regulation nervous system development. In particular, the role of pax-6 in the development and evolution of the eye.

Vertebrate Models 


Italian physician Luigi Galvani in his frog studies showed that muscles can be caused to twitch when electrically stimulated.

German physician and physicist Hermann von Helmholtz isolated the nerve conduction velocity to be between a range of 24.6 – 38.4 meters per second.


Ross G. Harrison was the first person to make observations of axonal growth whilst studying tadpoles in vitro.

Katz and Miledi whilst studying frogs observed the role of calcium ions in the release of neurotransmitters.

The neuropsychologist Roger W. Sperry, known for his split-brain research that lead his Nobel Prize in 1981, observed rats and frogs discovering how nerves pathfind.


The domestic chicken (gallus domesticus) have been used again and again the study of brain development because of how easy they are to study. Chickens are so easy to study because of how ‘simple’ it is for scientists to manipulate the embryo. Being able to manipulate the embryo means the scientists have been able to transplant genes, tissue and nerve growth factors to study the effects.

Konrad Lorenz an Austrian zoologist,ethologist, and ornithologist studied imprinting in chicks, which is when an animal comes to believe the first person, thing or animal they see is there mother.


English biologist Steven Rose also used chicks to study passive avoidance learning, which is when a person or animals learns to stop doing a certain behaviour when it results in punishment.

Nichole Le Douarin transplanted regions of nervous system between quails and the domestic chicken to create a chimera, which has led to critical insights into the development of the nervous system and the immune system. Other notable researchers that have worked with the domestic chicken are Viktor Hamburger and Rita Levi-Montalcini.

Mammals and Non-Human Primates

Hitzig and Fritsch both German physicians used dogs to map out the motor cortex of dogs.

Using cats, dogs and apes English neurophysiologist, histologist, bacteriologist, and a pathologist Sir Charles S. Sherrington made huge progress to our current knowledge of reflexes, motor control and localisation in addition to coining the term synapse.

German pharmacologist Otto Loewi who discovered of acetylcholine, used dogs to study chemical neural transmissions. This discovery came from the stimulation of the vagus nerve releasing vagustoff, which caused a reduction  in the heart rate. This vagustoff was later confirmed to be acetylcholine. English neuroscientist Henry Hallett Dale later expanded on this discovery to study the release of ACh from the motor nerves in cats, dogs and frogs. He came up with Dale’s principle that individual nerves release a single neurotransmitter, which of course, was later proved false.

British physiologist John Langley named the autonomic nervous system and studied cats, dogs and rabbits to formulate the receptor theory.

American psychologist Karl Lashley searched for the engram (physical embodiment of memory) using ablations in rats to see how it would affect their memory performance in maze tasks.


To famous psychological experiments involving mammals are those of American psychologist B.F. Skinner and Russian psychologist Ivan Pavlov. Pavlov conducted studies on dogs and coined the term what is now known as classical or passive conditioning via the pairing of stimuli. B.F. Skinner using a ‘Skinner Box’ and rats coined the term active or operant conditioning via reinforcement.

Kuffler (Hungarian-American neurophysiologist), Hubel (Canadian neurophysiologist) and Weisel (Swedish neurophysiologist) worked together on cats and monkey brains to map out receptive fields related visual processing.

Mice transgenics have also widely been used to study molecular dissection of behaviour and diseases in particular in relation to reward systems and development abnormalities.

Non-human primates are of particular interest to neuroscientists because they are of few animals with brains similar to ours, in particular they have a frontal lobe.

Neuroscience: The Action Potential

Action potential is something I find a lot of people who study psychology or neuroscience struggle with. For me, I just could never remember where it was sodium or potassium on the inside or outside of the cell membrane. Luckily, action potential is not as difficult to understand when you break it down into its major subsections.


Action potentials are generated by neurons and are always consistent in size and duration; their strength does not diminish as it propagates down the axon. The strength of the action potential is determined by the frequency it propagates down the axon; the frequency and pattern of the action potentials generate a code used by neurons to transfer information appropriately from one location to another. Neuroscientists use an oscilloscope to study action potential as it sensitive to changes in voltage over time. The action potential works its way down the axon until it reaches the axon terminal. At the axon terminal, a synaptic transmission is initiated.



Generating the Action Potential and All-or-None 

The perception of any sensation such as warmth or pain as well as any movement is the direct result of action potential. Depolarization of the neuron is what is necessary for an action potential to be generated, and it can arise in a variety of ways depending on the kind of neuron. The most common way to depolarize a neuron is by entry of sodium ions. The important thing is that the stimulus is strong enough to depolarize the neuronal membrane. Action potential works on what is known as all-or-none response, meaning it works on a threshold basis. As it is consistent in size, it relies on the stimulus exceeding a threshold called generator potential in order to fire, rather than the strength of the stimulus itself. This may seem confusing because yes, the strength of the stimulus must exceed the threshold , so in a way strength of the stimulus matters. However, what is important to remember is that once the threshold has been exceeded, the strength of the stimulus has no importance or effect on the strength of the action potential whatsoever.

Properties of Action Potential 

The membrane of a neuron at rest is around -65mV or -65 milli-volts with the regard to the outside. Volts is a good indicator that we are dealing with electrical current. During action potential, however, the membrane potential becomes briefly positive. This change from a negative to positive membrane potential is depolarization. Depolarization, a very rapid process, will continue until the membrane potential reaches 40 mV. To give you an idea how rapid the entire process of action potential including reaching back to -65mV it takes 2 milliseconds.

An action potential will only ever travel in one direction because of the refractory period. When the action potential travels away from the soma or cell body towards the axon terminals it is called orthodromic conduction. When the action potential travels towards the soma, the action potential is called antidromic conduction. Regardless of the direction it is traveling, action potential conductance rate varies, but the typical rate is 10m/s. The average length of an axon is about 2cm.

The Process 


1. Resting Potential: As stated before, the resting membrane potential is around -65 mV but it ranges depending on the neuron. Different textbooks will tell you different resting membrane potentials, but it’s not something you need to worry too much about. It is also important to note than Vm or the membrane action potential is equal to 0. Vm=0.

Threshold: The membrane potential at which there stimulus is strong enough to open the sodium channels. The opening of the voltage-gated sodium channels changes the ionic permeability of the membrane in favour of sodium.

2. Depolarisation

3. Rising Phase: As the membrane potential is negative at the resting phase, the opening of the sodium channels creates a great pull. This is because the sodium ions (Na+) are positive. The result is sodium ions rushing into the cell causing rapid depolarisation. This changes the membrane action potential towards the equilibrium value of sodium or ENa.


4. Falling Phase: The voltage-gated sodium channels become inactivated, and in turn the voltage-gated potassium channels open. This time around, there is a great pull on the potassium ions (K+, also positive) outside the cell as the sodium ions have made the membrane potential very positive. Potassium ions rush outside the cell, resulting in a negative membrane potential once more, close to  Eor the equilibrium value of potassium.

Undershoot: The membrane potential is more negative than -65 mV.

Absolute Refractory Period: The cell cannot fire during this period as there is a gradual restoration of the membrane potential back to -65mV and the Vm to 0. During this time, even if the stimulus is strong enough to exceed the threshold, the membrane will not fire. It lasts about 1ms.

Relative Refractory Period: The membrane potential stays hyper-polarised or at the undershoot until the potassium channels close. It can be difficult to initiate another action potential even after the absolute refractory period, longer than 1 ms.

Factors Influencing the Conduction Velocity 


The rate of the action potential depends on the strength of the depolarising current; specifically, it is reflected in firing frequency of the action potential. The maximum frequency, however, is 1000 Hz. Generally, axon potential conduction velocity increases diameter of the axon as well as the size of the axon itself and the number of ion channels. Smaller axons tend to require a much greater stimulus to reach the threshold necessary for depolarisation, as such as they are more sensitive to local anaesthetics.

The Cranial Nerves

cranial nerves


The majority of the cranial nerves emerge from the brain stem on the ventral surface of the brain. Cranial nerves I and II emerge from the forebrain and cranial nerve XI from the brain stem as well as the spinal cord. As they are nerves they are classified as part of the peripheral nervous system; however, two of the cranial nerves are also considered part of the central nervous system, I and II. Each nerve often has fibers performing many different functions. Also they have associated cranial nerve nuclei in the midbrain, pons and medulla of the brainstem.

I. Olfactory: a special sensory cranial nerve responsible for our sensation of smell.

II. Optic: a special sensory cranial nerve responsible for our sensation of vision.

III. Oculomotor: a somatic and visceral motor cranial nerve responsible for the movement of the eye and eyelid as well as the parasympathetic control of pupil size.

IV. Trochlear: a somatic motor cranial nerve responsible for the movements of the eye.

V. Trigeminal: a somatic sensory and motor cranial nerve responsible for the sensation of touch on the face and the muscles of mastication.

VI. Abducens: a somatic motor cranial neuron responsible for the movements of eye.

VII. Facial: a somatic and special sensory cranial neuron responsible for the movement of muscles of facial expressions as well as the sensation of taste in the anterior 2/3 of the tongue.

VIII. Auditory-vestibular: a special sensory motor neuron responsible for the sensation of hearing and balance.

IX. Glossopharyngeal: a somatic and visceral motor cranial neuron as well as a visceral and special sensory cranial neuron responsible for the movement of muscles in the throat and the parasympathetic control of salivary glands in addition to the detection of blood pressure changes in aorta and the sensation of taste in posterior one third of tongue.

X. Vagus: a visceral motor and sensory cranial neuron as well as a somatic motor neuron responsible for the parasympathetic control of heart, lungs and abdominal organs as well as the sensation of pain associated with the viscera and movement of muscles in the throat.

XI. Spinal accessory: somatic motor neuron responsible for the movement of muscles in the throat and neck.

XII. Hypoglossal: a somatic motor cranial neuron responsible for the movement of the tongue.

cranial nerves2


Bear, Mark F., Barry W. Connors, and Michael A. Paradiso. Neuroscience: Exploring the Brain. Philadelphia, PA: Lippincott Williams & Wilkins, 2007. Print.

Depression: Symptoms, Aetiology and Treatment Options


Depression is a serious affective disorder that affects millions of people in the world, approximately 5% of the population. In the United States alone approximately 33 million people will suffer from depression at some point in their life (Bear, 2007). In addition, the disorder is the leading cause of suicide. Despite its high prevalence, however, stigma still also remains high. A primary reason for the stigma surrounding any mental disorder is a misunderstanding of the symptoms and causes.


Even though depression strikes people differently, the cardinal symptoms are lowered mood and feelings of dejection, a lack of pleasure or interest rather than sadness. Accompanying symptoms include changes in appetite, fatigue, insomnia or hypersomnia, diminished concentration, feelings of worthlessness and/or guilt and recurrent thoughts of death and/or suicide (Bear, 2007). Depression can be one half of bipolar disorder but also occur on its own and in varying degrees of severity. Usually, for a diagnosis of major depression, the cardinal symptoms of depression must be present every day for approximately 2 weeks. Importantly, the cause of depression cannot be linked to a bereavement. This clear distinction is what separates depression from sadness.

Types of depression include chronic depression of dysthymia, major or clinical depression, atypical depression and manic depression. Chronic depression or dysthymia is usually less severe than major or clinical depression; however, it can be more disabling in that the symptoms are long-term (2 years+) or recurrent throughout a lifetime. Major or clinical depression is more severe; however, the symptoms do not last longer than 2 years and is not typically recurrent. Approximately 17% of sufferers have chronic symptoms.  It is important to note, however, that when depression is left untreated, recurrence is far more likely. Manic depression is found in bipolar disorder, to find out more click here. Finally, atypical depression is when a person suffers from the accompanying symptoms rather than the cardinal symptoms.

Aetiology and Treatment Options 

Biological basis 

Affective or mood disorders such as depression alter the typical function of the brain. Many different parts of the brain are usually affected at the same time, but the major system involved is the hypothalamic-pituitary-adrenal system (HPA). Exaggerated activity in the HPA system is common in people with anxiety and affective disorders. Specific to depression, blood cortisol levels are heightened as is the concentration of corticotropin-releasing hormones (CRH) in the cerebrospinal fluid.

Monoamine hypothesis

The monoamine hypothesis of depression states that a deficit in monoamines causes mood disorders. Monoamines include serotonin and catecholamines (inc. dopamine, noradrenaline, norepinephrine).  Current anti-depressants focus on this theory of depression. Anti-depressants inhibit the re-uptake of of monoamines, increasing the concentration of them in the synaptic cleft. The great benefit of anti-depressants is that they promote long-term, adaptive changes in the brain reducing the possibility of another depressive episode. Unfortunately, not all depressed people find anti-depressants effective. This can mean that either the treatment does not work for them at all or they require a greater dosage. Furthermore, it can takes week for depressants to take affect. Lastly, anti-depressants can raise levels of norepinephrine, which makes anti-depressants less effective. As anti-depressants are not always effective,  patients with prolonged depressive episodes may seek alternative treatment. Electroconvulsive therapy (ECT) and therapy are both options. ECT is mainly used in extreme cases because it can offer immediate relief. However, ECT is controversial due to the danger of memory loss. This is not surprising considering ECT is a localised seizure controlled by keeping the patient under anaesthesia. It is unknown exactly how ECT works; however, the hippocampus has been implicated. The hippocampus is involved in regulating CRH levels and the HPA system.

Types of anti-depressants include: selective serotonin re-uptake inhibitors, serotonin-noradrenaline re-uptake inhibitors, tricyclic anti-depressants and monoamine oxidase inhibitors. For people with bipolar disorder, lithium is also used to stabilise mood primarily the mania but has been shown stabilise mood overall.

Diathesis-Stress hypothesis 

The diathesis-stress hypothesis proposes that mental disorders have a genetic component that predisposes us to mental illness. Certain life stressors then makes us susceptible to mental illness actually presenting themselves. As such, traumatic childhoods full of abuse and/or neglect can leave a child at high risk for developing mental disorders. Tragically, children whose poor treatment is due to mentally ill caregivers, this cycle becomes hard to break. However, according to the diathesis-stress model, a trigger is not enough to bring forth mental illness without a genetic foundation. This genetic foundation goes hand in hand with the HPA system. Of course this does not mean that only traumatised children will suffer from mental health disorders. Individuals that have experienced a highly stressful life even such as divorce, moving away from home, changing schools, becoming ill, etc. will also be at risk are they predisposed to mental health issues.


In a healthy individual, cortisol activates hippocampal glucocorticoid receptors, which inhibit the the HPA system. However, in a depressed individual there is a flaw in the feedback system. On a molecular level there is a diminished hippocampal response to cortisol due to reduced number of  glucocorticoid receptors. Here the genetic component of depression comes into play; glucocorticoid receptors are the product of gene expression. Hence, an individual with few glucocorticoid receptors is more susceptible. Fittingly, the amount of glucocorticoid receptors are epigentically influenced, early sensory experience can alter the number as well. This means that a childhood where we are well looked after, loved, cared for, kept safe and happy can protect us from developing depression even if we disposed to at birth. This illustrates how important the interaction of nature and nurture is. Think Voldemort vs Harry Potter. Despite the traumatic death of his parents, the one year of unconditional love and Lily’s sacrifice protected him not just magically but neurologically. Interestingly, in an interview with Oprah Winfrey, JK Rowling discuss this exact point.



Antidepressants . (n.d.). Antidepressants. Retrieved July 18, 2014, from http://www.nhs.uk/conditions/Antidepressant-drugs/Pages/Introduction.aspx

Bear, M. F., Connors, B. W., & Paradiso, M. A. (Eds.). (2007). Neuroscience(Vol. 2). Lippincott Williams & Wilkins.

Pinel, J. P. (2010). Biopsychology (8th ed., International ed.). Harlow: Pearson Education.

What the Heck is an HPA Axis & What Does it Have to do with Stress?. (n.d.). About.com Fibromyalgia & Chronic Fatigue. Retrieved July 18, 2014, from http://chronicfatigue.about.com/od/cfsglossary/g/hpa_axis.htm

Bipolar Disorder

My most recent post showcased the artist Isti Kaldor who has bipolar disorder. This post will explain the basics of the disorder. Quite a few celebrities have come forward stating they have bipolar disorder including Catherine Zeta Jones, Demi Lovato and Stephen Fry. If you want to know the true scope, there is a wikipedia page dedicated to celebrities known to have it. Despite their very public work lives, with our limited insight into their personal lives it is difficult to really know much about the disorder. Stephen Fry, however, did a brilliant documentary on his experiences dealing with his bipolar disorder called Stephen Fry: The Secret Life of the Manic Depressive, which is available in full on YouTube.

Symptoms and Types 

As the title says, bipolar disorder is sometimes also called manic depression, but bipolar disorder is its official name. Characterised as a recurrent mood disorder, it consists of repeated episodes of mania interchanged with episodes of depression. The depressive episodes include similar but less severe symptoms of major depression such as changes in appetite, insomnia or hypersomnia, fatigue, feelings of worthlessness, guilt, inability to concentrate and suicidal thoughts. As such, the symptoms can be managed with anti-depressants. The manic periods, however, are the opposite in some respects. Symptoms consist of grandiosity, decreased need for sleep, talkativeness, flight of ideas, short attention span, and impaired judgement. It is believed that the correlation between bipolar disorder and celebrities is that those with the disorder usually experience these manic highs with bursts of creativity and inspiration. Unfortunately, the manic period can also result in promiscuity and complete loss of inhibition much like the effects of alcohol. As with any disorder, the range and complexity of symptoms varies greatly from person to person.

Bipolar comes in two general forms: type I and type II. Type I is marked by manic episodes (with or without incidents of major depression), and occurs in about 1% of the population, equally among men and women. Type II is marked by hypomania (milder form of mania that is not associated with marked impairments in judgment of performance) and is always followed by milder depressive periods.


Numerous twin studies and most notably the one conducted by McGuffin and colleagues (2003) have shown that there is a high concordance between monozygotic twins with “67% MZ vs. 19% DZ.” Also, even though there is a high correlation with depression and mania, the manic component appears to be significantly more heritable in monozygotic twins. We do know that bipolar disorder affects our neurochemical pathways as treatment of lithium and anti-depressants do help alleviate the drastic mood swings. However, the actual structural component is yet to be properly determined. Studies by Bearden et al., 2001 admit that even though “dysfunction is implicated in bipolar illness patients supported by reports of relatively greater impairment in visuospatial functioning, lateralization abnormalities, and mania secondary to RH lesions” there is still not enough conclusive evidence to draw a clear link between right hemisphere dysfunction and bipolar disorder.

Strakowski et al., 2005 on the other hand using MRIs have found compelling examples of damage to the prefrontal cortical areas, striatum and amygdala that predates that onset of symptoms, which suggests that abnormal brain structure could in fact play a quintessential role in onset of the disease. Furthermore, if further studies can confirm these findings, it could offer psychiatrists and neurologists a revolutionary way of pre-symptomatic diagnosis. As of 2012, Strakowski et al. have reached a “general consensus” that bipolar type I occurs due to abnormalities within networks that control emotional behaviour such as the prefrontal cortex and limbic area, specifically the amygdala.


To date the most effective treatments for bipolar disorder include lithium (used to target the manic episodes), anti-depressants such as SSRIs, monoamine oxidase and tricyclics. Other types of medication such as anti-anxieties and anti-psychotics are used in some cases depending on the severity of the symptoms. In addition to medication, therapy has also been proved to significantly reduce the psychological stress of the disorder.


Bear, Mark F., Barry W. Connors, and Michael Paradiso. Neuroscience: Exploring the Brain. Baltimore, MD: Lippincott Williams & Wilkins, 2006. Print.

Bearden, C. E., Hoffman, K. M. and Cannon, T. D. (2001), The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review. Bipolar Disorders, 3: 106–150. doi: 10.1034/j.1399-5618.2001.030302.x

Malliaris, Yanni,. “1.7 Aetiology of Bipolar Disorder.” 1.7 Aetiology of Bipolar Disorder. BipolarLab.com, 20 Aug. 2010. Web. 03 Aug. 2013.

Strakowski, S. M., Adler, C. M., Almeida, J., Altshuler, L. L., Blumberg, H. P., Chang, K. D., DelBello, M. P., Frangou, S., McIntosh, A., Phillips, M. L., Sussman, J. E. and Townsend, J. D. (2012), The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disorders, 14: 313–325. doi: 10.1111/j.1399-5618.2012.01022.x

Introduction to Basal Ganglia: Anatomy and the Motor Loop

To begin with…


Studies have shown that the motor loop through the basal ganglia helps initiate conscious movement. One model has shown that furthered inhibition of the thalamus via the basal ganglia underlies what is known as hypokinesia or the reduction of movement. Contrarily, decreased output by the basal ganglia leads to hyperkinesia or the excess of movement.

Now the basal ganglia consists of several structures ,which includes the caudate nucleus, the putamen, the globus pallidus and the subthalamic nigra. Some neuroscientists also include the substantia nigra as part of the basal ganglia even though technically it is part of the midbrain. This is because the substantia nigra plays a quintessential role in the control of movement. Together with the putatmen, the caudate nucleus makes up the striatum, which is the target of cortical input to the basal ganglia. The globus pallidus controls output to the thalamus, which helps create a loop of information from the cortex back to the cortex.


Motor Loop 

A simplified version of the motor loop:

Cortex -> Striatum -> Globus pallidus -> Thalamus -> Cortex

The impulse that drives the motor loop originates from the cortex (the frontal, parietal and prefrontal) and forms an excitatory connection with the putamen. The putamen cells then form an inhibitory connection with neurons in the globus pallidus, which then forms an inhibitory connection with the thalamus. More specifically, a part of the thalamus known as the ventral lateral nucleus or VLo. The VLo then forms the thalamocortical connection with the supplementary motor area or SMA, which is a medial region of cortical area 6 that directly sends axons to motor units.


This may seem counter-intuitive. Why would an inhibitory signal cause the activation of a motor unit? Well, basically at rest, neurons in the globus pallidus are active. Because the neurons globus pallidus are active, this inhibits the activity of the neurons in the thalamus, specifically in the VLo. So, when the impulse from the cortex excites the putamen, the neurons globus pallidus are inhibited. The inhibition of these neurons allows the VLo to become active or excited. The activation of the neurons in the VLo sends neural activity via the thalamocortical connection to the SMA.


Bear, Mark F., Barry W. Connors, and Michael A. Paradiso. Neuroscience: Exploring the Brain. Philadelphia, PA: Lippincott Williams & Wilkins, 2007. Print.

The Brain: Lower-Level Brain Structures

On average humans have a 1:45 ratio between brain to body. This implies that there is a correlation between intelligence and brain to body ratio. However, there are exceptions to this implied correlation. In fact, intelligence is better gauged by the complexity of brain structures.

Primitive vertebrates like sharks, only have structures for basic survival functions – breathing, resting, and feeding. Lower mammals such as dogs are slightly more complex with a brain allowing for emotion and memory. Humans have structures that enable all basic functions, memory, emotion but also structures for information processing and foresight.

The brainstem is the oldest part of the brain as well as central core of it. It begins where the spinal cord swells as it entres the skull; the brainstem is vital for basic automatic survival functions.

  • The medulla is the base of the brainstem: controlling heart rate and breathing.
  • The brainstem-crosser over point is where the nerves from the opposite sides of the body meet.
  • The reticular formation is the nerve network in the brainstem that extends up to the thalamus. It plays an important role in controlling arousal (control of consciousness), specifically our sleep cycle. Other vital roles of the reticular formation includes motor control, visceral control (instinctual), and sensory control.
  • The pons or “bridge” connects the medulla with the cerebral cortex. In addition, the pons helps connect the right and left hemisphere as well controlling autonomic functions such as arousal.
  • The thalamus is the brain’s “sensory switchboard,” located on top of the brainstem. It directs messages to the sensory receptive areas in the cerebral cortex and transmits responses from the sensory areas to the cerebellum and medulla.

brain stem

The cerebellum or the “little brain” is attached to the rear of the brainstem and helps coordinate voluntary movement and balance. The cerebellum of kind of nonverbal memory and learning. It also manages sustaining functions with the spinal cord.

The limbic system is at the border of the brainstem and the cerebral hemisphere and is associated with emotions and drives.

  • The amygdala consists of two almond shaped clusters that influence aggression and fear.
  • The hypothalamus sits below the thalamus and directs maintenance activities such as appetite, thirst and body temperature. Furthermore, it helps govern the endocrine system via the pituitary gland.

Neuroscientists and neuropsychologists can stimulate the pleasure centres in our brain to calm patients. It is also understood that addictive drugs trigger our pleasure system.

brain basic and limbicHow Nootropics Impact the Brain

A class of supplements and drugs called “nootropics” can have a positive impact on parts of the brain. Drugs like piracetam have displayed resistance to adverse brain conditions such as cerebral hypoxia. These nootropic compounds have a affinity brain tissue in the hippocampus and cortex. Nootropic supplements, such as Ashwagandha, can be found online from sites such as fitpowders.com and amazon.com.