Pituitary
The different functions performed by the anterior and posterior pituitary in terms of sex
The anterior pituitary which is also known as the adenohypophysis, is basically an interior lobe (glandular) which alongside the posterior pituitary, makes up the pituitary gland. The posterior pituitary releases oxytocin which stimulates and smooth muscle contraction in the mammary glands and the uterus. The anterior pituitary on the other hand stimulates release of thyroid hormones, FSH and LH to stimulate sex cell production and release of sex hormones; it also stimulates sex cell production as well as secretes prolactin to stimulate milk production. In addition, the posterior pituitary which is a small extension of the hypothalamus with neurosecretory cells that create 2 hormones that are stored and later released by the posterior pituitary. Among its functions are; Antidiuretic hormone that prevents loss of water in the body and the Oxytocin which triggers uterine contractions during delivery and when breastfeeding.
The posterior pituitary is the true glandular part of the pituitary gland. Its functions are controlled by inhibiting hormones and releasing hypothalamus’ hormones. It produces six hormones; Follicle stimulating hormone (FSH). This hormone stimulates gonad’s cells for the production of gametes (sperms in males and ova in females). Luteinizing hormone stimulates gonads in order to produce sex hormones (testosterone in males and estrogens in female). The thyroid stimulating hormone is basically a tropic hormone which is responsible for stimulations of the thyroid gland. In terms of sex, prolactin has numerous effects on the body, its main function is to stimulate the mammary glands of the breast to produce milk. The anterior pituitary stimulates release of thyroid hormones, FSH and LH to stimulate sex cell production as well as the release of sex hormones and the posterior pituitary on the other hand inhibits hormones and releasing hypothalamus’ hormones. However, the regulatory functions of the posterior pituitary are majorly achieved through secretions of certain peptide hormones which acts on target hormones and glands including gonads (Starr, 2012, p. 115).
Epilepsy
- What are the neurological underpinnings of epilepsy at a micro and macro level
At a macro level, neurological underpinnings of epilepsy bring about the latest advances in neuroimaging functional brain networks that are applied in epilepsy. Simultaneous electroencephalography and functional magnetic resonance imaging (EEG-FMRI) are used for non-invasively map activities in epileptiform at millimeter resolution throughout the brain. With the growing array of molecular tests that are now available in the epilepsies, physicians pretty much need to know the actual tests that are needed by each patient. The most important clinical group of genetic testing is the epileptic encephalopathies, a test with a cumulative number of characteristic epilepsy syndromes being recognized. Currently, the political underpinnings of human disease are being expanded in epilepsy. For instance, advanced technological research is promising to identify all the molecular defects which contribute to epilepsy’s genetic architecture.
At a micro level, the discovery of molecules has been illuminated by clinical genetic studies which largely include genetic, for instance, the GGE (genetic generalized epilepsies) which can influence by genetic factors. Presumably, GGE accounts for close to 30% of all cases associated with epilepsy and they seem to be the most challenging groups in the field of epilepsy genetics to solve. This is due to the fact that they follow the complex inheritance and numerous genes are most likely to contribute whether with or without an environmental or acquired component (Bennett, 2008, p. 245).
The GGE is composed of well-defined syndromes such as generalized tonic-clonic seizure, childhood absence epilepsy, juvenile myoclonic epilepsy and juvenile absence epilepsy. In addition to these definitions, it is much arguable that at a clinical level, molecular testing is very useful. On the other hand of the normal self-limited focal and generalized epilepsies, there are numerous monogenic syndromes that are severe where molecular testing plays a key role today in clinical practices. The epileptic encephalophies for instance, which primarily begin in childhood and infancy is very significant. Among its examples is; epilepsy limited to female with mental retardation, dravet syndrome and specific infantile spasms phenotypes. In such settings, causative genetic mutation setting which is in contrast to vulnerability change or variation identifies the causes of the child’s disorder. With all the advancement in technology and identification of more molecular causes, it is much likely that almost all patients with epilepsy could have certain mutations such as monophonic denovo providing an alternative explanation for various cases with GGE.
- How do GABA agonists work to decrease symptoms
Primarily, Gamma-Amino Butyric acid (GABA) basically acts as a neurotransmitter in the nervous system reducing particular nerve signals. As the principal inhibitory neurotransmitter, GABA maintains the inhibitory tone which offsets neuronal excitation. It mainly controls nervous signals in the central nervous system and in the retina, therefore insufficient GABA normally causes epileptic seizure and a lot of anxiety. These activities are enhanced by inhibition of adult neurons as the immature neurons are excited. In addition to this, seizures that are generated with functional GABAergic synapses in the immature hippocampus include fast oscillations which are needed in transforming a simple network to that of epilepsy. As the most abundant neurotransmitter in the nervous system particularly in the cerebral cortex where sensation is interpreted, GABA regulates nervous signals particularly in the central nervous system and in the retina. It has a quieting influence on epilepsy as it inhibits nerve transmission in the brain thereby calming the nervous system which heightens epilepsy. Some recreational and medical drugs reduce the natural level of GABA which include; barbiturates, alcohol and marijuana. GABA is quite unique to the nervous system of mammals. In addition, hypnotics and many sedatives are GABA agonists.
In order to decrease symptoms, GABA agonists hinder the transmission of nerve impulse from a neuron to the other. Basically, GABA has quite an opposite personality; it greatly relaxes the mind by calming nerves that enhance seizure. It influences the absence of seizure/epilepsy through the following mechanisms; GABA receptors cause tonic inhibition by responding to ambient GABA which could be obstinately active at seemingly low levels. Normally, disorders caused by a seizure are predominantly characterized by low levels of GABA. Oral GABA greatly inhibits tremors and seizure which present the extreme end of nervous system over-stimulation.
- How does split brain/callosotomy work to decrease symptoms
Callosotomy which is also known as split-brain surgery is sometimes an option to be considered on occasions when a person with uncontrollable and extreme forms of epilepsy affects all the two sides of the brain. A corpus callosotomy exposes the brain using a certain procedure known as a craniotomy. It is after the patient is put to sleep with anaesthesia that the surgeon removes a piece of bone and then pulls a section of the dura back by making an incision in the scalp. It's basically done to separate the sides of the brain (hemispheres). For instance, a serious type of seizure known as a drop attack causes the person to fall suddenly with high risk of energy. This surgery helps the hemispheres share information and it also enhances the spread of seizure impulse from both sides of the brain at intervals. Primarily, callosotomy is an operation that cuts the corpus callosum thereby causing interrupting the binge of seizures from one hemisphere to another.
Unlike other procedures such as the epilepsy-treating procedures, callosotomy does not involve the removal of brain tissues. To begin with, this procedure is basically a partial callosotomy such that, it involves the removal of 2/3 of the corpus callosum if the original removal did not decrease the seizures as intended. One Certain seizure spread to parts or originate from various parts of the brain that are responsible for particular functions including movement of the language. Removal of these could lead to loss of language function or paralysis. In some cases case, this procedure takes a different turn and it takes two stages. During the first operation, 2/3 of the structure is cut while the back section is well-maintained allowing the hemispheres to continue sharing visual information. Is the serious seizure does not feel this effect, and then in the second operation, the corpus callosum that remains can be cut. Due to this process, seizures normally become less severe since they cannot spread to opposite both sides of the brain.
Marijuana
Why marijuana possesses much less of a health risk than alcohol
Both alcohol and marijuana have very different and complex actions on the brain. All the same, alcohol is by far more dangerous compared to marijuana. It alters brain chemistry and affects neurotransmitters of the brain. It is both psychologically and physically addictive. Neurologists suggest that though marijuana appears to me very dangerous, it is does not quite affect brain cess to a great extent as alcohol does. Many people die from alcohol use but nobody dies from marijuana. Studies depict that marijuana actually has Neuro-protective properties meaning that instead of damaging cells, it works to protect brain cells from harm. For instance, recently, teens who were found to smoke marijuana and take alcohol as well suffered quite significantly less damage particularly to the white matter in their brains. Beyond question, it is exceedingly evident that alcohol damages brain cells.
Neurologists have discovered that ten months of alcohol consumption that produced a significant alcohol level was sufficient enough to be considered intoxicated neurogenesis by over 50%. Further than that, this decreased neurogenesis lasted for several weeks of self-restraint. Neurological studies show that both marijuana and alcohol can be considered hallucinogen or rather narcotic, although much of these effects are attributed to alcohol that has more effect than marijuanaparticularly on the central nervous system causing addiction and behavior change. In addition, numerous studies show that marijuana is safer than alcohol in many ways, it takes many years for marijuana smokers to develop a nerve complication as compared to alcohol. One year of alcohol consumption could lead to developments of nervous complications and other significant effects attributed to it. Prolonged consumption of alcohol and marijuana have different effects both in the short and long terms, however their side effects vary. Consumption of marijuana produces tetrahyfdrocannabinol (THC) which is absorbed into the blood stream. This chemical activates proteins in the brain and the spinal cord of the user which produce short term effects such as heightened state awareness and euphoria (Drug, 2007. P. 612). Compared to alcohol effects, marijuana has none of the adverse side effects of opiates which are more on alcohol consumption.
Dopamine
How dopamine (DA) works in both schizophrenia (I/paranoid) and cocaine administration
Persons with schizophrenia are normally treated using medication that blocks (DA) dopamine neurotransmission. Chronic administration of majority of DA antagonists basically alters functions of the dopaminergic thereby causing exceedingly sensitive DA agonists. However, since the properties of the DA agonist of cocaine appear to be seemingly involved in its behavioural effects, treatments of the chronic DA agonist may enhance cocaine effects. Pharmacotherapies for cocaine and schizophrenic psychoses are very complex but quite similar due to their behavioural outcomes and similarities in their brain neurochemistry. As shown in clinical studies and in preclinical studies, their neurochemical neuronal mechanisms of action involve predominantly dopaminergic dysfunction and effects of secondary neuroadaptive effects which seem to greatly involve central serotonergic function.
Arguably, the treatment of schizophrenic psychosis demand needs complex solutions that encompass the multiplicity of various variables which are associated with its course, onset, prognosis and psych-neurobiology which is basically the same case for cocaine psychosis. To a great extent, similarities between cocaine and co-morbidity of schizophrenic psychoses appear quite often in the clinical literature. Certain reports report that cocaine prompt a psychotic syndrome which is hallucinatory, delusional and transient and covaries with the rigorousness of cocaine-induced psychotic paranoia. Subsequently, it is evident from studies that behaviour of cocaine intoxicated patients and acute asceticism mimics both negative and positive symptoms of schizophrenia. Cocaine is a psychomotor stimulant that elevates mood and increases locomotors with rewarding ecstasy. Cocaine profoundly influences dopaminergic neurotransmission thereby implicating the dopamine (DA) transporter. Predominantly pertinent to relationships between cocaine-induced psychosis and schizophrenic are biochemical data that show that these two disorders are quite analogous particularly in regards to their neurochemical action (Lajtha, 2009, p. 178). Therefore, Pharmacotherapies for cocaine and schizophrenic psychoses are very complex but quite similar due to their behavioural outcomes and similarities in their brain neurochemistry.
Hypothalamus
How SDN and MPOA differ between female and male rodents at anatomical and functional levels
Sexually dimorphic nucleus (SND) is a cluster of cells that is located in the medial preoptic area of the brain particularly of the hypothalamus which is said to be somewhat related to animals sexual behaviour. Calbindin has quite a special significance for the study of differences in sex particularly in the brain since it serves as a biomarker for the sexually dimorphic nucleus of the medial preoptic area of the rat (SDN-MPO). Males in this area express more and larger neurons as compared to females and significantly, the neurons are mainly visualized immunoreactivity of their calbindin. Hypothalamus arises from cells along the third ventricle. Structural differences at a light microscope level between female and male MPOA are in number and volume of the nucleus and size which are primarily modified by early hormone exposure. An androgen-dependent mechanism could also influence the expression of calbindin in rats since lumping androgen with that antagonist flutamide results to decreases in calbindin levels in the MPOA of the female and male rats. When preparations are examined, many strains of mice seemingly do not display sexual dimorphism in the MPO-SDA. Nevertheless, close to the rats, calbindin is a marker of sexual dimorphic of the SDN-MPOA which shows depicts a more calbindin expression than females. However, testicular production of steroids of a critical period of the steroids in the neonatal male mouse is quite similar to the rat, hence the difference in sex in mice which can pretty much depend on gonadal secretions (Kalat, 2013, p. 324). Subsequently, this is moreover proven in knockout (SF-1KO) mice that really do not differentiate adrenal glands and gonads and as a result, they are not exposed to steroids especially during neonatal period. Sex differences are discovered in protein expression and calbindin gene expression in the cerebellum juvenile and frontal cortex. In the cortex and cerebellum, female rats have about 2-fold more expressions than males.
John F. Kennedy
Why the conspiracy theorists are wrong and there is profound evidence that indeed there was a one shooter
The circumstances surrounding John F. Kennedy’s assassination spawned endless suspicions of a conspiracy since November 22, 1963. A lot of theorists have come up with their thoughts, ideas and assumptions to this conspiracy, but what remains is that profound evidence is of the essence in determining the cause of the entire saga. To start with, these conspiracies and suspicions were seemingly alleviated particularly when an official investigation initiated by the Warren Commission clinched the following year that indeed there was no conspiracy whatsoever. Nevertheless, theorists have argued that there was no shooter, however, the single-bullet theory or better known as the magic theory that was introduced by the Warren Commission, depicts that a single bullet killed President John F. Kennedy and wounded Texas Governor John Connally. Secondly, the lack of damage to the presidential limousine gave conclusions that the two dignitaries were likely struck by one bullet.
Presumably, this theory posits that the bullet that killed John F. Kennedy ‘exit 399 or CE 399’ was the cause of the non-fatal wounds to the president and all the wounds on the governor. This theory claims that a three-centimeter (1.2’) long copper-jacketed lead-core 6.5 rifle bullet was fired right from the 6th floor of the Texas School Book Depository, it penetrated through Kennedy’s neck as well as Governor Connally’s chest and wrist, it finally passed through the governor’s thigh. Evidence to these claims can be backed by its discovery on a gurney in the corridor in Dallas at Parkland Memorial Hospital. Thereafter, the bullet became the major exhibit of the Commission and was identified as CE 399. It is through the discovery of this bullet that there is persuasive evidence that indeed there is profound and persuasive evidence that a single bullet wounded Governor Connally and killed President John F. Kennedy.
Many pro-conspiracy theorists believe that the single bullet theory is essential to the conclusion of this evidence that President John F. Kennedy was wounded around 210 and 225 while the Governor was wounded in the chest and on his back before 240 time frame. Subsequently, more evidence depicts that all this was acted by Oswald the perpetrator alone. Oswald only had a single chance to fire one bullet from his rifles and a second chance was not possible whatsoever, there definitely would not have been enough time to fire two shots from his bolt action rifle. In a time period ranging from 4.7 to 7 seconds, the entire act had been completed. It was concluded by the Warren Commission that all the shots fired at the president actually originated from the 6th floor window at the Texas School Book Depository particularly at the southeast corner.
Based on the physical evidence, several conspiracy theories claim that one shooter was actually located in a building across Dallas Street (the Dal-Tex Building). In addition to this evidence, assassination researchers claim that the presidential limousine had a crack in the windshield and a bullet hole in its windshield right above the rear-view mirror. Based on John F. Kennedy’s assassination, credible sources shows that without indubitable evidence, Lee Harvey Manniclicher-Carcono rifle whose serial number was C2766 was actually located inside the Texas School Book Depository the building that overlooked the assassination when John F. Kennedy was shot (Bugliosi, 2007. P. 148).
References
Bennett, M. R., & Hacker, P. M. S. (2008). History of cognitive neuroscience. Chichester, U.K: Wiley-Blackwell.
Bugliosi, V. (2007). Reclaiming history: The assassination of President John F. Kennedy. New York: W.W. Norton & Co.
Drug courts: A new approach to treatment and rehabilitation. (2007). New York: Springer.
Kalat, J. W. (2013). Biological psychology. Belmont, CA [etc.: Wadsworth Cengage Learning.
Lajtha, A., Javitt, D. C., &Kantrowitz, J. T. (2009). Handbook of neurochemistry and molecular neurobiology. New York: Springer.
Starr, L. (2012). Animal structure and function. Pacific Grove, Calif: Brooks/Cole.
