Prepulse Inhibition Model

The research is discussing the effects of prenatal stress (PS) on the development of socioemotional symptoms as well as neurodevelopmental disorders. The study arises from existing literatures where a significant relationship has been established between prenatal stress and social deficits such as autism and attention-deficit hypersensitivity disorder among children and schizophrenia among adolescents. King et al. identifies exposures to environmental hardships and stressful events as the underlying factor in the development of PS (274). The aspect has a negative impact on the immune and endocrine system as well as neurological development (Charil et al. 56). Studies have revealed that PS affects several aspects of brain development in the fetal stage. It increases rate of cell death and reduces rate of proliferation in the hypothalamus-pituitary axis (Schoenfeld and Gould 15).

Outline and evaluate one or more biological explanations of schizophrenia (8 marks AO1/16 marks AO1)

The pons is the region above the brainstem. The pons contains the locus coeruleus, a region of cells that belong to the reticular formation. The neurotransmitter norepinephrine are necessary for arousal and attention. These neurons are found in the brain and spinal cord.

Schizophrenia is a complex and highly debilitating mental illness that we are currently unable to treat in any way that guarantees success or return to previous function. It affects around 1% of the population and is associated with a thirteen-fold increase in the likelihood of suicide, so its effective control is paramount (Gogos et al., 2015). There have been several hypotheses as to the cause of schizophrenia. Many link genetic and environmental factors, and dysregulations of neurotransmitters dopamine, glutamate, and serotonin (Egbujo, Sinclair, & Hahn, 2016). The dopamine hypothesis currently suggests that hyperactive dopamine transmission in the basal ganglia leads to psychosis and underactive dopamine transmission in the prefrontal

Erlenmeyer-Kimling also noted that environment and early developmental damage could play a role in the onset on schizophrenia. This disease may have a series of triggers that could bring on the onset of the disease. These triggers could include complications during pregnancy and/or labor, prenatal exposure to a virus (especially in the fifth month when brain development occurs), and stress throughout the stages of life. (Dincin 103)

Research has shown that one of the main factors of schizophrenia is genetics. Despite the fact that there has been no specific gene linked to the cause of schizophrenia, there is a gene related to the risk of one developing schizophrenia known as the brain derived neurotropic factor (Egan, Weinberger, Lu, 2003). This brain deriving factor is known to effect the hippocampus, this aids in the creation of impairments of individuals with schizophrenia. Perhaps one of the most interesting elements in the development of schizophrenia is that it truly developed; it is a psychological disorder that has many factors that work in conjunction with a susceptibility gene before the onset (Bray, 2007).

Schizophrenia is a mental illness in which an individual is characterized with abnormal social behavior and failure to differentiate between what is real and what is not. Individuals with schizophrenia can develop additional mental problems such as anxiety disorders, major depressive illness or substance abuse disorders. There are many factors that contribute to the risk of developing schizophrenia, in where a combination of both genetic and environmental factors play a big role in its development. Many genes are believed to be part of the development of schizophrenia each of minor effect and unknown spread and manifested, since it’s not just one cell who’s at fault but a conjunction of many that are. Environmental factors that contribute

Biological theorists believe that individuals may have a genetic predisposition for the schizophrenia if a close family member has been diagnosed with the disorder. Stress during adolescent years seems to provoke the disorder among individuals who have a family history of the disorder. In addition, this theory suggests biochemical abnormalities related to the dopamine neurotransmitters may also contribute to the illness as the brains neurotransmission of the dopamine is too frequent in occurrence (Comer, 2005). CAT and MRI scans have also indicated that abnormal brain structuring may also play a role in the development of schizophrenia due to a common occurrence of enlarged ventricles within schizophrenia sufferers (Comer, 2005). Various parts of the brain may not develop for function properly which seems lead to Type II schizophrenia. Studies have also pointed towards the idea that exposure to certain viruses before birth may lead to the eventual development of schizophrenia (Comer, 2005).

Biological perspective is the one that people focused on the most in the last couple decades. Moreover, genetic factor researchers believe that some people inherit a biological predispozitions to schizophrenia and develop the disorder later when they face huge stress, particulary in late adolescence or early adulthood. Family studies discovered that schizophrenia and schizophrenia-like brain abnormalities are more common among relatives of people with the disorder. Also, the more closely related the relatives are to the person with schizophrenia, the more likley they are to develop the disorder.

generated in the parietal lobe in response to sensory input. For example, a response to extreme

Schizophrenia (SCH) is a chronic mental disorder affecting around 1% of the population (Andreasen & Black, 2006), it is considered to be one of the most burdening disorders for the individuals, with it being recognised as one of the top 10 causes of disability(van Os & Kapur, 2009). Therefore investigating and developing a further understanding into the disorder has great benefits. Schizophrenia research incorporates various methods of investigation, which have all contributed to understanding of various aspects such as the etiology of disorder and its progression. Known risk factors of SCH range from genetics (Owen, Craddock & O’Donovan, 2010), neural disconnectivity (Friston & Frith, 1995), neurodevelopmental (Weinberger, 1986).

In terms of motor control, the basal ganglia is composed of interconnected nuclei located in the telencephalon, diencephalon, and midbrain which include the striatum, globus pallidus (GP), entopeduncular nucleus (globus pallidus internal in humans), subthalamic nucleus, and the substantia nigra (figure1) (6,8). Although there are multiple structures that partake in the modulation of movement, the basal ganglia serves to integrate information deriving from the parietal, frontal, and temporal cortex. In particular, electrical stimulation from the cortex to the striatum derive from regions implicated in the planning and execution of motor movement (6). All of this information converges and activates GABAergic medium spiny neurons (9). Of note,

To test the possibility that inhibition effect was generated from the use of only two alternative peripheral stimuli, following experiment was carried out. A central box and four peripheral boxes were used in the experiment and the positive IOR result ruled out the possible explanation that inhibition limited to the two alternative boxes.

Within the human anatomy, an intricate and complex network of specialised nerve fibres and neurons works in collaboration with the central nervous system and peripheral system, designed to carry out the various actions humans perform every day. The nervous system is also known as the master control unit of the human body, as it operates other major functions such as the circulatory and respiratory systems (Jakab, 2006). It is composed of the central nervous system (CNS) and the peripheral nervous system (PNS). The neurons established within the various sections of the nervous system, is structured with three main parts: a dendrite which is a cluster of branches that operates by receiving information from the

Animal models have been used as a primary research tool in investigating pathogenesis and developing treatments for human diseases. To mimic neuropsychiatric disorders in animal models, especially in the case of a complex disorders such as schizophrenia have been a tough task. This challenge persists due to the uncertainty of the pathophysiology and etiology that is presented with the disease. In addition to the unpredictability of the manifestation of the disease, symptoms that do occur in humans cannot be directly correlated with animal models. This presents a challenge where symptoms cannot be directly measured in animals more precisely in rodents. Despite the challenges that were present, researchers have went on forth to examine the disease using subtle approaches. Hence rodents don’t naturally develop schizophrenia, scientists must induce this through pharmacological, genetic, or environmental manipulations. The tools that are most used in pharmacological manipulations to induce schizophrenia are: ketamine and amphetamine. In this perspective, we will focus on how reliable pharmacological manipulations are in construct validity, face validity and predictive validity in respect to ketamine and amphetamine. Understanding the validity of the animal models will help understand the pathogenesis of the disease and bring novel insights for treatment. The sooner we construct a better representable model of schizophrenia, it