Assembling the Emotions

2006 ◽  
Vol 32 ◽  
pp. 185-212 ◽  
Author(s):  
Vincent Bergeron ◽  
Mohan Matthen

Endogenous depression is highly correlated with low levels of serotonin in the central nervous system. Does this imply or suggest that this sort of depression just is this neurochemical deficit? Scorning such an inference, Antonio Damasio writes:If feeling happy or sad … corresponds in part to the cognitive modes under which your thoughts are operating, then the explanation also requires that the chemical acts on the circuits which generate and manipulate [such thoughts]. Which means that reducing depression to a statement about the availability of serotonin or norepinephrine in general- a popular statement in the days and age of Prozac- is unacceptably rude (1995, 161).Damasio's thought is that depression is essentially a modification of how we perceive the world, reason about it, and make decisions about how to act in it - in other words, that it is essentially cognitive. A reduced level of serotonin might cause the said modification, but no adequate account of depression would identify the malady with its cause. A proper account would minimally need to say how cognitive processing is affected by a reduced level of serotonin.

Vaccines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 120
Author(s):  
Anis Daou

The vaccination for the novel Coronavirus (COVID-19) is undergoing its final stages of analysis and testing. It is an impressive feat under the circumstances that we are on the verge of a potential breakthrough vaccination. This will help reduce the stress for millions of people around the globe, helping to restore worldwide normalcy. In this review, the analysis looks into how the new branch of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) came into the forefront of the world like a pandemic. This review will break down the details of what COVID-19 is, the viral family it belongs to and its background of how this family of viruses alters bodily functions by attacking vital human respiratory organs, the circulatory system, the central nervous system and the gastrointestinal tract. This review also looks at the process a new drug analogue undergoes, from (i) being a promising lead compound to (ii) being released into the market, from the drug development and discovery stage right through to FDA approval and aftermarket research. This review also addresses viable reasoning as to why the SARS-CoV-2 vaccine may have taken much less time than normal in order for it to be released for use.


2019 ◽  
Author(s):  
Liza Malong ◽  
Ilaria Napoli ◽  
Ian J White ◽  
Salome Stierli ◽  
Alessandro Bossio ◽  
...  

The specialised blood barriers of the nervous system are important for protecting the neural environment but can hinder therapeutic accessibility1,2. Studies in the central nervous system (CNS) have shown the importance of the cellular components of the neuro-vascular unit for blood-brain barrier (BBB) function. Whilst the endothelial cells (ECs) confer barrier function with specialised tight junctions (TJs) and low levels of transcytosis, pericytes and astrocytes provide complete coverage of the ECs and both deliver essential signals for the development and maintenance of the BBB3–9. In contrast, the blood-nerve barrier (BNB) of the peripheral nervous system (PNS) remains poorly defined10. Here, we show that the vascular unit in the PNS has a distinct cellular composition with only partial coverage of the BNB-forming ECs. Using a mouse model, in which barrier function can be controlled11, we show the BNB, while less tight than the BBB, is maintained by low levels of transcytosis and the TJs of the ECs, with opening of the barrier associated with increased transcytosis. Importantly, we find that while ECs of the PNS have higher transcytosis rates than those of the CNS, the barrier is reinforced by resident macrophages that specifically engulf leaked material. This identifies a distinct role for macrophages as an important component of the BNB acting to protect the PNS environment with implications for improving therapeutic delivery to this tissue.


CNS Spectrums ◽  
2001 ◽  
Vol 6 (12) ◽  
pp. 953-953
Author(s):  
Michael Trimble

Freud writes in his startlingly innovative book, Wit and Its Relation to the Unconscious, that “…our philosophical inquiries have not awarded to wit the important role that it plays in our mental life.” He pointed out the difficulties of studying the phenomenon scientifically, and went on to analyze the meanings of jokes and why we laugh. He emphasized the “pleasure in economy” that the central nervous system derives from the pithy nature of the witty synthesis. Since then, several authors have brought forward their own theories, Arthur Koestler among them. However, neuroscientists have shown little interest in the subject.This needs urgent attention. It is therefore welcome that at least one group of scientists is taking jokes seriously. They set up a “Laugh Lab” Web site to investigate humor, and respondents from all over the world were asked to vote for the “best” of several jokes displayed on the site. Their responses will be analyzed and hypotheses tested.


1943 ◽  
Vol 89 (374) ◽  
pp. 42-51 ◽  
Author(s):  
Donald Blair

In March, 1939. there was admitted under my care at the St. Pancras Hospital Mental Observation Unit a case of torulosis of the nervous system. This is a very rare disease in this country and the present case is only the third recorded in British medical history (Greenfieldet al., 1938; Smith and Crawford, 1930), and the first one to have come under mental hospital supervision. Although such a rarity here, torulosis is more common in the United States, and cases have been reported from nearly every part of the world.


Author(s):  
Elmira Erfanovna Alimova ◽  
Elena Evgenievna Al-Rabadi

Currently, according to the World Health Organization, about 20% of the world's population takes non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDs are lipophilic substances that easily penetrate the blood-brain barrier and can cause side effects from the central nervous system. Neurotoxicity (headache, dizziness, insomnia, depression, depersonalization, psychosis, and tremor occur during the treatment with indomethacin; visual impairment, drowsiness - during the treatment with meloxicam; hearing loss - when taking salicylates) ranks second after gastrotoxicity. The article describes the mechanisms of neurotoxicity that occur when taking NSAIDs.


2010 ◽  
Vol 84 (21) ◽  
pp. 11030-11044 ◽  
Author(s):  
Susan J. Bender ◽  
Judith M. Phillips ◽  
Erin P. Scott ◽  
Susan R. Weiss

ABSTRACT Coronavirus infection of the murine central nervous system (CNS) provides a model for studies of viral encephalitis and demyelinating disease. Mouse hepatitis virus (MHV) neurotropism varies by strain: MHV-A59 causes mild encephalomyelitis and demyelination, while the highly neurovirulent strain JHM.SD (MHV-4) causes fatal encephalitis with extensive neuronal spread of virus. In addition, while neurons are the predominant CNS cell type infected in vivo, the canonical receptor for MHV, the carcinoembryonic antigen family member CEACAM1a, has been demonstrated only on endothelial cells and microglia. In order to investigate whether CEACAM1a is also expressed in other cell types, ceacam1a mRNA expression was quantified in murine tissues and primary cells. As expected, among CNS cell types, microglia expressed the highest levels of ceacam1a, but lower levels were also detected in oligodendrocytes, astrocytes, and neurons. Given the low levels of neuronal expression of ceacam1a, primary neurons from wild-type and ceacam1a knockout mice were inoculated with MHV to determine the extent to which CEACAM1a-independent infection might contribute to CNS infection. While both A59 and JHM.SD infected small numbers of ceacam1a knockout neurons, only JHM.SD spread efficiently to adjacent cells in the absence of CEACAM1a. Quantification of mRNA for the ceacam1a-related genes ceacam2 and psg16 (bCEA), which encode proposed alternative MHV receptors, revealed low ceacam2 expression in microglia and oligodendrocytes and psg16 expression exclusively in neurons; however, only CEACAM2 mediated infection in human 293T cells. Therefore, neither CEACAM2 nor PSG16 is likely to be an MHV receptor on neurons, and the mechanism for CEACAM1a-independent neuronal spread of JHM.SD remains unknown.


2021 ◽  
Author(s):  
Jose Martinez-Navio

Early in the course of infection, human immunodeficiency virus (HIV) is able to enter the central nervous system where it stablishes a permanent reservoir. Current antiretroviral therapies do not efficiently cross the blood-brain barrier and therefore do not reach the HIV located in the central nervous system. Consequently, HIV infection can often be associated with neurocognitive impairment and HIV-associated dementia. The purpose of this review is to brief the reader into the world of neurological complications arising from HIV infection. Mechanisms by which HIV directly or indirectly impairs the central nervous system are discussed, as well as other factors influencing or contributing to the impairment, and the animal models currently used to perform research on the topic.


2003 ◽  
Vol 26 (4) ◽  
pp. 408-409
Author(s):  
David A. Booth

It is tough to relate visual perception or other achievements to physiological processing in the central nervous system. The diagrammatic, algebraic, and verbal pictures of how sights seem to Lehar do not advance understanding of how we manage to see what is in the world. There are well-known conceptual reasons why no such purely introspective approach can be productive.


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