scholarly journals Drive and Instinct—How They Produce Relatedness and Addiction

2021 ◽  
Vol 12 ◽  
Author(s):  
Thomas Ringwood ◽  
Lindsay Cox ◽  
Breanna Felldin ◽  
Michael Kirsch ◽  
Brian Johnson

Addictive drugs are responsible for mass killing. Neither persons with addiction nor the general populace seem conscious of the malevolence of governments and drug dealers working together. How could this be? What is the place of psychoanalysis in thinking about deaths from addiction and in responding to patients with addiction? To answer these questions, we revise concepts of SEEKING, drive, instinct, pleasure, and unpleasure as separable. We review the neurobiological mechanism of cathexis. We discuss how addictive drugs take over the will by changing the SEEKING system. We review how opioid tone in the central nervous system regulates human relationships and how this endogenous hormonal system is modified by external opioid administration. We differentiate the pleasure of relatedness from the unpleasure of urgent need including the urgent need for drugs. We show how addictive drug-induced changes in the SEEKING system diminish dopaminergic tone, reducing the motivation to engage in the pursuit of food, water, sex, sleep, and relationships in favor of addictive drugs. With this neuropsychoanalytic understanding of how drugs work, we become more confidently conscious of our ability to respond individually and socially.

Author(s):  
Sarah A. Luse

In the mid-nineteenth century Virchow revolutionized pathology by introduction of the concept of “cellular pathology”. Today, a century later, this term has increasing significance in health and disease. We now are in the beginning of a new era in pathology, one which might well be termed “organelle pathology” or “subcellular pathology”. The impact of lysosomal diseases on clinical medicine exemplifies this role of pathology of organelles in elucidation of disease today.Another aspect of cell organelles of prime importance is their pathologic alteration by drugs, toxins, hormones and malnutrition. The sensitivity of cell organelles to minute alterations in their environment offers an accurate evaluation of the site of action of drugs in the study of both function and toxicity. Examples of mitochondrial lesions include the effect of DDD on the adrenal cortex, riboflavin deficiency on liver cells, elevated blood ammonia on the neuron and some 8-aminoquinolines on myocardium.


Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 704
Author(s):  
Yingyu Zhou ◽  
Wanyi Qiu ◽  
Yimei Wang ◽  
Rong Wang ◽  
Tomohiro Takano ◽  
...  

As a kind of metabolically triggered inflammation, obesity influences the interplay between the central nervous system and the enteral environment. The present study showed that β-elemene, which is contained in various plant substances, had effects on recovering the changes in metabolites occurring in high-fat diet (HFD)-induced obese C57BL/6 male mice brains, especially in the prefrontal cortex (PFC) and hippocampus (HIP). β-elemene also partially reversed HFD-induced changes in the composition and contents of mouse gut bacteria. Furthermore, we evaluated the interaction between cerebral metabolites and intestinal microbiota via Pearson correlations. The prediction results suggested that Firmicutes were possibly controlled by neuron integrity, cerebral inflammation, and neurotransmitters, and Bacteroidetes in mouse intestines might be related to cerebral aerobic respiration and the glucose cycle. Such results also implied that Actinobacteria probably affected cerebral energy metabolism. These findings suggested that β-elemene has regulatory effects on the imbalanced microbiota-gut-brain axis caused by obesity and, therefore, would contribute to the future study in on the interplay between cerebral metabolites from different brain regions and the intestinal microbiota of mice.


1999 ◽  
Vol 43 (5) ◽  
pp. 1091-1097 ◽  
Author(s):  
Hideki Kita ◽  
Hirotami Matsuo ◽  
Hitomi Takanaga ◽  
Junichi Kawakami ◽  
Koujirou Yamamoto ◽  
...  

ABSTRACT We investigated the correlation between an in vivo isobologram based on the concentrations of new quinolones (NQs) in brain tissue and the administration of nonsteroidal anti-inflammatory drugs (NSAIDs) for the occurrence of convulsions in mice and an in vitro isobologram based on the concentrations of both drugs for changes in the γ-aminobutyric acid (GABA)-induced current response in Xenopus oocytes injected with mRNA from mouse brains in the presence of NQs and/or NSAIDs. After the administration of enoxacin (ENX) in the presence or absence of felbinac (FLB), ketoprofen (KTP), or flurbiprofen (FRP), a synergistic effect was observed in the isobologram based on the threshold concentration in brain tissue between mice with convulsions and those without convulsions. The three NSAIDs did not affect the pharmacokinetic behavior of ENX in the brain. However, the ENX-induced inhibition of the GABA response in the GABAA receptor expressed in Xenopus oocytes was enhanced in the presence of the three NSAIDs. The inhibition ratio profiles of the GABA responses for both drugs were analyzed with a newly developed toxicodynamic model. The inhibitory profiles for ENX in the presence of NSAIDs followed the order KTP (1.2 μM) > FRP (0.3 μM) > FLB (0.2 μM). These were 50- to 280-fold smaller than those observed in the absence of NSAIDs. The inhibition ratio (0.01 to 0.02) of the GABAA receptor in the presence of both drugs was well-fitted to the isobologram based on threshold concentrations of both drugs in brain tissue between mice with convulsions and those without convulsions, despite the presence of NSAIDs. In mice with convulsions, the inhibitory profiles of the threshold concentrations of both drugs in brain tissue of mice with convulsions and those without convulsions can be predicted quantitatively by using in vitro GABA response data and toxicodynamic model.


1969 ◽  
Vol 18 (6) ◽  
pp. 1315-1324 ◽  
Author(s):  
L. Beani ◽  
C. Bianchi ◽  
P. Megazzini ◽  
L. Ballotti ◽  
G. Bernardi

2014 ◽  
Vol 31 (04) ◽  
pp. 219-224 ◽  
Author(s):  
A. Ibegbu ◽  
A. Animoku Abdulrazaq ◽  
Ayuba Micheal ◽  
Brosu Daniel ◽  
A. Adamu Sadeeq ◽  
...  

Abstract Introduction. Mercury is one of the most hazardous environmental contaminants to living organisms and the central nervous system has been shown to be the main target. Objective. The present work was aimed at evaluating the effect of ascorbic acid on mercury chloride-induced changes on the cerebellar cortex of adult Wistar rats. Material and method. Thirty Wistar rats of average weight of 200g and were randomly divided into 6 groups of 5 rats each. The animals in Group 1 (control) were administered with distilled water, Groups 2 and 3 were administered with 52mg/kg and 26.25mg/kg body weight of HgCl respectively while Groups 4 and 5 were administered with 52mg/kg of HgCl and 5mg/kg of ascorbic acid and 26.25gm/kg of HgCl and 5mg/kg of ascorbic acid respectively, while Group 6 was administered with 5mg/kg of ascorbic acid. The administration was through oral route, daily for 3 weeks. Results. The result of the biochemical parameters showed a significant increase (P < 0.05) on the mean SOD and LPO values after the administration of mercury chloride and Ascorbic acid. Histological observation of the cerebellar cortex, showed normal histo-morphology in Groups 1 and 6 while, the cerebellum in Groups 2, 3, 4 and 5 showed some degenerative, necrotic and cellular changes. Conclusion. However, ascorbic acid administration has shown to ameliorate the induced degenerative changes in the cerebellum caused by mercury chloride toxicity in Wistar rats.


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