SBA Answers and Explanations
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury in SBAs for the MRCS Part A, 2018
The neuromuscular junction (the synapse between somatic motor neurones and skeletal muscle) operates by way of acetylcholine acting through nicotinic acetylcholine receptors. The substantia nigra is a dense area of dopaminergic neurones which forms part of the basal ganglia; degeneration leads to Parkinson’s disease. The periaqueductal grey is a region rich in endogenous opioids which is believed to play a pivotal role in attenuation of painful stimuli through descending inhibition from higher centres. The noradrenergic-rich locus coeruleus is believed to play a key role in attention. The nucleus accumbens is dopamine-rich and plays an important role in addiction and reward. The adrenal medulla is an endocrine gland but is effectively a specialized second-order (postganglionic) sympathetic nerve terminal that secretes approximately 70 per cent adrenaline, 30 per cent noradrenaline. Excess catecholamines are secreted by the adrenal medulla in a condition known as a phaeochromocytoma, which is a rare tumour of the adrenal gland. A thorough grounding of the aforementioned chemical neurotransmitters is imperative if one is to understand certain disease states and how particular drugs act within the nervous system.
Herbal Medicines in Neuropsychiatric Illness: The Case of L-Stepholidine
Vikas Kumar, Addepalli Veeranjaneyulu in Herbs for Diabetes and Neurological Disease Management, 2018
Cholinergic system has a primary role in hallucinations and delusional thinking. Alteration in cholinergic parameters may be primary component of the pathophysiology of schizophrenia or a down-stream effect from pathology in other neurotransmitter systems or structures. Dopaminergic system regulates the cortical cholinergic cell groups. The basal forebrain cholinergic complex, which projects throughout the cerebral cortex, is regulated by GABA-mediated output from nucleus accumbens. Output from nucleus accumbens is highly dependent upon its dopaminergic input. Abnormal dopaminergic tone in nucleus accumbens might alter the activity of cholinergic projections to the cortex thereby linking an alteration in cortical function to subcortical dopamine dysregulation.52 It has been found that cholinergic blockade impairs cognitive function in normal human control subjects, including marked memory impairment and attention deficits. Learning and memory system traditionally associated with the hippocampus and hippocampal function is also found to be dependent upon cholinergic input. All these finding suggest that cholinergic input to the hippocampal formation is the critical component of learning and memory and may be impaired in schizophrenia. Thus, the attention, learning, and memory deficits in schizophrenia might be attributed to abnormalities in a variety of cholinergic pathways.53
Theories of Tobacco Addiction
Rajmohan Panda, Manu Raj Mathur in Tobacco Cessation, 2019
Our brains are wired to ensure that we will repeat life-sustaining activities by associating those activities with pleasure or reward. Whenever this reward circuit is activated, the brain notes that something important is happening that needs to be remembered, and teaches us to do it again and again. The “rewarding” effect of nicotine is attributed to its ability to activate the dopaminergic pathways projecting from the ventral tegmental area of the midbrain to the cerebral cortex and the limbic system.1,5,6 The increase in dopamine in the nucleus accumbens is mediated by receptors in cell bodies in the ventral tegmental area (VTA). Food, for example, stimulates reward via the VTA which leads to dopamine overflow in the nucleus accumbens, which leads to pleasure. The “amount” of pleasure depends on how enjoyable the food is, and the degree of hunger. In comparison, nicotine acts directly on the cell bodies in the VTA resulting in a sustained response. When tobacco is used, it can release 2–10 times the amount of dopamine that natural rewards, such as eating and sex, do. In some individuals, this occurs almost immediately (as when nicotine is smoked), and the effects can last much longer than those produced by natural rewards. The resulting effects on the brain's pleasure circuit dwarf those produced by naturally rewarding behaviors. The effect of such a powerful reward strongly motivates people to smoke again and again.4–6
Tianeptine Abuse and Dependence in Psychiatric Patients: A Review of 18 Case Reports in the Literature
Published in Journal of Psychoactive Drugs, 2018
Janusz Springer, Wiesław Jerzy Cubała
The main reason for recreational tianeptine use seems to be the desire to achieve an opioid-like anxiolytic effect. Tianeptine exhibits μ-opioid receptor and δ-opioid receptor agonism (Gassaway et al. 2014). The drug is also known to increase dopaminergic transmission in the nucleus accumbens and the cerebral cortex (Invernizzi et al. 1992). Sensitization plays a key role in the development of reinforcement, reward, and drug dependence. The reinforcing effect of addictive substances involves μ-opioid receptor activation (Soderman and Unterwald 2008; Zubieta et al. 1996) and the reward effect requires activation of the dopamine D1 receptor (Invernizzi et al. 1992; Sacchetti et al. 1993). The nucleus accumbens, frontal cortex, and ventral midbrain, all of which are intricately involved in the reward and addiction circuitry, are enriched in these receptors. Each receptor is believed to facilitate different aspects of the so-called reward circuit via interactions with opioids and neurotransmitters, including dopamine, whereas the activation of the μ-opioid receptor is associated with euphoria and reward (Gassaway et al. 2014; Trigo et al. 2010).
Does Music Matter? A Look at the Issues and the Evidence
Published in Developmental Neuropsychology, 2019
Lauren Julius Harris
Are there laterality differences in the reward system and, if so, are they general or specific for music? The caudate, where Kokal et al. (2011) found changes, is part of the dorsal striatum, and the changes found were on the right side. Greater dopaminergic responses to reward also have been reported in the ventral striatum where the task was gambling and the rewards were monetary and “unpredictable” (Martin-Soelch et al., 2011). In that study, the effects were found in the nucleus accumbens, part of the ventral striatum, and in the prefrontal cortex, which receives extensive projections from basal ganglia. It would be of interest to know whether, in Salimpoor et al.’s (2011) and Blood and Zatorre’s (2001) studies, activation was also greater on the right, and whether, for speech, there is a complementary greater induction of striatal dopamine release on the left. A recent study answers the latter question in the affirmative (Simonyan, Herscovitch, & Horwitz, 2013). It would be of further interest to know whether the effects are the same in men and women in light of previously-mentioned evidence of sex differences in musical preferences and responses (e.g., Kellaris & Rice, 1993) and evidence for a laterality by sex interaction in dopaminergic responses to reward (Martin-Soelch et al., 2011).
Cocaine induced heart failure: report and literature review
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Sherif Elkattawy, Ramez Alyacoub, Abraham Al-Nassarei, Islam Younes, Sarah Ayad, Mirette Habib
Cocaine is a highly addictive stimulant that alters human behavior through the limbic system’s activity, a structure in the brain involved in motivation, emotion, learning, and memory. The nucleus accumbens (NA) is a specific area within the limbic system that receives connections through dopaminergic neurons. When stimulated, the accumulation of dopamine at the NA causes euphoria, conditioning the brain to establish a reward pathway in association with a stimulant. Cocaine inhibits dopamine transport protein (DAT) embedded within presynaptic neurons of the NA, forming a reward pathway; thus, explaining the drug’s highly addictive nature and potential for abuse [1, 5]. Although the overall incidence of recreational cocaine use has been declining over the years within the United States, the global prevalence of cocaine is still approximately 0.4%. Many studies have provided significant evidence explaining the relationship between cocaine use and the onset of cocaine-induced morbidity (including cardiovascular, neurovascular, psychiatric, and infectious illnesses) and mortality over time.[2,3,4,6,7]
Related Knowledge Centers
- Basal Forebrain
- Dopaminergic Pathways
- Mesolimbic Pathway
- Nucleus
- Septum Pellucidum
- Basal Ganglia
- Hypothalamus
- Preoptic Area
- Olfactory Tubercle
- Striatum