Neurotransmitters

N-Methyl-3, 4-methylenedioxyamphetamine (MDMA), or ecstasy is a recreational drug of abuse. It is a synthetic substance that affects the body's systems, which its mechanism of action and treatment should be more investigated. MDMA provides an immediate enjoyable feeling by stimulating the release of neurotransmitters, such as dopamine and serotonin in the brain. Unfortunately, abnormal regulation of the brain neurotransmitters, as well as the increased oxidative stress causes damage to the brain neurons after the MDMA exposure. Only a few studies have been done regarding its treatment. Thus, the treatment of MDMA complications should be further explored mainly by targeting its mechanism of action in the neurotransmitter systems. Hence, this study presents a short review regarding the recent findings on the role of neurotransmitters to cause MDMA neurotoxicity. The results will be useful for future research in elucidating the potential treatment based on the targeted mechanisms to treat the neurotoxic effects of MDMA.

Portulaca oleracea (purslane) belonging to family “Portulacaceae” was considered to be an anti-magic herb used to protect against variety of diseases. Here, we investigated the neuronal activities of P. oleracea in adult rats. Animals were treated with 1.5 mL/kg of aqueous extract of purslane (leaves and stem) for 12 days. Cerebellum, pons and medulla, cerebral cortex, thalamus and hypothalamus, midbrain and spinal cord were isolated to estimate the concentration of calcium, acetyl cholinesterase, dopamine, norepinephrine and serotonin in them. Purslane was able to induce a significant decrease in calcium concentration of the brain cortex. Dopamine, norepinephrine and serotonin were significantly altered in the studied brain regions after treatment of rats with purslane. Acetyl cholinesterase was increased in all brain regions except in the cerebellum.  Our results suggest the potential role of purslane mediated changes in the neuronal tissues.

We describe a hybrid material that consists of mo-lybdenum sulfide flowers placed on graphene nanosheets and multiwalled carbon nanotubes (GNS-CNTs/MoS 2). It was deposited on a glassy carbon electrode (GCE) which then is well suited for sensitive and selective determination of dopamine. The GNS-CNTs/MoS 2 nanocomposite was prepared by a hydrothermal method and characterized by scanning electron and transmission emission microscopies, energy-dispersive X-ray spectroscopy, cyclic voltammetry, differential pulse voltammetry and electrochemical impedance spec-troscopy. Electrochemical studies show the composite to possess excellent electrochemical properties such as a large electrochemically active surface, high capacitance current, a wide potential window, high conductivity and large porosity. The electrode displays excellent electrocatalytic ability to oxidize dopamine. The modified GCE, best operated at a working potential as low as 0.15 V (vs. Ag/AgCl), responds linearly to dopamine in the 100 nM to 100 μM concentration range. The detection limit is 50 nM, and the sensitivity is 10.81 (± 0.26) μA⋅μM −1 ⋅cm −2. The sensor has good selectivity, appreciable stability, repeatability and reproducibility. It was applied to the determination of dopamine in (spiked) biological and pharmaceutical samples.

Essence of love is one of topic that still been asking for by numerous physiologist, biologist and even philosophers. Love will deserve different meaning if love is interpreted with the different angle. This topic is considered as an eternally elusive subject, as it is hard to find the real meaning of love and how love works. This study was focused on the essence of love from physiologic angle, which discuss about body's mechanism and it's change as structural change of brain, release of neurotransmitters and hormones, heart rate variability, pupils dilatation, and shallow breathing. Obviously, love has an important role on maintaining homeostasis and more startling role, love is necessary for human to survive while lack of love may cause psychopathologic conditions.

The human body has approximately 1 trillion neurons, each of which has a cell body with a nucleus that contains the genetic material that determines how the cell functions (Feldman, 2008).  By thinking of the nervous system as the highway and the neurons as the vehicles on that highway, we can see how “the nervous system is (considered to be) the pathway for the instructions that permit our bodies to carry out such precise activities” (p. 61). In this paper, we discover why neurons are called “the basic elements of behavior” by examining them as the nerve cells that allow our brains to transport and coordinate the messages of our thoughts, actions, and deeds.

The reward centers of the nervous system play an important role in the evolution of species: They produce pleasurable sensations in the presence of certain stimuli associated to survival and reproduction in order to teach an animal that it's convenient to generate those circumstances, and thus increase the likelihood of survival of the individual and the species. But being humans the most complex living organisms on earth, we have developed reward responses for a wide range of stimuli that go a long way beyond mere survival. These are called extrinsic rewards and maybe, if we force it, they can be traced back to those primal instincts. This is because of a learned conditioning and it depends on culture. For example, we can say that we seek social recognition because it solidifies our chances of getting a mate and having children to perpetuate our DNA, or that we seek financial stability to maximize our chances of surviving for a longer time. But those aren't the only extrinsic rewards that motivate our behaviors. There is indeed an enormous array of activities that will activate these centers in different ways and levels of intensity, depending on cultural conditioning and personal preferences. These can go from completing a hard level on a video game, appreciating a strange piece of abstract art, or attaining academic goals to being selflessly generous, eating vegan or, in general, postponing instant gratification in pursuit of something greater. While pleasure can sometimes act as a signaling of the right way for survival, (like in the case of food for nourishment or sex for reproduction), it can also be deceptive at times. The most delicious foods aren't necessarily the ones that are best for our health. And consuming certain drugs can produce pleasurable sensations but end up killing us or ruining our lives. For navigating this complex structure of rewards associated to sometimes contradicting stimuli humans have developed a more comprehensive concept than just pleasure: the concept of happiness. The pursuit of happiness guides human behavior and lays behind every decision we make. On a simplified vision we can think of happiness as the optimization of the quality, intensity and frequency of rewards experienced by our brains throughout our lives. We choose to sacrifice instant gratification if we sense that the long-term gratification we will obtain out of it is greater. In our example about consumption of harmful drugs, choosing not to take them increases happiness because cognitively we have learned about the disasters of addiction and we consider that long term, and throughout our lives, the sum of rewards we can get without them exceed the ones consuming them can give us minus the pain they'd cause. Happiness as a long-term project provides the rational answer. However, empathy makes some of those sacrifices be real, in the sense that the gratification derived from our sacrifice is actually smaller than the one that we would have had by being selfish. But contributing to the gratification of others is important enough to make it worth it. What is it in the brain that can make us (sometimes) feel happier by sacrificing our immediate wants? Can we be happy most of the time? How can we optimize the different types of rewards we perceive throughout our lives? How to build a model of happiness that is sustainable both socially and in time? To begin to find these answers it's important to understand that the concept of happiness englobes a series of qualitatively different positive emotions, chemically associated to different neurotransmitters. Happiness isn't yes or no, pleasure or pain, black or white, one or

Epilepsi, birçok konjenital/edinsel hasarlanma nedeniyle beynin belli bölgelerinde reaktif astrosit(hasarlanmış glial hücre) oluşumuyla ilişkilidir.Bu yazıda glial hücrelerin nasıl hasarlanıp metabolizmalarının bozularak epilepsiye yol açtıklarını anlamak tedavi stratejileri geliştirmek açısından önemlidir.

Recent advances in the study of alcoholism have thrown
light on the involvement of various neurotransmitters in the
phenomenon of alcohol addiction. Various neurotransmitters
have been implicated in alcohol addiction due to their
imbalance in the brain, which could be either due to their
excess activity or inhibition. This review paper aims to
consolidate and to summarize some of the recent papers
which have been published in this regard. The review
paper will give an overview of the neurobiology of alcohol
addiction, followed by detailed reviews of some of the recent
papers published in the context of the genetics of alcohol
addiction. Furthermore, the author hopes that the present
text will be found useful to novices and experts alike in the
field of neurotransmitters in alcoholism.

Neurochemistry and drug addiction. Neurocognitive approach. Cognitive Neuroscience. Research for the Postgraduate Program in Cognitive Sciences of the University of Costa Rica. This research establishes a theoretical basis for the biochemical and neurophysiological bases of behavior and mental phenomena, as well as analyzing the neuropathologies derived from the consumption of toxic substances. Plausible explanations are given for the relationships between toxic and addictive and addictive behaviors, and their neurophysiological and genetic bases. // Neuroquímica y toxicodependencia. Enfoque de neurocognoscitivo.  Neurociencias Cognoscitivas. Investigación para el Programa de Postgrado en Ciencias Cognoscitivas de la Universidad de Costa Rica.  Esta investigación, establece una fundamenta teórica de las bases bioquímicas y neurofisiológicas de la conducta y de los fenómenos mentales, así como analiza las neuropatologías derivadas del consumo de tóxicos. Se plantean explicaciones plausibles de las relaciones entre tóxicos y conductas dependientes y adictivas, y sus bases neurofisiológicas y genéticas. // Rodolfo J. Rodríguez-Rodríguez. E-Mail: rodolfojrr@gmx.com

RESUMEN
El presente artículo se propone dar cuenta del elusivo fenómeno de la conciencia desde la original perspectiva de la neurofenomenología de Francisco Varela, quien a partir de nociones tales como neuroplasticidad, enacción y emergencia, explica, cómo ocurren los procesos cerebrales que fundan la conciencia y la “unidad” de la vivencia. Describiendo como la conciencia aparece en el vivir encarnado: en la regulación con el cuerpo entero; en sus relaciones sensorio-motoras con el mundo y en una red ínter-subjetiva de acciones y de lenguaje.
Dr. Adolfo Vásquez Rocca
Keywords:  Neurociencias, ciencias cognitivas, ética, yo, cuerpo, neuroplasticidad, enacción, acciones corporeizadas,  biología cultural,  saber-cómo.
Neuroscience, cognitive science, ethics, self, body, neuroplasticity, enaction, actions embodied experiences, cultural biology,  know-how.
-Francisco Varela: neurophenomenology, enactive approach to cognition, minds without me and the elusive phenomenon of consciousness.
DR. ADOLFO VÁSQUEZ ROCCA

Abstract:  Nanomaterial-modified detection systems represent a chief driver towards the adoption of electrochemical methods, since nanomaterials enable functional tunability, ability to self-assemble, and novel electrical, optical and catalytic properties that emerge at this scale. This results in tremendous gains in terms of sensitivity, selectivity and versatility. We review the electrochemical methods and mechanisms that may be applied in the detection of neurological drugs. We focus on understanding how specific nano-sized modifiers may be applied to influence the electron transfer event to result in gains in sensitivity, selectivity and versatility of the detection system. Specific sections are dedicated to electrodes based on the carbon materials, supporting electrolytes, and on electrochemical detection paradigms for neurological drugs and neurotransmitters. We finally discuss emerging trends and future challenges such as the development of strategies for simultaneous detection of multiple targets with high spatial and temporal resolutions, the integration of microfluidic strategies for analyte preconcentration, the real-time monitoring of neurotransmitter secretions from active cell cultures under electro- and chemotactic cues, aptamer-based biosensors, and the miniaturization of the sensing system for detection in small sample volumes andfor enabling cost savings due to manufacturing scale-up. The Supp. Information includes a list of the key properties of the analytes, viz. pKa values, half-life of drugs and their electro-chemical mechanisms. It also defines analytical figures of merit of the drugs and neurotransmitters. The review contains 198 references in the main manuscript and 207 references in the Supp. Information.

Neurochemistry refers to the chemical processes that occur in the brain and nervous system. This section of study determines how neurochemicals influence the network of neural operation. The brain transfers numerous chemical information via neurons to communicate. The main role of neurochemistry activities takes place in the brain, which allows it to perform numerous actions. Foundation of brain is a little bit different from man to man and several things can play a role in the levels of various neurotransmitters in the brain. It is supposed that differences in brain chemistry may accountable for a variety of behavioral disorders. A particular cell called neurons is the basis of brain. Neurotransmitters have the capability that it can trigger when ordered to do so, along with receptors for specific neurotransmitters. By sending messages with neurotransmitters to signal various cell activities, brain perform its functions. Neurotransmitter spreads chemical messages from neuron to neuron to broadcast certain work and thus it works. A neuron may accept many chemical messages, both positive and negative from the other neurons contiguous it. They are accountable to get the neuron to reply in different ways, or they may work combine to produce a certain effect. Since all of this occurs just within a split second, the neurotransmitter must be cleared away rapidly so that the same receptors can be activated again and again. Psychoactive drugs work by briefly influencing a man's neurochemistry, which thusly causes changes in a man's mind-set, cognition, perception and behavior. Neuropeptides are endogenous protein molecules that are utilized for neuronal signaling. These molecules exert more prolonged and diverse effects on behavior than neurotransmitters. Therefore the objective of this appraisal is to show study of the brain's chemical makeup especially neurotransmitters, psychopharmaceuticals, neuropeptides and their activities to nervous tissue.

While our personality traits such as honesty are much more dependent on the environment and circumstances, it has become clear that our temperaments have a solid biological foundation. Unfortunately, genetics has turned out to be much messier than hoped for, but it has become clear that genes are involved in neurotransmitters, such as dopamine (DAT) and serotonin transporter genes (5-HTTLPR). I have found several approaches to temperament and neurotransmitters/hormones. One of the first approaches I found was Helen Fisher, whose classification combined with mine looks like this: While testosterone (male) and estrogen (female) hormones are problematic (plus, they are hormones and not neurotransmitters), they do nicely correspond to the NT/NF distinction in the Myers-Briggs/Keirsey inventory. Looking for another classification based on I came across Erich Braverman, whose four temperaments are very close to Keirsey's. However, the mapping of neurotransmitters to temperament is very different and confusing.

Parkinson’s disease is a neurodegenerative disease caused by the death of neurons, ie, cells critical to the production of dopamine, an important neurotransmitter in the brain. Here, we present a brief review of the dopamine synthetic pathway, binding to the dopamine receptors, and subsequent action. The production of dopamine (a monoamine neurotransmitter) occurs in the ventral tegmental area (VTA) of the substantia nigra, specifically in the hypothalamic nucleus and midbrain. Compared to other monoamines, dopamine is widely distributed in the
olfactory bulb, midbrain substantia nigra, hypothalamus, VTA, retina, and the periaqueductal gray area. Dopamine receptors are large G-protein coupled receptor family members, of which there are five subtypes including D1, D2, D3, D4, and D5. These subtypes are further divided into two subclasses: D1-like family receptors (types 1 and 5) and D2-like family receptors (types 2, 3, and 4). Four different pathways and functions of the dopaminergic system are presented in this review. In the oxidation of dopamine, 5,6-indolequinone, dopamine-o-quinone, and aminochrome are formed. It is difficult to separate the roles of 5,6-indolequinone and dopamine-o-quinone in the degenerative process of Parkinson’s diseases due to their instability. The role of aminochrome
in Parkinson’s disease is to form and stabilize the neurotoxic protofibrils of alpha-synuclein, mitochondrial dysfunction, oxidative stress, and the degradation of protein by lysosomal systems and proteasomes. The neurotoxic effects of aminochrome can be inhibited by preventing the polymerization of 5,6-indolequinone, dopamine-o-quinone, and aminochrome into neuromelanin, by reducing aminochrome catalysis by DT-diaphorase, and by preventing dopamine oxidative deamination catalyzed by monoamine oxidase. In addition to these, the conversion of dopamine in the neuromelanin (NM) shows both protective and toxic roles. Therefore, the aims of this review were to discuss and explain the role of dopamine and explore its physiology and specificity in Parkinson's
disease, as well as its role in other physiological functions

This is an extract about URIC ACID, ARGININE, CITRULLINE POSSIBLE RELATION WITH SOME DISEASES like arthritis reumathoid, irritable bowel syndrome etc.
created by JoanCarles Testagorda Garcia of the work Anatomia Magna vol.I created by JoanCarles Testagorda Garcia. The total content of this extract (9pages) and the total content, the total original ideas, equations, reasonings of the work Anatomia Magna vol.I more than 150pages are created by JoanCarles Testagorda Garcia.

Human brain is well encapsulated within a thick, bony skull. The choroid plexus secretes the cerebrospinal fluid (CSF) which surrounds the brain. The fluid passes down through the four ventricles with the help of subarachnoid space and finally enters the cerebral veins through the arachnoid villi. Brain lacks lymphatic system so CSF acts as a partial substitute. Dura mater is a tough, protective connective tissue firmly attached to the skull and includes the subarachnoid space filled with the CSF, arteries and web-like connective tissue known as archanoid mater. The pia mater is a very delicate and permeable membrane composed of collagen, elastin and fibroblasts that rests on the floor of subarachnoid space and allows diffusion between CSF and the interstitial fluid of brain tissue. The pia mater is also interrupted by astrocyte processes. The dura mater, arachnoid mater and the pia mater are collectively known as meninges.

Recent evidences suggest that glutamatergic dysregulation implicated in neural plasticity and cellular resilience may contribute to the pathophysiology of Major Depressive Disorder (MDD). Riluzole, which exerts its effect by targeting glutamate neurotransmission, has shown antidepressant effect in recent preclinical, observational and open label studies. This study aimed to assess the efficacy and tolerability of riluzole in patients with MDD. Sixty-four inpatients with diagnosis of moderate to severe major depressive disorder participated in a parallel, randomized, controlled trial, and sixty patients underwent 6 weeks treatment with either riluzole (50 mg/bid) plus citalopram (40 mg/day) or placebo plus citalopram (40 mg/day). All participants were inpatients for the whole duration of the study. Patients were assessed using Hamilton depression rating scale (HDRS) at baseline and weeks 2, 4 and 6. The primary outcome measure was to assess the efficacy of riluzole compared to placebo in improving the depressive symptoms. General linear model repeated measures demonstrated significant effect for time _ treatment interaction on HDRS [F (1.86, 107.82) ¼ 8.63, p < 0.001]. Significantly greater improvement was observed in HDRS scores in the riluzole group compared to the placebo group from baseline HDRS score at weeks 2, 4 and 6 (p < 0.001, p ¼ 0.001, p ¼ 0.002, respectively). Significantly greater response with greater speed to treatment was observed in the riluzole group than the placebo group. No serious adverse event occurred. This study showed a favorable safety and efficacy profile in patients with major depressive disorder. Larger controlled studies with longer treatment periods are needed to investigate long term safety, efficacy and optimal dosing.

This work proposes a mathematical model about how a reaction is created in the human brain in response to a particular incoming Information/Event using quantum mechanics and more precisely path integrals theory. The set of action potentials created in a particular neuron N2 is a result of temporal and spatial summation of the signals coming from different neighboring neurons Nx with different dendrite-paths. Each dendrite-path of N2 is assumed to be determined by its respective synapse with its neurotransmitters and assumed to have an action S due to the neurotransmitter types (for example: excitatory or inhibitory). An external incoming signal information being initially modulated by receptor neurons (in eyes, ears...) travels through the neighboring neurons that are linked to the excited receptor neurons. A potential reaction responses are subsequently created thanks to a final deformed signal in the motor neurons by all the correlated neural paths. The total deformation at each neuron is created by different incoming dendrite-paths and their structures (inhibitory or excitatory neurotransmitters and their type), and of course the existence or not of the signal and its frequency coming from each path. Using path Integrals theory, we compute the probability of existence of the signal-Information or the potential reaction to the incoming information at each neuron. In this paper we also compute how much the signal-Information has been distorted between two neighboring linked neural points including if it arrives or not to the neighboring neurons. We propose an Information entropy similar to Shannon one and we demonstrate that this entropy is equivalent to timespace curvature in the Brain.

The recent years the interest in neurocognitive and brain science research is relatively increased. In this study the relation of DNA and genetic factors that are interrelated to brain development and cognitive functions is analyzed. Author’s main purpose is to localize and analyze the function of the particular parts of brain which are related to specific cognitive functions. Especially the connection of specific brain cortexes with mathematical perception and mathematical learning difficulties also known as dyscalculia is analyzed and evaluated as well. Future directions in order to evaluate and enhance the theoretical outcomes by visualizing the brain activity within the use of brain imaging techniques are also discussed.

An explorative review of literature of pharmacological aspects of acetylcholine (ACh) and dopamine (DA) neurotransmitter systems on the methods of causation of motor dysfunction, ranging from dyskinesia to tremulous jaw movements. The current author comments on the ACh system with reference to nicotinic ACh receptor (nAChR) blockade, competitive antagonism and tacrine-induced jaw tremor research. The DA system implication is also reviewed and raises current topical issues models of neuro-circuitry and ACh-DA interactions. To conclude, the ACh and DA systems and their interactions require future research to establish concrete mechanisms and the complexities of these system interactions to be explored in relation to dysfunctional motor behaviour.

Since the late 1970s glycine has been considered an important inhibitory neurotransmitter in brain stem and medulla. The description of its involvement in the mechanism of action of the potent neurotoxin strychnine pushed further the concept of inhibitory transmitter. The significant concentrations of glycine in forebrain motivated investigators to evaluate different aspects of glycinergic transmission under the ontogenetic, physiologic and pathologic standpoints. This review encompasses a few of these aspects as the role of the different glycine receptors (GlyRs) in intracellular chloride balance, glycine transporters, GABA/Glycine co-release, glycine/NMDA receptor interaction, glycine receptors in acute alcohol effects and advocates a more relevant role for glycine as a stimulatory transmitter in forebrain areas. Finally, the possible co-release of glycine and GABA is considered as an important process to understand the role of glycine in forebrain neural transmission.

Mealtimes and feeding schedules may interfere with the circadian system and impact sleep. The practice of intermittent fasting (IF) in its different formats is increasing worldwide. However, most studies addressing the effect of IF on circadian rhythms, daytime sleepiness, and sleep architecture have been conducted during diurnal IF for Ramadan. In this article, we analyze the effect of diurnal IF on the circadian clock, sleep, and daytime sleepiness. In free-living, unconstrained environments that do not control for lifestyle changes such as sleep/wake schedules, sleep duration, and light exposure, studies have demonstrated sudden and significant delays in bedtime and wake time during diurnal intermittent fasting for Ramadan. However, subsequent studies that accounted for lifestyle factors and sleep/wake patterns have reported no changes in markers of the biological clock, daytime sleepiness, or sleep parameters. Nevertheless , several researchers have demonstrated a reduction in the proportion of rapid eye movement stage sleep as the significant alteration in sleep architecture during fasting.

Vasoactive intestinal peptide (VIP) is an important modulator of hippocampal synaptic transmission that influences both GABAergic synaptic transmission and glutamatergic cell excitability through activation of VPAC 1 and VPAC 2 receptors. Presynaptic enhancement of GABA release contributes to VIP modulation of hippocampal synaptic transmission. EXPERIMENTAL APPROACH We investigated which VIP receptors and coupled transduction pathways were involved in VIP enhancement of K +-evoked [ 3 H]-GABA release from isolated nerve terminals of rat hippocampus. KEY RESULTS VIP enhancement of [ 3 H]-GABA release was potentiated in the presence of the VPAC 1 receptor antagonist PG 97-269 but converted into an inhibition in the presence of the VPAC 2 receptor antagonist PG 99-465, suggesting that activation of VPAC 1 receptors inhibits and activation of VPAC 2 receptors enhances, GABA release. A VPAC 1 receptor agonist inhibited exocytotic voltage-gated calcium channel (VGCC)-dependent [ 3 H]-GABA release through activation of protein G i/o , an effect also dependent on PKC activity. A VPAC 2 receptor agonist enhanced both exocytotic VGCC-dependent release through protein G s-dependent, PKA-dependent and PKC-dependent mechanisms and GABA transporter 1-mediated [ 3 H]-GABA release through a G s protein-dependent and PKC-dependent mechanism. CONCLUSIONS AND IMPLICATIONS Our results show that VPAC 1 and VPAC 2 VIP receptors have opposing actions on GABA release from hippocampal nerve terminals through activation of different transduction pathways. As VPAC 1 and VPAC 2 receptors are located in different layers of Ammon's horn, our results suggest that these VIP receptors underlie different modulation of synaptic transmission to pyramidal cell dendrites and cell bodies, with important consequences for their possible therapeutic application in the treatment of epilepsy.

Throughout this report I will be discussing reasons why our current psychiatric system needs improvements
concerning the use of psychiatric drugs and how they may not be the answer to the symptoms of schizophrenia. This
is an important topic to study considering the health dangers that patients are faced with today as a result of their
illness and the medication used for it. I have researched the high success rates of alternative, minimum medication
programmes, like open dialogue, which have greater focus on psychotherapies, as opposed to antipsychotic
drugs. I have discussed the fundamental flaws with our accepted ideas of schizophrenia, and the implications this
neurobiological research has for treatments. I have highlighted the problems with the psychiatric pharmaceutical
industry, (particularly drug trials) which markets drugs in a misleading way, creating a paradigm where psychiatrists
rely heavily on antipsychotics to stabilise their patients. This is not the best solution for the long term health of patients.
I have concluded in this report that improvements to our system through increased integration of psychotherapies
and lower dosages of psychiatric drugs, would greatly impact the quality of treatment that schizophrenic patients
receive.

Currentimagingtechniqueshavelimitedabilitytodetectneurotransmittersreleasedduringbrainprocessing.Itisacriticallimitationbecauseneurotransmittershavesignificantcontroloverthebrainactivity.Inthiscontext,recentdevelopmentofsingle-scandynamicmolecularimagingtechniqueisimportantbecauseitallowsdetection,mapping,andmeasurementofdopaminereleasedinthebrainduringtaskperformance.Thetechniqueexploitsthecompetitionbetweenendogenouslyreleaseddopamineanditsreceptorligandforoccupancyofreceptorsites.Dopaminereleasedduringtaskperformanceisdetectedbydynamicallymeasuringconcentrationofintravenouslyinjectedradiolabeledligandusingapositronemissiontomography(PET)camera.Basedontheligandconcentration,valuesofreceptorkineticparametersareestimated.Theseestimatesallowdetectionofdopaminereleasedinthehumanbrainduringtaskperformance.

Reversal learning has been studied as the process of learning to inhibit previously rewarded actions. Deficits in reversal learning have been seen after manipulations of dopamine and lesions of the orbitofrontal cortex. However, reversal learning is often studied in animals that have limited experience with reversals. As such, the animals are learning that reversals occur during data collection. We have examined a task regime in which monkeys have extensive experience with reversals and stable behavioral performance on a probabilistic two-arm bandit reversal learning task. We developed a Bayesian analysis approach to examine the effects of manipulations of dopamine on reversal performance in this regime. We find that the analysis can clarify the strategy of the animal. Specifically, at reversal, the monkeys switch quickly from choosing one stimulus to choosing the other, as opposed to gradually transitioning, which might be expected if they were using a naive reinforcement learning (RL) update of value. Furthermore, we found that administration of haloperidol affects the way the animals integrate prior knowledge into their choice behavior. Animals had a stronger prior on where reversals would occur on haloperidol than on levodopa (L-DOPA) or placebo. This strong prior was appropriate, because the animals had extensive experience with reversals occurring in the middle of the block. Overall, we find that Bayesian dissection of the behavior clarifies the strategy of the animals and reveals an effect of haloperidol on integration of prior information with evidence in favor of a choice reversal.

Evidence suggests that alcohol affects brain function by interacting with multiple neurotransmitter systems, thereby disrupting the delicate balance between inhibitory and excitatory neurotransmitters 6. It's often said that depression results from a chemical imbalance, but that figure of speech doesn't capture how complex the disease is. Research suggests that depression doesn't spring from simply having too much or too little of certain brain chemicals. Rather, depression has many possible causes, including faulty mood regulation by the brain, genetic vulnerability, stressful life events, medications, and medical problems. Short-term alcohol exposure tilts this balance in favor of inhibitory influences. After long-term alcohol exposure, however, the brain attempts to compensate by tilting the balance back toward equilibrium 7. These neurological changes occur as the development of tolerance to alcohol's effects. When alcohol consumption is abruptly discontinued or reduced, these compensatory changes are no longer opposed by the presence of alcohol, thereby leading to the excitation of neurotransmitter systems and the development of alcohol withdrawal syndrome. Long term alcohol intake also induces changes in many neurotransmitter systems that ultimately lead to the development of craving and alcohol-seeking behavior. It's believed that several of these forces interact to bring on depression 9. To be sure, chemicals are involved in this process, but it is not a simple matter of one chemical being too low and another too high. Rather, many chemicals are involved, working both inside and outside nerve cells. There are millions, even billions, of chemical reactions that make up the dynamic system that is responsible for your mood, perceptions, and how you experience life. With this level of complexity, you can see how two people might have similar symptoms of depression, but the problem on the inside, and therefore what treatments will work best, may be entirely different. Researchers have learned much about the biology of depression 7. They've identified genes that make individuals more vulnerable to low moods and influence how an individual responds to drug therapy. One day, these discoveries

Personal genomic analysis was used for molecular diagnosis and pharmacogenomics in a 53-year-old female suffering from alternating depressive and dysphoric episodes. A total of 52 genes and 108 SNPs were analyzed in the whole genome. Results from the pharmacogenomic analysis were consistent with the pharmacological history and indicate mutations associated with low monoaminergic tone, but also a hyperactive 5HT2A receptor, a feature that associates to a high probability of developing a bipolar condition, especially under 5-hydroxytryptamine potentiating pharmacology. This aligns with the patient developing dysphoria with high clomipramine. The pharmacokinetic genomics pointed out to some absorption, distribution, metabolism, and excretion (ADME) alterations that can lower or nullify drug&#39;s activity. A personalized regimen was proposed, with a positive outcome after 1 year.