Keywords

Behavior, drug, neurodegenerative disorder, addiction

Introduction

There is a lot of social vices occasioned by Arab spring, Boko Haram in Nigeria, Nigerian Fulanis herdsmen – farmers clashes, Aum Shirinkyo in Japan, demonstration following announcement of the present American president, threat from North Korean president, British exit from European Union, Catarlan and Scottish secessionists, ISIS/Talaban war, South Sudan ethnic war, religious and racial sentiments shown by some leaders and public figures and general increase of moral decadence among youths. Threatening, Reactionary, Unforgiving, Machiavellian and Partisan mind brain set has been theorized (Gonclaves and Boggio, 2017), to be responsible for political crises with attendant consequences on global current and future events (Coutinho et al., 2013) in relation to world politics (Jost et al., 2014). Habit is the way, manner, process of doing things in consistent form. Hence attitude can translate to habit and habit can translate to character. Character is the combination of factors that makes a person’s nature or personality (Robinson and Davidson, 2007). Habitual behaviour is a function of corticosteroidal loops that comprise sensorimotor, (BA 1-3) associative and limbic pathways (BA 23, 24, 31, 34, 35, 37, 38), whereas striatum comprises caudate (dorsomedial striatum), putamen (dorsolateral striatum) and mucleus accumbens (ventral striatum). But dopaminergic midbrain comprises substatantia nigra and ventral tegmental area. These pathways are responsible for goal-directed/flexible behaviour to habitual behaviour as well as Parkinson’s Disease (PD) and Huntington Disease (HD), respectively (Foerde, 2008). Senile dementia pathogenesis may so be along the pathway (BA 46, 47) (Strytzer, 2009). Habituation is the capability of brain to ignore irrelevant or extraneous information inundated sensority. Whereas the brain capacity to enhance or store certain memories traces through facilitation of synaptic circuits is called memory sensitization (Guyton and Hill, 2006). Human Immunodeficiency Virus / Immune Deficiency Syndrome (HIV/AIDS) affects about 37 million people worldwide (Bland, 1986). Despite anti-retroviral therapy, HIV-positive individuals do experience neuro HIV disorders such as cognitive impairment, substance abuse and dependence. Therefore, HIV –I transgenic (HIV-I Tag) rat, a model of neuro HIV has proven that HIV-I proteins in the CNS increases the sensitivity and susceptibility of HIV-positive individuals to substance abuse (Cappelletti et al., 2017).

Relationship between Drug and Habit Formation

During habit formation, thought, action and choice are less dependent on cognitive resources (knownuton and Diedrichson, 2008). Hence parts of brain in connection with habit when affected pathologically can lead to abnormal habit which ranges from breach of peace passing through hooliganism to war. Drugs that could affect this part of brain are alcohols, narcotics, hypnotics, stimulants and depressants. Area 32 (dorsal anterior cingulate) for emotional judgement, area 34 (dorsal endocrinal area) for memory and emotional assessment, area 35 (ferirhinal area) for happiness, sadness and disgust, area 38 (temporopolar area) for social and emotional processing, self-other distinction, memory retrieval and humour comprehension, area 46 (middle frontal area) for motivation attention and cognitive tasks and area 47 (orbital area) for emotional, affection and memory (Strotzer, 2009; Ozson et al., 2007) are responsible for recognition and acceptance of activities that can be turned to habits.Attitudes translate to habits which in turn translate to characters are functions of brain that is a key to mind and behaviour. The responsible parts which are area 7 (superior parietal area) involves episodic memory retrieval, area 9 (granular frontal area) for memory, cognitive task and personality, area 10 (frontopolar area) for central executive, area 11 (prefrontal area) for social behaviour, area 19 (preocipital area) for face recognition, area 20 (inferior temporal area) for emotional mind of colour and facial expression, area 23 (ventral posterior cingulate area) for face familiarity and emotional processes, area 24 (ventral anterior cingulate area) for emotional assessment of fair perception, area 27 (presubicular area) for memory eroding, area 28 (anticlinal area) for memory encoding and consolidation first affected on Alzheimer’s disease, area 31 (dorsal posterior cingulate area) for episodic memory retrieval and recognition of familiar faces are responsible for habit formation and change. Dispositional resistance to change predicts responses to other changes (Oreg, 2000), which has potential benefits of performing routine tasks with detrimental effects on non-routine tasks (Oreg, 2018).

Formation and Change of Habit

The role of striatum in the formation and change of habit cannot be over emphasized. The pathways are both direct and indirect with interneuron play that involves dopaminergic inputs, potential context and amygdala indicating that habits occur in graded strength, compete with strategies for translation to behaviour. Hence habit can be of different phenotypes expressed by signalling pathways in the brain (Amaya and Smith, 2018). Habit originates from dorsal striatum similar to putamen of primates (Knowlton and Patterson, 2016), which plays role in action-response phenomenon, punishment and contingency (Smith and Graybel, 2016). However, dorsomedial striatum caudate homologue is responsible for habitual measures that will lead to achievements of specific parts (Balleine and O’Doherty, 2010). The pathways involve dopamine and dopamine (D2) and adenosine (x2) receptors (Lovinfer, 2010). Neocortex (inflalimbic) and amygdala modulate basal ganglia for habits formation and changes (Amaya and Smith, 2018. Stronger habits could rise from strong and competing challenges (Gremel and Costa, 2013).

Formation and change of habit involve cognitive and attentional mechanisms, self-control, environmental pressures and intrapsychic forces (Cardeen and Wood, 2008). Cognitive process of habit formation, effortless self-control habit, changing habits, implementation, intentions, reminders, rewards are driven by persons and the environment (Rozin et al., 2011). Children should be helped to realize and give account of their specific goals (Hertsberg et al., 2015). During observation, neural structures are recruited for actual execution and observation which take place in the frontal lobe but not restricted to the ventral premotor cortex, although, it involves somatic pic motor circuits (Bucarso et al., 2001). Drugs, diet and stress promote habitual control to which is prevalent across neuropsychiatric disorders. Hence neural determinants of habitual control may change behaviour (Corbot, 2018). Striatum of the nasal sash is responsible for learning by receiving inputs from cortical returns. It comprises direct and indirect pathways from kinematics to habits. Not all highly trained behaviour sequences are habits (O’Hare et al., 2015).Motivational control of action is governed by cue-driven, outcome-insensitive habits and value based, goal directed behaviours. Habits are driven by putamen-thalamic motor regains and value-based decision making is a function of caudate network translating to restoring flexibility in rigid habits (Cecedi and Tricomi, 2018). Therefore, distinguishing cue and value driven action, discordance in contemporary methods, cortico-striatal connectivity, deficits in fail-directed control, compulsion-driven pathologies are very crucial to regulating actions control which are evident in neural abnormalities that impact on value-based decision making (Gillan et al., 2015).Our daily behaviour is based on habit learning and representations are functions of corticostriatal system via direct and indirect basal ganglia, some attentional mechanisms are habitual (Seger, 2018). Respiratory sinus arrhythmia (RSA) is a measure of parasympathetic influence on the heart rate that decreases when a person faces challenges. But skin conductance response (SCR) is a measure of sympathetic arousal that increases when a person meets challenges (Bahr, 2015), suggesting the roles of parasympathomimetic via vagal nerves which decreases diastole and sympathomimetic study increases both systole and diastoles indicating that meeting a challenge is more hectic and requires dissipation of energy than facing a challenge.

Brain and Habit Formation

Habit formation is computed by brain as evidenced by neurobiology which suggests that similar mechanisms for habitual learning and control apply across diverse psychological domains. For example, sensory system stimulates Hebbian and reinforcement learning leading to habit strength that selects action on environment which is interpreted by sensory systems (Pauli et al., 2018). Mastering a motor skill is a function of a decrease in variability that can reveal control priority (Sternad, 2018). Amblygonscarpus andogensis was administered to rats that displayed stereotype activities from amphetamine. The stereotype activities about 1-2hr after administration of the theatrics sign find that amphetamine can change goal-directed habit which can be unified by the extract (Ebbo et al., 2010). Also, condensed nitrogen carbocycles can be converted to various heteroatoms that can change habits invariably changing the mind and brain leading to temporary or permanent madness (Saganuwan, 2011).

Habit and Excitatory Neurotransmitter

Spinal plasticity affects locomotion which is both neuronal and synaptic that support and maintain acquisition of motor skills. This is achieved by reconciliation between spinal cord function and spinal cords, long-recognized reliability (Norton and Wolpan, 2018). Skills’ learning is dependent on memory retention of skill-use experiences overtime. The memory has to be consolidated and robust against unnecessary interference. Sleep consolidate skill learning by reducing the effects and protection of interference and aiding abstraction and generalization of skill learning (Heald, 2008). Mother’s opinion involving face to face contact is required to build a therapeutic relationship (Clarke et al., 2014). Social anxiety about the self-increased physiological arousal impacts on speech fluency. Respiratory sinus arrhythmia (RSA) is a measure of parasympathetic influence on the heart that reduces during challenge condition whereas skin conductance response (SCR) is a measure of sympathetic arousal that increases during challenge (Buhr, 2015). Habits are formed by brain and mind and can be notified by environment, drug and diets. Sympathometics, symnatholytics, parasympathetic and parasympathelytics can shape habit.

Drugs are agents that modify biochemical and structural functions of body system (Bereczkei et al., 2015). Drug seeking initially becomes volitional, progressively habitual and then compulsive (addiction) is from the nucleus accumbens to the dorsolateral striatum with endophenotypes related to cannabinoids, opioids and adenosine which are implicated in the regulation of striatal plasticity and habit formation (Fouyssac et al., 2007). However, adrenaline, an adrenergic neurotransmitter secreted by adrenal medulla is responsible for perception of fear and flight. Sympathomimetic drugs are amphetamine, ephedrine, cocaine, cathinone which cause euphoria, an intense excitement and happiness, which is reactionary. When the affected person becomes addicted “compulsive use of drugs”, the tendency for forgiveness may be lacking, leading to further chance of motivating resultant psychopathy. Right amygdala is responsible for fear processing! A J-shaped relationship for increasing wine, beer and vascular risk in dose-response fashion has been established (Costango et al., 2011). Organ donors with type 1 diabetes are associated with illicit drug abuse and suicide (Jacobsen et al., 2017). Selective serotonin reuptake inhibitors (SSRIs) cause suicidality, hostility, agitation and mania (Bostwick, 2006). Psychotropic drugs motivate violence, cause medical illness including psychiatric disorders can be treated by psychotropic drugs (CCHR, 2006). Emotional stress associated with a chronic illness or painful condition alters patient’s temperament (Dorman, 2002). Psychotropic drugs could also cause violence and suicide in soldiers, vets (CCHR) and medical residency trainees (Yaghmour et al., 2017). Drug addiction is associated with mood swing, depression, suicidality and conflict (Cantao and Bolti, 2016) and overdose could cause suicide with respect to age, sex and country (Varnik et al., 2011).

Drugs cause obsession

Obsession is a state of preoccupying someone in mind to a disturbing extent. Compulsivity is caused by imbalance between brain’s goal directed and habit-learning system and could be affected by stress and anxiety (Gilan el al., 2016). However, addiction is a brain maladaptive, functional, reorganizational process in reward-related habit, executive control (Yalachkov et al., 2007). Chronic stress increases dendritic complexity that may facilitate the recruitment of habit and addiction related neurocircutries through neuronal restructuring of the striatum (Taylor et al., 2014). Both ventral striatal and central nucleus pathways of the amygdala control habit (Belin et al., 2013). Dopamine, a neurotransmitter released from negro-striatal pathway is used in treatment of Parkinson’s disease (PD) and may cause obsessive-compulsive disorders such as gambling and sexual activity. Dopamine agonists such as pramipexole, ropinirole, amphetamine and cocaine when taken in large doses for a long time can cause schizophrenia characterized by behavioral (social isolation, hostility, lack of restraint) cognitive (delusion, amnesia, mental confusion, false belief of superiority), mood (anger, anxiety, apathy), psychological (paranoia, fear, depression, hallucination, delusion) and speech (circumstantial, incoherent, rapid and frenzied speech). Altered dopamine (D1) receptor activity agonist or antagonist in basolateral amygdala may impair fear suppression (Ng et al., 2018). Midbrain dopamine signaling maintains motivation of ongoing bouts (Fischbach – Weiss et al., 2017). Addiction is a chronic brain disease with strong genetic, neurodevelopmental and sociocultural components. Drugs of abuse triggers supraphysiologic surges of dopamine in the nucleus accumbens, which activates direct striatal pathway via D1 receptors and inhibits the indirect striato-cortical pathway via D2 receptors. Repeated intake triggers glutamatergic inputs to the striatum and midbrain dopamine neurone (Volkow and Morales, 2015). The neurotransmitters responsible for addiction are dopamine, serotonin, gammaaminobutyric acid, acetylcholine, oxytocin, nociceptin, substance P, hypocretin, norepinephrine, dynorphin, corticotropin-releasing factor, glutamate, endocannabinoids, neuropeptide Y and opioids (Koob and Volkow, 2016). Theory of mind is the ability to make inference about the mental states of others in order to predict their behaviour. An individual difference in spontaneous mentalization correlates with Machiavellianism. Therefore, those who have a stronger motivation for putting themselves into the mind of others can mislead and exploit them (Esperger and Bereczkei, 2011).

Drug Addiction is mediated via Neuron

Neuronal has to do with neuron, a specialized nerve that transmits nerve impulse. Neural transition of reinforcement for drug addiction may depend on the neuroplasticity in both cortical and striatal structures induced by chronic self-administration of drugs (Everitt and Robbins, 2005). The imbalance between ins and outs of the striatum is responsible for drug addiction (larger et al., 2015). Threatening, reactionary, unforgiving, motivating psychopathy is a neuropsychological disorder that has do with neuronal modulation or damage caused by drugs, stress, or aging. The pathway is nigrostriatal, including right amygdala, anterior cingulate, dorsal striatum, dorsal lateral prefrontal cortex, inferior frontal gyrus, insular and nucleus accumbens. Drugs that are associated with increased suicidal ideations are also associated with increased suicidal attempts (Robertson and Allison, 2009). Anaesthetics, sedatives, tranquilizers and anticonvulsants act via NMDA glutamate excitatory system or the GABA inhibitory system can cause large number of neurons to die by apoptosis, especially during the first trimester and first several years at birth (Olney et al., 2004). Drugs, alcohol and suicide represent growing share of U.S. mortality (Monnat, 2017). Takotsubo cardiomyopathy could complicate drug-induced suicidal attempt (Roman et al., 2013).Aging “to grow older” is a continuous physiological process that affects all the organs. As one is aging, the brain mass decreases and invariably the function decreases, leading to Alzheimer disease (senile dementia) with characteristics similar to that of schizophrenia.

The Role of Lymbic System in Drug Addiction

Stress and depression cause dendritic loss and atrophy and decreased glial cells in the hippocampus and prefrontal cortex, affecting the function of nucleus accumbens and hypothalamus. Conversely, stress could cause increased denditric arborization and new synapse formation in the amygdala, amplifying the function of this structure. These paradoxical neurohistological changes can cause anhedonia, amotivation, anxiety, fear, cognitive deficits that characterize depression (Andrade and Rao., 2010). Basolateral amygdala-insular cortex supports parallel association in driving stimulus outcome versus stimulus-response associations within and between individuals (Nasser et al., 2018). The phasic dopamine signal functions more to signal violation of expectancies, to drive real-world associations between events (Sharp and Schoenbaum, 2018). The medial prefrontal cortex coordinates goal directed behavior mediated by dopamine release in the nucleus accumbens in a complex frequency and dose dependent manner (Hill et al., 2017). Drugs that affect limbic system are eltoprazine, tramadol among others (Korte et al., 2016).

Disorders caused by Drug Addiction

Disorder, lack of order or an illness is related to Threatening, Reactionary, Unforgiving, Motivating, Psychopathy. The neuropsychosocial disorders are stress, anxiety, somatoform, dissociative, sexual dysfunction, personality, schizophrenic, paranoid organic brain, affective, mental retardation, child and adolescent disorders (Mahmood, 2008), which may have implications of attention deficit and hyperactivity disorder (ADHD), alcoholism (triggering transmitters), autism (a mind unaware of itself and others), Deja vu (true hallucinations), dyslexia (an island of disability within an ocean of competence), handedness (left turn signals), perfect pitch (turned in the genes), photographic memory (data , data everywhere), seasonal affective disorder (the winter blues) and synesthesia (when the notes have colors and letters make pictures) (Bragdon, 2003).Psychopathy is a personality disorder characterized by egotistical trait, impaired empathy, antisocial behavior. Psychopathy is a component of the dark triad. But Machiavellianism is characterized by cooperation with partners in a Trust game associated with dorsal lateral prefrontal cortex and utilization of competitive strategies in the inferior frontal gyrus. Other components are narcissism, characterized by lack of awareness of his personality predicament, behavior and effect.

Treatment of disorders caused by Drug Addiction

Dorsolateral and dorsomedial striatum histone deacetylase (HDAC) negatively regulates transcriptional process underlying habit formation. HDAC3 may be targeted for prevention or reverse of maladaptive compulsive behavior (Malvaeg and Wassum, 2018). Cells inherit molecular memories of previously experienced conditions linked to histone variants and DNA replication (Velamis and Goodrich, 2017). The detection of a mismatch between our predictions and realities allows to learn from our error and it is a function of midbrain dopamine neurons which encode multiple types of errors signals and contribute to multiple forms of error – driven learning (Keiflin and Janak, 2017). Dopamine prediction errors reflect more dimensions of an expected outcome (vector) than scalar reward value (Langdon et al., 2018). . There is no clear evidence of an association between antiepileptic drugs and increased risk of suicide due to clinical and methodological heterogeneity (Ferrer et al., 2014). Waiting and stopping impulsivity are regulated by increased chatecholamine release in the prefrontal cortex and dopamine release in the nucleus accumbens and decreases motivation for reward and waiting impulsivity, but increases stopping impulsivity (Korte et al., 2017). Anterior cingulate is responsible for nicotine reversal of ethanol – induced learning deficits. In addition, the anterior cingulate, dorsal hippocampus and ventral hippocampus mediate drug-induced changes in anxiety (Gulick and Gould, 2011). Statins may lower risk of developing depression (Yang et al; 2018). Behaviour represents the response of a particular brain to an environment (Carr, 1983). Group work with population at risk (Grief and Ephross, 1997) may be associated with that requires self-control, which involves socialization, cognitive variables (cause – effect relations) and emotion regulation (Nenar and Keng, 2000). Piroxicam has both inhibitory and excitatory effects on CNS (Saganuwan and Orinya, 2015) hence can be used in the treatment of diseases associated with CNS depression and excitation (Saganuwan, 2017a; 2017b) which is based on change of functional group (Saganuwan, 2017c).

Drug Addiction and Law

The spiral model of behavioral changes are pre-contemplation, contemplation, preparation and action (Banyard, 1996) which are routine, repetition and relaxation based (Ross, 1984). The treatment of disorders caused by drug addiction requires critical counseling and psychotherapy (Corey, 1990). But taking action to avoid troubles is the most important step of the peer pressure reversal (Scott, 1985) as drug addiction could lead to neonaticide, homicide, infanticide and filicide (Mckee, 2006). Dementia is an abnormal condition marked by multiple cognitive deficits that include memory impairment. It is seen in 15% of people over 65years (Weiten, 2007). However, motor control emerges from interaction between the individual, the task and the environment (Shumway-Cook and Woollacott, 1995). Psychosocial problems could be solved via interaction leading to conflict resolution (Pettijohn, 1998). Over 1000 American kids have lost parents in the Iraq war (Junn and Boyatzis, 2006), unveiling informational, normative social influence and emergencies by dissecting and breaking the rules (Aronson et al., 2010) that can help solving neuropsychosocial problems that would avoid 3rd global war. All these are dependent on personality and personal growth (Frayrer and Fadiman, 1998).

HIV-Associated psychosis

N – myc downstream regulated gene 2 (NDRG2) fused with TAT protein (TAT-NDRG2) can be used to treat brain problem (Carey et al., 2013). Trans-activator of transcription (TAT) implicated in neuro-pathogenesis of HIV-I infection damages neuron and impairs learning and memory by reducing gray matter density in the sublenticular extended amygdala, amygdala, amygdala – hypocampal area, piriform, perilentorhinal cortices and hypothalamus in mice (Carey et al.,2012). TAT interaction with opioids potentiates neuro-inflammation and neurodegeneration CNS via C-C chemokine receptor type 5 (CCR5). Morphine caused increase in endogenous CCR­5 chemokine ligands (CCL3, CCL4, CCL5 and CCL2). But maraviroc attenuated the cytokines indicating that CCR5 mediates HIV – I TAT- induced alterations has antinociceptive potency and rewarding properties of opioids (El-Amine et al., 2018). The HIV-1 TAT induced dysfunction of mesolimbic dopaminergic pathway impaired reward processes and contributed to methamphetamic abuse in HIV-human. Dopamine adenosine receptor interactions and neuronal recruitment represents target for treatment of amphetamine abuse in HIV humans. The pathway is via nucleus accumbens, caudate putamen and ventral tegmental area (Farokninejad et al., 2017).TAT modulate the function of dopamine transporter and damage dopamine – rich regions of the CNS, hence may cause Parkinsonism (Bland, 1986).

Mediation of neurotransmitters in HIV-associated psychosis

Neurodegenerative diseases are irreversible as seen in HIV infection that involves glial cells and macrophages (Fitting et al., 2010). HIV-TAT protein induced sensorimotor deficits associated with acute and persistent neuro inflammation in limbic and extralimbic parts of brain (Gaskil et al., 2017).It also mediates cognitive abnormalities observed in HIV infected individuals (Gonek et al., 2017).TAT expression decreased dopamine in caudate putamen, increased serotonin in the hippocampus and increased conversion of glutamate to glutamine in all regions of the brain cells, whereas selegiline decreased serotonin metabolism. TAT-induced alterations in glutamate signaling and facilitates reversal learning (Gupta & Kulhara, 2007). Therefore, treatment of HIV-induced psychosis may be by inhibition of both postsynaptic dopamine receptors and presynaptic ether-a-go-go (erg) potassium (K) channels (Hahn et al., 2016).The human face receives sensory information from the environment, which is transmitted to the cortex (Hothersall et al., 2017) HIV-I TAT alters the intrinsic capacity of mu-opioid-receptors signaling in response to agonist binding via beta-arrestin-2 function (Huang et al., 2018). HIV-TAT disrupts blood brain barrier integrity and causes phagocytosis, microlysis and increased perivascular macrophages (Kesby et al.,2016).

TAT induced oxidative stress, DNA damage and chromosomal aberrations in HIV-I infected individuals (Kesby et al., 2015). Pathogenic role of methamphetamine promotes cardiac left ventricular dysfunction greater than TAT-induced effects (Kesby et al., 2017). TAT expression leads to reward deficits (Koczor et al., 2015), disrupts mu and kappa, receptors, proopiomelanocortin, proenkephalin and prodynorphin transcript level in cortex, hippocampus and striatum. The abnormality of dendrocytes and reduction in spine density caused by TAT/morphine is responsible for neurodegenerative changes in neuro AID and may exacerbate neurological imparinats in HIV patients who abuse opioids (Liebrand et al., 2017). However, heterodimerization of the kappa opioid receptor and neurotensin receptor I contributes to a novel β-arrestin -2-biased pathway (Liu et al., 2016). Human HSP 70-2 (chaperone) expressed in the CNS when added to human neuroblastomas offered protection against hydroxydopamine stress (Meng et al., 2017). Residues W1320 and Y328 on the mu-receptor influenced opiate ligand bias by DAMGO increasing relative β-arrestin 2 activity at the W320A mutant and endomorphin – I gaining activity with Y328F. Therefore, endomorphin – 2 was involved in a directional shift from cAMP bias towards β-arrestin 2 at W320A (Miller, 1987). TAT enhanced delivery of the Cterminus of HDAg-l inhibited hepatitis D2 virus and may have therapeutic potential against HDV infection (Nath & Steiner,2014). Signifying that a co-infection of HIV and HDV may help in elimination of the latter and proffer immunity against HDV infection.

TAT-haFGE14-154 upregulated ADAM 10 and attenuated Alzheimer phenotype of App/PS mice via neuro protection pathway (NCA, 2007). In vivo exision of HIV-I proviral DNA by sg RNAs/SsaCas9 in solid tissues achieved via AA V delivery may serve as a guide towards having lasting solution for HIV infection (Paris et al., 2015). Memory changes produced in the hippocampus may result from interaction of stimulation of the reward centre via inhibition of drive sTATes in the frontal lobe and association with the drive sTATes in the limbic system (Saganuwan and  Onyeyili, 2014)). The common pathway of mechanisms actions of drugs of abuse is via dopamine in the limbic system to which may be therapeutically targeted in abuse treatment (Shepard et al., 2007). Severe infection can cause nerve hypersensitivity syndromes and chronic pain disorders (Siemionon et al. 2011; Vigorito et al., 2015), which may also affect theta cells in the hippocampal area that is sensorimotor and cause abnormal motor movement (Yin et al., 2017).

Conclusion

Drugs that act via corticosteroidal, limbic and mesolimbic pathways including sympathomimetics, sympatholytics, parasympathetics and parasympatholytics could change habit. Sympathomimetics and parasympatholytics increase systolic and diastolic pressure when challenges are met, whereas parasympathomimetics and sympatholytics decrease systolic pressure as well as systole and diastole when challenges are faced. Decreased systole and diastole could be responsible for criminal mind and behaviour which are functions of brain.

References

1. Amaya KA, Smith KS (2018) Neurobiology of habit formation. Behavioural Sciences 20: 145-152.
2. Aovirade C, Rao SK (2010) How antidepressant drug act: a primer on neuroplasticity as the eventual mediator of antidepressant efficacy Ind J Psychiat 52(4): 378-388.
3. Aronson E, Wilson TD, Akert RM (2010) Social Psychology, 7th ed., person, USA p 623.
4. Balleine BW, O’Doherty JP (2010) Human and lodegt homologies in action control: Corticostriatal determinants of goal-directed and habitual action. Neuropsychopharmacology 35(1): 45-69.
5. Banyard P (1996) Applying Psychology of Health, Hodder and Stoughton 202.
6. Belin D, Belin – Rauscent A, Murray JE, Everitt BJ (2013) Addiction: failure of control over maladaptive incentive habits. Curr Opin Neurobiol 23: 564-572.
7. Bereczkei T, Papp P, Kincses P (2015) the neural basis of the Machiavellians’ decision making in fair and unfair situations. Brain Cogn 98: 53-64.
8. Bestwick JM (2006) Do SSALs cause suicide in children? The evidence is under-whelming. J Clin Psychol 62 (2): 235-241.
9. Bragdon AD, Brains that Work, a Little Bit Differently: Recent Discoveries About Common Brain Diversities, Barnes and Noble Books, New York, USA P125.
10. Buccino G, Binkofski F, Fink GR, Fadiga L, Fogassi L, Gallese V, Seitz RJ, Zilles K, Rizzolatti G, Freund HJ. Actions observation activates premotor and parietal areas in a somatopic manner: an FMRI study. European Journal of Neuroscience 2001; 13: 400-404.
11. Buhr AP. 10th Oxfor Dysfluency Conference, ODC 2014. 17-20 July, 2014, Oxford, United Kingdom. Attention to self and speech fluency. Procedia-Social and Behavioural Sciences 2015; 193: 336.
12. Buhr AP. Attention to self and speech fluency. Procedia Social and Behavioural Services 2015; 193: 336.
13. Bland BH. The Physiology and Pharmacology of hippocampal formation theta rhythms. Progress in Neurobiology 1986; 26: 1-54.
14. Cappelletti P, Binda E, Tunesi M, Albani D, Giordano C, Molla G, Pollegioni LR. Recombinant human TAT-HSP 70-2: a tool for neuroprotection. Protein Expression and Purification 2017; 138:18-24.
15. Carey AN, Liu X, Mintzopoulos D, Paris JJ, Muschamp JW, Mclaughlin Ji, Kaufman MJ. Conditional TAT protein expression in the GT-tg biogenic mouse brain induces gray matter density reduction. Progress in Neuro-psychopharmacology and Biological psychiatry 2013; 43(3): 49-54.
16. Carey AN, Sypek Ei, Singh HD, KAutman MJ, Mclaughlin JP. Expression of HIV-TAT protein is associated with learning and memory deficits in the mouse. Behavioural Brain Research 2012; 229: 48-56.
17. Cantao L, Botti NCL. Suicidal behavior among drug addicts. Rev Bras Enferm (Internet) 2016; 69(2): 366-373.
18. Carden L, Wood W. habit formation and change. Behavioural Sciences 2018; 20: 117-122.
19. Carr JE, Dengerink A. Behavioural Science in the Practice of Medicine, Elsevier Biomedical New York USA P474.
20. CCHR A, Review of How Prescribed Psychiatric Medications Could be During Members of the Armed Forces and Vets to Acts of Violence and Suicide 2014:29.
21. Clarke G, Millard S, Kelman E. Mother’s perspectives of a webcam service for children who stammer. Procedia. Services and Behavioural 2015; 193: 296-299.
22. Corbit LH. Understanding the balance between goal-directed and habitual behavioural control. Current Opinion on Behavioural Services 2018; 20: 161-168.
23. Corey G. Theory and Practice of Counselling and Psychotherapy, 4th ed., Brooks/Cole Publishing Company, Pacific Grove, USAP 475.
24. Costanzo S, Castelnuovo AD, Donati NB, Lacoviello L, de Gaetano G. Wine, beer or spirit drinking in relation to fatal and non-fatal cardiovascular events: a meta-analysis. Eur J Epidemiol 2011; 26:833-850.
25. Coutinho JF, Sampaio A, Ferreira M, Soares JM, Gonclaves OF. Brain correlates of pro-social personality traits: a voxel-based morphometry study. Brain Imaging Behav 2013; 7:293-299.
26. Ebbo AA, Elsa, AT, Ladan MJ, Etuk UF, Saganuwan SA. Antipsychotic effects of aqueous stem bark extract of Amblygonocorpus androgenises in wistar albino rats. Journal of Medical Plants Research 2011; (11)3 1033-1038.
27. Esperger Z, Bereczkei T. Machiavelianism and spontaneous mentalization: one-step ahead of others. Eur J Per 2011. Dol: 10. 1002/pers. 859.
28. Everitt BJ, Robbins TW. Neural systems of reinforcement for drug addiction from actions to habits to compulsion. Nature Neurosci 2005; 8 (11): 1481-1489).
29. El-Amine R, Germini D, Zakharova VV, Tsfasman T, Sheval EU, louzada RAN, Dupay C, Bilhou-Nabera C, Hamade A, Najjar F, Oksenhendler E, Lipinski M, Cheronyak BV, Vassetzky YS. HIV – I TAT protein induces DNA damage in human peripheral B-lymphocytes via mitochondrial ROS production. Redox Biology 2018 (15): 92-108.
30. Farokninejad F, Benbanani AB, Denbidi RR, Takshid MA. Expression and purification of TAT-NDKG2 recombinant protein and evaluation of its anti-proliferative effect on LNCap cell line. Protein Expression and Purification 2017; 138:25-33.
31. Fitting S, Xu R, Bull C, Buch SK, El-Hage N, Nath A, Knapp PE, Hauser KF,. Interactive comorbidity between opioid drug abuse and HIV-I TAT. American Journal of Pathology 2010; 177 (3): 1397-1410.
32. Ferrer P, Ballarin E, Sabate N, Vidal X, Rotten Kolber N, Amelio J, Hasford J, Smiedl G, Ibanez L. Antiepileptic drugs and suicide: a systematic review of adverse effects. Neuroepidemiology 2014; 42: 107-120.
33. Fischbach – Weiss S, Reese RM, Janak PM. Inhibiting mesolimbix dopamine neurons reduces the initiation and maintenance of instrumental repondaing Neuroscience 2017; 1-10.
34. Foerde K. What are habits and do they depend on the striatum? A view from the study of neuropsychological populations. Behavioural Sciences 2018; 20: 17-24.
35. Fouyssac N, Everitt BJ, Belin D. Cellular basis of the intrastriatal functional shifts that underlie the development of habit: relevance for drug addiction. Curr Opin Behav Sci 2017; 13:144-151.
36. Frager R, Fadiman J. Personality and Personal Growth, 4th et., Longman, P602.
37. Geceli AO, Tricomi E. Habits and goals: a motivational perspective on action. Behavioural Sciences 2018; 20: 110-116.
38. Gillan CN, Robbins TW, Sahakian BJ, vanden Heuvel OA, van Wingen G. The role of habit in compulsivity. Eur Neuropsypharmacol 2016; 26:828-840.
39. Gillau CM, Apergis-Schmte AM, Morein-Zamir S, Urcelay GP, Sule A, Fineberg NA, Sahakian BJ, Robbins TN. Functional neuroimaging of avoidance Rabits in obsessive-compulsive discoverer. Am I Psychiatry 2015; 172: 284-293.
40. Gonclaves OF, Boggio PS. Is there a T.R.U.M.P. brain? Implications for mental health and world peace. Porto Biomed J 2017; 2(6): 247-249.
41. Greif GL, Ephross PH. Group Work with Populations at Risk, Oxford University Press, New York P346.
42. Gremel CM, Costa RM. Orbito frontal and striatal circuits dynamically encode the shift between goal-directed and habitual actions. Nat Commun 2013: 4.
43. Gulick D, Gould TJ, Nicotine acts in the anterior cingulate, but not dorsal or ventral hippocampus, to reverse ehanol-induced learning impairments in the plus-maze discriminative avoidance task. Addict Biol 2011; 16 (1). 176-188.
44. Guyton AC, Hall JE. Pocket Comparison to Textbook of Medical Phsiology, 3rd Ed., Saunders, New Delhi, India P730.
45. Gaskil PJ, Miller DR, Gable-George J, Yano H, Khoshbouei H. HIV, TAT and dopamine transmission. Neurobiology of Disease 2017; 105: 51-73.
46. Gonek N, Mclane VD, Stevens DL, Lippold K, Akbarali HI, Knapp PE, Dewey WL, Hauser KF, Paris JJ. CCR5 mediates HIV-I TAT-induced neuro-inflammation and influences morphine tolerance, dependence and reward. Brain, Behavior and Immunity 2017: 1-15.
47. Gupta S, Kulhara P. Cellular and molecular mechanism of drug dependence: an overview and update Indian Journal of Psychiatry 2007; 49 (2): 85-90.
48. Hahn YK, Paris JJ, Lichtman AH, Hanser KF, Sim-Selley LJ, Selley DE, Knapp PE. Central HIV-1 TAT exposure elevates anxiety and fear conditioned responses of male mice concurrent with altered mu-opioid receptor mediated G. protein activation and ß-arrestin 2 activity in the forebrain. Neurology of Disease 2016; 92:124-136.
49. Hothersall JD, Torella R, Humphreys S, Hooley M, Brown D, McMurray G, Nickolls SA. Residues W320 and Y 328 within the binding site of the µ-opioid receptor influence opiate ligand bias. Neuropharmacology 2017; 118:46-58.
50. Huang HC., Lu H.F., Lai Y.H., Lee C.P., Liu H.K., Huang C. TAT-enhanced delivery of the C terminus of HDHg L inhibits assembly and secretion of hepatitis D virus. Antiviral Research 2018; 150:69-78.
51. Hertsberg N, Hollister JE, Zebrowski PM, Berguez A, Millard SK. Perspectives on therapeutic progress: 11-14 year-olds’ reflections. Procedia, Social and Behavioural 2015; 193: 344.
52. Hill DF, Parent KL, Atcherley CW, Cowen SL, Heien NL. Differential release of dopamine in the nucleus accumbens evoked by low-versus high-frequency medial prefrontal cortex stimulation. Brain Stim 2017. 1-9.
53. Jacobsen LM, Haller MJ, Parish A, Gurko MJ, Levine R, Wasserfall C, Campbell-Thompson M, Kaddis J, Pugliese A, Atkinson NA, Sahatz DA. High Illicit drug abuse and suicide in organ donors with type 1 diabetes. Diabetes Care 2017; 40, 123.
54. Jost JT, Nam HH, Amodio DM, Van Bavel JJ. Political neuroscience: the beginning of a beautiful friendship. Polit Psych 2014; 35 (1): 3-42.
55. Junn EN, Boyatzis CJ Child growth and Development, 13th ed., Contemporary Learning Series, Dubazae, USA P207.
56. Keiflin R, Janak PH. Error-driven learning: dopamine signals more than value – based errors Curr Biol 2017; 27: 30005-329.
57. Knowlton BJ, Diedrichen J. Editorial overview: habits and skills. Current Opinion in Behavioural Sciences 2018; 20: iv-vi.
58. Knowlton BJ, Patterson TK. Habit formation and the striatum. Curr Top Behav Neurosci 2016; 1-21.
59. Koob GF, Volkow ND. Neurobiology of addiction: a neurocirculatory analysis. Lancet psychiat 2016: 3:760-763.
60. Korte SM, Prins J, vanden Bergh FS, Dosting RS, Dupree R, Korte-Bouws GAH, Westphal KGC, Olivier B, Denys DA, Garland A, Gunturkin O. The 5-HTIA/IB-receptor agonist eltoprazine increases with catecholamine release in the prefrontal cortex and dopamine release in the nucleus accumbens and decreases motivation for reward and “waiting” impulsivity, but increases “stopping” impulsivity. Fur J Pharmacol 2017; 794:257-269.
61. Kesby JP, Markou A, Semenova S, TMARC Group. Effects of HIV/TAT protein expression and chronic selgiline treatment on special memory, reversal learning and neuro transmitter levels in mice Behavioural Brain Research 2016; 311: 131-140.
62. Kesby JP, Markous A, Semenova S. The effects of HIV-I regulatory TAT protein expression on brain reward function, response to psychostimulants and delay-dependent memory in mice. Neuropharmacology 2016; 109:205-215.
63. Kesby JP, Najera JA, Romoli B, Fang Y, Basova L, Birmingham A, Marcondes MCG, Dulas D, Semenova S. HIV – I TAT protein enhances sensitization to methamphetamine by affecting dopaminergic function. Brain, Behavior and Immunity 2017; 65: 210-221.
64. Koczor CA, Fields A, Jedrzejczak MJ, Jiao Z, Ludaway T, Russ R, Shang J, Torress RA, Lewis W. Methamphetamine and HIV-TAT alter murine cardiac DNA methylation and gene expression. Toxicity and Applied pharmacology 2015; 288 (3): 409-419.
65. Liebrand CR, Paris JJ, Ghandour MS, Knapp PE, Kim W-K, Hauser KF, McRae MP. HIV-I TAT disrupts blood-brain barrier integrity and increases phagocytic perivascular macrophages and microglia in the dorsal striatum of transgenic mice. Neuroscience Letters 2017; le40:136-143.
66. Liu H, Tian Y, Ji B, Lu H, Xin Q, Jiang Y, Ding L, Zhang J, Chen J. Bai B. Heterodimerization of the kappa opioid receptor and neurotensin receptor I contributes to a novel ß-arrestin-2-biased pathway. Bioclinicaet Acta 2016; 1863:2719-2738.
67. Langdon AJ, Sharpe MJ, Schoenbaum G, Niv Y. Model-based predictions for dopamine. Curr Opin Neurobiol 2018; 49:1-7.
68. Loringer DM. neurotransmitter roles in synaptic modulation, plasticity and learning in the arousal striatum. Neuropharmacology 2010; 58: 951-961.
69. Mahmud J. Abnormal Psychology, APH Publishing Corporation, New Delhi P334.
70. Malvaez N, Wassum KN. Regulation of habit formation in the dorsal striatum. Curr Opin Behav Sci 2018; 20: lg7-74.
71. Mckee GR. Why Mothers Kill. A Forensic Psychologist’s Casebook, Oxford University Press, New York, USA P290.
72. Monnat SM. Drugs, alcohol and suicide represent growing share of U.S. mortality. Carsey Res 2017; 112:1-6.
73. Meng T, Cao Q, Lei P, Bush AI, Xiang Q, Su Z, He X, Rogers JT, Chin I-N, Zhang Q, Huang Y. TAT-haFGF, 14-154 up regulates AID10 to attenuate the Alzheimer phenotype of App/PS, mice through the P13k-CREB-IREIa/xBPi pathway. Molecular Therapy: Nucleic Acids 2017; 7:439-452.
74. Miller NS. The relationship of addiction, tolerance and dependence to alcohol and drugs: a neurochemical approach. Journal of Substance Abuse Treatment 1987; 4: 197-207.
75. Nath A, Steiner J. Synaptodentric injury with HIV-TAT protein: what is the therapeutic target. Experimental Neurology 2014; 251: 12-14.
76. Neuro Centre of America (NCA). Nerve hypersensitivity syndromes and chronic pain disorders. Neurosensory Centre of Eastern Pennsylvania Kingston 2007.
77. Nasser HN, Lafferty DS, lesser EN, Bacharach SZ, Calu DJ, Disconnection of basolateral amygdala and insular cortex disrupts conditioned approach in pavlovian lever auto-shaping. Neurobiol learning Memory 2018; 147:35-45.
78. Ng KH, Pollock MW, Urbaxzyk PJ, Sangha S. Altering D1 receptor activity in the basolateral amygdala impairs fear suppression during a safety line. Neurobiol learning Memory 2018; 147:26-34.
79. Norton JJS, Wolpaw JR. Acquisition, maintenance and therapeutic use of a simple motor skill. Current Opinion in Behavioural Services 2018; 20: 138-144.
80. Nusbaum HC, Uddin S, Van Hedger SC, Heald SLM. Consolidating skill learning through sleep. Current Opinion in Behavioural Services 2018; 20: 174-182.
81. O’Hare J, Calakos N, Tin HH. Recent insight into corticostriatal circuit mechanisms underlying habits. Current Opinion in Behavioural Services 2018; 25: 40-46.
82. Olney JW Young C, Wozniak DF, Jevtovic-Todorvic/Ikonomidou, C. Do pediatric drugs cause developing neurons to commit suicide? Trends Pharmacol Sci 2004; 25(3) : 135-139.
83. Oreg, S.(2018). Resistance to change and performance : toward a more even-handed view of dispositional resistance. Journal of Applied Behavioural Sciences 54 (1): 88-107
84. Oreg, S. (2003). Resistance to change :developing an individual differences measure . Journal of Applied Psychology 88:680-693.
85. Olson IR, Plotzker A, Ezzyat Y. The enigmatic temporal: a review of findings on social and emotional processing. Brain 2007; 130: 1718-1731.
86. Pauli WM, Cockburn J, Pool ER, Perez OD, O’Doherty JP. Computational approaches to habits in a mode of free world. Current Opinion in Behavioural Sciences 2018; 20: 104-109.
87. Petti John TF. Notable Selections in Social Psychology, 2nd ed., Dushkin/Mc Graw-Hill, Guilford, USA P 352.
88. Paris JJ, Singh HD, Carey AN, Mclaughlin JP. Exposure to HIV-1 TAT brain impairs sensorimotor gating and activates microglia in limbic and extralimbic brain regions of male mice. Behavioural Brain Research 2015; 291:209-218.
89. Robertson HT, Allison DB. Drugs associated with more suicidal ideations are also associated with more suicide attempts. Plus one 2006; 4(10):e7312.
90. Robins P. Drugs of choice, drugs of change: Egyptian consumption habits since the 1920s. Third World Q. 2017:39.
91. Robinson M, Davidson G. Chambers 21st Centuries Dictionary, Chambers Edinburgh, UK P1654.
92. Romano N, Zorzoli F, Bertona R, Villani R Takotsubo cardiomyopathy as an early complication of drug-induced suicide attempt. Case Report Med 2013; 946378.
93. Ross BM. Our Special Child: A Guide to Successful Parenting of Handicapped children, Fleming H. Revell Company, New Jersey USA P252.
94. Rozin P, Scott S, Dinglem M, Urbanek JK, Jrang H, Katenbach M. Nudge to obesity 1: Minor changes in accessibility decrease food intake. Judgon Decis Mak 2011; 6:323-332.
95. Saganuwan SA. Functional chemical group that may likely become a source for the synthesis of novel central nervous system (CNS) acting drugs. CNSAMC 2017C;17 (3):178-186.
96. Saganuwan SA. Functional chemical groups that may likely become a source for the synthesis of novel central nervous system (CNS) acting drugs. Central Nervous System Agent in Medical Chemistry 2017; 17 (3).
97. Saganuwan SA. In vivo piroxicam metabolites: possible source for synthesis of central nervous system (CNS) acting depressants 2017b;17 (3):172-177.
98. Saganuwan SA. Piroxicam: source for synthesis of central nervous system (CNS) acting drugs. CNSAMC 2017;17 (2):135-140.
99. Saganuwan SA. Toxico-neurological effects of piroxicam in monogastric animals. J Exper Sci 2016;10:121-128.
100. Saganuwan SA, Onyeyili PA. Understanding of malaria and its therapeutic regimens: The way forward: International Journal of Tropical Diseases and Health 2014; 4(7): 802 – 840.
101. Shepard PD, Canavier CC, Levitan ES. Ether-a-go-go related gene potassium channels: what’s all the buzz about? Schizophrenia Bulletin 2007: 33: 167: 1263-12-69.
102. Siemionon MZ, Gharb BB, Rampazzo A. The face as a sensory organ In: the Know-How of Face Transplantation, Springer-Verlag, London 2011.
103. Scott S. Peer Pressure Reversal, Human Resource Development Press, Amherst, Massachusetts, 1985: 185.
104. Seger CA. Corticostriatal foundations of habits. Current Opinion on Behavioural Sciences 2018; 20: 153-160.
105. Sharpe MJ, Schoebaum G. Evaluation of the hypothesis that phasic dopamine constitutes a cached-value signal. Neurobiol Learning Memory 2017. https://doi.org/10.1016/j.nlm.2017.12.002.
106. Shumway-Cook A, Woollacoot M. Motor Control: Theory and Practical Applications, Lippincott Williams and Wilkins, A Wolters Kluner Company 1995: 473.
107. Smith KS, Graybiel FM. Habit formation. Dialogues Clin Neurosci 2016; 18: 33-43.
108. Sternad D. It’s not (only) the mean that matters: variability, noise and exploration in skill learning. Current Opinion in Behavioural Services 2018; 20: 183-195.
109. Strotzer M. One century of brain mapping using Brodmann areas. Clinical Neurol 2009; 3: 179-186.
110. Taylor SB, Anglin JM, Paode PR, Roggert AG, Olive MF, Conrad CD. Chronic Stress may facilitate the recruitment of Rabit-and addiction related neurocircuitness through neuronal restructuring of the striatum. Neuroscience 2014; 280:231-243.
111. Varnik A, Sisask M, Varnik P, Wu J, Kolves K, Arensman E, Maxwell M, Reisch T, Gusmao R, Van Audenhove C, Scheerder G, Vander Feltz-Cornells CM, Coffey C, Kopp M, Szekey A, Roskar S, Heger U. Drug Suicide: a sex equal cause of death on 16 European countries. BMC Public Health 2011; 11:61.
112. Vigorito M, Connaghan KP, Chang SL. The HIV-I transgeneric rat mood of neuro HIV. Brain, Behaviour and Immunity 2015; 48:336-349.
113. Volken ND, Morales M. The brain on drugs: from reward to addiction. Cell 2015; 162: 712-725.
114. Weiten W. Psychology: Themes and Variations, 5th ed., Wads worth, Thomson Learning, Belmont USA 2001P697.
115. Wenar C, Kerig P. Developmental Psychopathology: From Infancy Through Adolescence, 4th ed, McGraw-Hill Higher Education, Singapore P490.
116. Yager LM, Garcia AF, Wunsch AM, Ferguson SM. The ins and outs of the striatum; role in drug addiction. Neuroscience 2015; 301;529-541.
117. Yaghmour NA, Brigham TP, Richter T, Miller RS, Philibert I, Baldwin Jr, DC. Causes of death of residents in ACGME-accredited programs 2000. Through 2014; implications for the learning environment. Acad Med 2017; 92: 976-983.
118. Yalachkov Y, Kaiser J, Naumer MJ. Functional reorganization of reward and habit-related brain networks in addition. Addict, Sust Behave Health P193-200.
119. Yang CC, Jick SS, Jick H. Lipid-lowering drugs and the risk of depression and suicidal behavior. Arch Intern Med 2013; 163:1-7
120. Yin C, Zhang T, Qu X, Zhang Y, Putatunda R, Xiao X, Li F, Xiao W, Zhao H, Dai S, Qin X, Mo, X, Young, W-B, Khalil, K, Hu W. In vivo excision of HIV-I provirus by SaCas9 and multiplex single guide RNAs in animal models. Molecular Therapy 2017; 25(5): 1168-1186.