Questions related to Neuropsychopharmacology
Hi everyone ^_^
I was wondring if there is a specific technique to study the chemical change responsible for DID and I want to know if I could follow a specific procedure to the neurochemicals behinde this disorder and how the alteration vary between a normal person and a DID patient? also, the most important thing is finding a specific drug to cure this disorder. I know that there are drugs that help the patients endure anixty and depression come with this disorder but there is no direct and specific cure for DID.
I read that contextual treatment helped the patient somehow to know themselves and some of them return the control and can change from one personlaity to the other when they want but it didn't work for most of them although it benfits them somehow but not cure them. So; I read a lot of artiles and reviews from the litreture but most of them focused in the contextual treatment not chemical based treatment!!
I don't know if this is right or not but I think this return to neuropsychopharmacology and I'm a chemistry master student so I want to know if there is a possibility to study this in my thesis project and if I need a high tech equipments to do that?
Zipurshy RB, Reilly TJ, Murray RM. The myth of schizophrenia as a progressive brain disease. Schizophr Bull 2013;39:1363-72
Andreasen NC, Liu D, Ziebell S, et al. Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study. Am J Psychiatry 2013; 170:609-15
Dorph-Petersen KA, Pierri JN, Perel JM, et al. The influence of chronic exposure to antipsychotic medications on brain size before and after tissue fixation: a comparison of haloperidol and olanzapine in macaque monkeys. Neuropsychopharmacology 2005;30:1649-61
I have 2 group of mice, one of them should have seizure like behaviors, however, I didn't notice that phenotype, so I want to induce seizure in mice, and check if there are some difference between the 2 groups, anyone can give me some suggestions? thanks a lot! Hailong Hou
Can anyone recommend a drug that either a) increases tonic dopamine in the striatum and has a short half-life, or b) decreases tonic DA but does not affect phasic DA?
Recently I learned of the potent CYP1A2 induction effects of proton-pump inhibitors (ie. omeprazole etc). These medications can significantly reduce olanzapine and clozapine concentrations. Which medications are we overlooking when it comes to CYP1A2 induction?
Papakostas et al showed adjunctive LMF to be effective in treatment of mdd in 2012 with a NNT of 6 patients. The 2014 follow up article in J Clin Psych by Papakostas et al assessed biomarkers of LMF responders showing no statistically significant difference in HDRS-28 scores between MTHFR 677 CC (wild type) and MTHFR 677 TT (varient, reduced activity) patients.
Reduced or inactive MTHFR activity is not specific to depressive disorders.
Where does this leave us when depressed patients present with reduced or inactive MTHFR? I am thinking it should not lead towards LMF supplementation.
I have been thinking about using Clarity to compare the expression of specific protein before and after addictive drug treatment, to kind of visualizing aberrant plasticity at molecular level. But wondering if the resolution of Clarity would be good enough for this purpose, since the abnormal circuits are the primary reports from the Clarity methodology.
"Conscious activity" here means Primary Consciousness (G. Edelman), or Sentience in the sense of the capacity of Feeling. There is no doubt that higher cognitive functions are carried by neurons.
Several lines of evidence have related astroglial function with conscious processes. I make a brief summary of the most interesting studies, many of them discussed in my previous publications (Pereira Jr. and Furlan, 2009; 2010; Pereira Jr, 2013; 2014). These results come from several independent respected laboratories. Schummers et al (2009), in a work carried on the M. Sur Lab in MIT, found that astrocytes in the visual cortex are more sensitive to external stimuli than neurons. Thrane et al. (2012) from the M.Nedergaard Lab in Rochester-USA found that astrocytes are more sensitive to three commonly used general anesthetics than neurons. Sfera et al. (2015) argue that conscious delirium derives from a combination of cholinergic inflammatory processes and astroglialfunction failure. A conference summary of empirical results indicating the involvement of glial cells in mental activities appeared in Douglas Fields et al. (2014).
By means of the feedback on neurons, astrocyte information processing can have an effect on learning, memory and behavior (for a recent review, see Robertson, 2013).Takata et al. (2011) found that astrocytes mediate cholinergic neuromodulation into cortical plasticity. Han et al. (2013) inserted human astrocytes in the mouse forebrain and found an improvement of cognitive performance. In this regard, Lee et al.(2014), from the T.Sejnowski Lab in the Salk Institute found that toxic deactivation of astroglial functions impairs recognition memory, a task that involves conscious recall and processing of novelty.
Astrocytes also seem to be involved in the instantiation of emotional feelings and psychosomatic responses, as in the case of chronic pain (see Chen et al., 2012; 2014; Ji et al., 2013). As the mediation between neurons and blood is made by astrocytes through the blood-brain barrier, astrocytes constitute the effector part of the hypothalamus (Panatier et al., 2006; Gordon et al., 2009) and nucleus accumbens (Bull et al, 2014), controlling the release of neuropeptides and their effects on conscious mood and feelings(e.g. hunger.; see Yang et al., 2015; Wang et al., 2015)and their related somatic responses, as the up-regulation of stress-related proteins (Zhao et al., 2008). More recently,Orstroff et al. (2014) from the J. LeDoux Lab in New York University discovered that astroglial processes retract from synapses with neurons that mediate fear signaling in the amygdala, and Will et al. (2015) related the number of astrocytes in the hypothalamus with the experience-learned ability to reach male orgasm.
Bull C, Freitas K, Zou S, Poland RS, Syed WA et al. (2014 Rat Nucleus Accumbens Core Astrocytes Modulate Reward and the Motivation to Self-Administer Ethanol after Abstinence. Neuropsychopharmacology (2014) 39: 2835–2845.
Chen MJ, Kress B, Han X, Moll K, Peng W, Ji RR,Nedergaard M. Astrocytic CX43 hemichannels and gap junctions play a crucial role in development of chronic neuropathic pain following spinal cord injury. Glia60(11):1660-70.
Chen G, Park CK, Xie RG, Berta T, Nedergaard M, Ji RR. (2014) Connexin-43 induces chemokine release from spinal cord astrocytes to maintain late-phase neuropathic pain in mice. Brain137(Pt 8):2193-209.
Douglas Fields R, Araque A, Johansen-Berg H, Lim S, Lynch G, Nave K,Nedergaard M, Perez R, Sejnowski T, Wake H. (2014) Glial Biology in Learning and Cognition. Neuroscientist. 20(5): 426–431.
Fellin T, Pascual O, Gobbo S, Pozzan T, Haydon PG and Carmignoto G.
(2004) Neuronal Synchrony Mediated by Astrocytic Glutamate Through
Activation of Extrasynaptic NMDA Receptors. Neuron 43(5): 729-43.
Gordon, G.R., Iremonger, K.J., Kantevari, S., Ellis-Davies, G.C., MacVicar, B.A., Bains, J.S. (2009) Astrocyte-mediated distributed plasticity at hypothalamic glutamate synapses. Neuron 64: 391–403.
Han X, Chen M, Wang F, Windrem M, Wang S, Shanz S. et al. (2013) Forebrain engraftment by human glial progenitor cells enhances synaptic plasticity and learning in adult mice. Cell Stem Cell 12:342–53.
Ji RR, Berta T, Nedergaard M. (2013) Glia and pain: is chronic pain a gliopathy? Pain 154 Suppl 1:S10-28.
Lee HS, Ghetti A, Pinto-Duarte A, Wang X, Dziewczapolski G, Galimi F, Huitron-Resendiz S, Piña-Crespo JC, Roberts AJ, Verma IM, Sejnowski TJ, HeinemannSF (2014) Astrocytes contribute to gamma oscillations and recognition memory. ProcNatlAcadSci U S A111(32):E3343-52.
Ostroff LE, Manzur MK, Cain CK, Ledoux JE. (2014) Synapses lacking astrocyte appear in the amygdala during consolidation of Pavlovian threat conditioning. J Comp Neurol. 522(9):2152-63.
Panatier, A. (2009) Glial cells:indispensable partners of hypothalamic magnocellularneurones.J.Neuroendocrinol. 21:665–672.
Pereira Jr. A (2013) Triple-Aspect Monism: A Conceptual Framework for the Science of Human Consciousness. In A. Pereira Jr. & D. Lehmann (Eds.)The Unity of Mind, Brain and World: Current Perspectives on a Science of Consciousness (pp. 299-337). Cambridge, UK: Cambridge University Press.
Pereira Jr. A (2014) Triple-Aspect Monism: Physiological, mental unconscious and conscious aspects of brain activity. Jnl. Integr.Neurosci., 13(2), 201-227.
Pereira, A. Jr., &Furlan, F.A. (2009) On the role of synchrony for neuron-astrocyte interactionsand perceptual conscious processing. J. Biol. Phys.35 , 465– 481.
Pereira, A. Jr., &Furlan, F.A. (2010) Astrocytes and human cognition: Modeling informationintegration and modulation of neuronal activity. Prog.Neurobiol. , 92 , 405– 420.
Pereira, A. Jr., Barros, R.F. & Santos, R.P. (2013) The calcium wave model of the perception-action cycle: Evidence from semantic relevance in memory experiments. Front. Psychol. 4: 1–-4.
Robertson JM. (2013) Astrocyte domains and the three-dimensional and seamless expression of consciousness and explicit memories. Med Hypotheses 81(6):1017-24.
Schummers,J,Yu, H and Sur, M (2008) Tuned responses of astrocytes and their influence on hemodynamic signals in the visual cortex. Science 320: 1638–1643.
Sfera, A, Osorio, C, Price, AI, Gradini, R and Cummings, M (2015) Delirium from the gliocentric perspective. Frontiers in Cellular Neuroscience 9: 171.
Takata, N., Mishima, T., Hisatsune, C., Nagai, T., Ebisui, E., Mikoshiba, K., Hirase, H. (2011) Astrocyte calcium signaling transforms cholinergic modulation to cortical plasticity in vivo.J. Neurosci. 31(49), 18155–18165.
Thrane, AS, Thrane VR, Zeppenfeld D, Lou N, Xu Q, Nagelhus EA & Nedergaard, M. (2012) General anesthesia selectively disrupts astrocyte calcium signaling in the awakemouse cortex. Proc. Natl. Acad. Sci. USA, 109, 18974–18979.
Wang, F. Smith, N.A., Xu, Q., Fujita, T., Baba, A., Matsuda, T., Takano, T., Bekar, L. &Nedergaard, M. (2012) Astrocytes modulate neural network activity by Ca2+-dependent uptake of extracellular K+. Sci Signal., 5, 26.
Wang Y, Hsuchou H, He Y, Kastin AJ, Pan W (2015) Role of Astrocytes in Leptin Signaling.J MolNeurosci. [Epub ahead of print]
Will RG, Nutsch VL, Turner JM, Hattori T, Tobiansky DJ, DominguezJM(2015).Astrocytes in the medial preoptic area modulate ejaculation latency in an experience-dependent fashion.BehavNeurosci. 129(1):68-73.
Yang L, Qi Y and Yang Y (2015).Astrocytes Control Food Intake by Inhibiting AGRP Neuron Activity via Adenosine A1 Receptors.Cell Rep. 11(5):798-807.
Zhao Y, Xiao J, Ueda M, Wang Y, Hines M, Nowak TS Jr, LeDoux MS. (2008) Glial elements contribute to stress-induced torsinA expression in the CNS and peripheral nervous system. Neuroscience 155(2):439-53.
Adler et al., (1999) found that formal thought disorder can be induced by administering ketamine to healthy volunteers. Is anyone aware of any literature that shows the long term effects of ketamine administration? Does ketamine only induce formal thought disorder directly after use? Or can ketamine produce an episode of formal thought disorder, even when it has not been used for a while?
I cannot find any studies that illustrate this, but I do not want to assume that there is no research in this area.
Selective norepinephrine and serotonin reuptake inhibitors (SNRI's) are commonly used in the treatment of cataplexy because cataplexy is the result of down dysregulated norepinephrine, itself the result of missing or greatly diminished orexinergic signaling.
However, cataplexy is also occasionally treated with Phentermine, which is a norepinephrine releasing agent.
What happens when a person takes both a releasing agent and a reuptake inhibitor (not necessarily specific to this example, but generally)? Is the result a greater concentration/availability of the protein you're after than you'd get with either individually?
Does anyone have figures for receptor affinities for older antipsychotics? I would be very grateful as I cannot find any data for drugs like zuclopenthixol, droperidol> I expect that they have significant histamine blockade but cannot see any on various published diagrams.
Cross addiction refers to the presence of two or more addictions - a common trait among addicts. Many cross addicted patients develop secondary dependencies in an effort to deal with their Cross addiction refers to the presence of two or more addictions - a common trait among addicts. Many cross addicted patients develop secondary dependencies in an effort to deal with their primary addiction..
What are the somatic and psychological factors that cause a cross addiction after primary addiction?
We use many agents "off label" (eg carbamazepine for bipolar) yet given history of abuse and psychotic reactions to both ketamine and phencyclidine we need to be cautious. In what situations should clinicians cross the line and administer ketamine?
The patient has responded to several APs regarding positive features but the negative features are quite treatment resistant to risperidone, olanzapine, amisulpride, ziprasidone, and aripiprazole. Thanks.
The synthetic cannabinoids (SC) currently being marketed as alternatives to plant cannabis have a higher risk of adverse outcomes than phyto (plant) cannabinoids.
The SC products on the market are much stronger agonists at the CB1 receptor than THC, and none contain a synthetic equivalent to the phyto-cannabinoid CBD, but is part of the increased risk also due to SC substances acting at other receptor sites?
I was wondering if there was any association between phenylketonuria (PKU) and stuttering. I have tried searching the literature, but unfortunately couldn't find much at all (other a paragraph on p58 of Multilingual Aspects of Fluency Disorders by Howell et al). In your opinion, is it possible for PKU (or its various subtypes) to cause a person to stutter? Why or why not? I am mostly interested in the genetic and pharmacological side of things but would really appreciate any input on the topic.
It is well established that depressed individuals tend to focus their attention on unhappy and unflattering information, to interpret information negatively, and to harbour pervasively pessimistic belief.
Should we consider negative processing biases when rodent models are used to determine antidepressant-like effects of drugs/extracts? If so, how?