Consciousness
Von Economo neurons/ Intelligence?
Neurobiology of music
Neuroplasticity
Neural back firing
Aging
Nootropic drugs
Glia signalling
Neurorobotics/prosthetics
Brain imaging technology uses and limitations/ fMRI, EEG ect…
Brain training?
The brain and meditation
The neurobiological basis of focused attention
What is the function of the default network
Dissociation
Mirror neurons
Neural coding ( eg of motor cortex)
Microtubules
Calendar
Exam Sept 23 rd
Presentations

Cecelia Courville
Ideas to Research for PSY 456
1.
Autism

Research into the qualifications to be classified autistic including physical/biological and psychological characteristics, the psychological effects of physical symptoms, and correlations between psychological symptoms and areas of the brain.
2.
Phantom Limb

Looking into the idea of still being able to feel a part of the body that is no longer
3.
Korsakoff’s syndrome fugue state

The physical and psychological implications of amnesia conditions such as Korsakoff’s syndrome.
The basic idea I would like to research in respect to autism is the difference in early brain development between children who do and do not have autism. In addition to this question I would like to look into the early development in general for a person with autism from birth to approximately three or four years of age. I have found studies and papers about the early brain development in children with autism at early ages. These include some deal with early symptoms relating to perception and sociability, others that study the neurodevelopment in infancy, and articles relating to the development and regression associated to brain development in children with autism.
The basic idea I would like to research relating to the neurologic symptom of phantom limb, is the biology of the brain behind this event. I have found research in the area relating to conditions such as stroke and epilepsy. I have also found information in regards to amputees experiencing the symptom of phantom limb. The research looks at the neurologic basis of this condition and the brain activity associated with it, this includes perception and never feedback. In amputees it is debated whether this phenomenon occurs in the brain, or if it is the muscles in what remains of the limb that are reacting to the motor commands. Research in stroke patients leads to results suggesting that the phantom limb symptom is the result of activation of parts of the brain associated with motor skills.
The basic idea I would like to research relating to amnesia is particular types of amnesia including dissociative amnesia, global amnesia and Korsakoff’s syndrome. I have found research relating to these areas of amnesia and the brain activity that occurs during these states. At this time I have found less information regarding fugue states, but would also like to look into that as well providing there is enough research. I would focus mostly on trauma induced amnesia but also go into other events that can cause these states. This would include regions of the brain affected by the trauma and relating to amnesia.

Here are two of my most promising research topics.
I have changed my pcp topic from the long term effects of pcp use to just the effects of pcp use on brain chemistry. There is a great deal of research available on how pcp affects the different neurotransmitters of the brain over a short term period of time as well as a long term period of time. THere are also studies that discuss how pcp is used to induce schizophrenia in lab animals for the testing of antipsychotic medications. There seems to be sufficient research done on pcp in order to determine some of the effects that the drug has on our brian chemistry and neurotransmitter levels.
For my second topic I believe I would like to research the cause and individual variations of auditory hallucinations in people suffering from schizophrenia.
This could be interesting because I know that auditory hallucinations are somewhat common but can vary from mean and menacing voices that suggest taking one's own life and perpetuate feelings of worthlessness to in rare cases happy voices or even visual hallucinations that accompany the auditory ones. From what
I have seen so far there is a great deal of research done in this area so it should not be too difficult to find articles that help to explain the occurrence of these strange symptoms.
-Alex
Hi Dr. Hakan,
These are the three projects I thought would be interesting.
When Deep Brain Stimulation (DBS) is entered into PsycINFO over 2,000 articles are retrieved. If you add coma to the search, results go down to 10. But, if therapy is added to the search over 600 articles are found. I think DBS could be a interesting project since it is being used on not only coma patients, but also with anything from alcoholism, Parkinson’s, OCD, tremors, major depression, and even tics.
When stroke is entered into PsycINFO, over 21,000 results appear. Over 6,000 appear if you add treatment to the search. While viewing the articles it became apparent that there is plenty of information to be found on stroke research. Some articles are written on both pre and post-hospital interventions as well as pharmacological and non-pharmacological treatments.
Stem Cell Research is more narrow in that only about 3,500 results show up with
PsycINFO, and only 1,200 if you add treatment. But, the articles written are interesting and seem to cover a broad scope of neurological problems. Articles on
Stem Cells are currently being researched in issues such as brain and spinal cord injuries as well as Leukemia and host-tissue transplantation.

Hi Dr. Hakan,
Here are my potential project topics:
1. COTARD'S SYNDROME
-What is the physiological basis of this disorder?
-What does electroshock therapy do to the brain and why does it seem to help these patients?
-What is ariprprazole monotherapy and why does it help patients?
-What do medications like quetiapine and venlafaxine do to the brain, and why does this help Cotard's syndrome?
-Physiologically, why is Cotard's related to bipolar disorder and schizophrenia?
-If this topic is too narrow, I will expland it to Cotard's, Capgras, and Fregoli syndrome.
-References:
Charland-Verville, V., Bruno, M., Bahri, M., Demertzi, A., Desseilles, M., Chatelle, C., & ... Zeman, A.
(2013). Brain dead yet mind alive: A positron emission tomography case study of brain metabolism in
Cotard's syndrome. Cortex: A Journal Devoted To The Study Of The Nervous System And Behavior
49 (7), 1997-1999. doi:10.1016/j.cortex.2013.03.003
,
Simpson, P., Kaul, E., & Quinn, D. (2013). Cotard's syndrome with catatonia: A case presentation and discussion. Psychosomatics: Journal Of Consultation Liaison Psychiatry doi:10.1016/j.psym.2012.03.004
, 54 (2), 196-199.
Bandinelli, P., Trevisi, M., Kotzalidis, G., Manfredi, G., Rapinesi, C., & Ducci, G. (2011). Chronic Koro-like
Syndrome (KLS) in recurrent depressive disorder as a variant of Cotard's delusion in an Italian male patient. A case report and historical review. Rivista Di Psichiatria , 46 (3), 220-226.
Chou, P., Lin, B., Lan, T., & Chan, C. (2011). Chronic Cotard's syndrome: Recovery from 2 years' bed ‐ ridden status. Psychiatry And Clinical Neurosciences , 65 (3), doi:10.1111/j.1440-1819.2011.02206.x
Wani, Z. A., Khan, A. W., Baba, A. A., Khan, H. A., Ain Wani, Q., & Taploo, R. (2008). Cotard's syndrome and delayed diagnosis in Kashmir, India. International Journal Of Mental Health Systems ,
2 doi:10.1186/1752-4458-2-1

Fàzzari, G., Benzoni, O., Sangaletti, A., Bonera, F., Nassini, S., Mazzarini, L., & ... Girardi, P. (2009).
Improvement of cognition in a patient with Cotard's delusions and frontotemporal atrophy receiving electroconvulsive therapy (ECT) for depression. doi:10.1017/S1041610209008990
International Psychogeriatrics , 21 (3), 600-603.
De Berardis, D., Serroni, N., Campanella, D., Marasco, V., Moschetta, F., & Di Giannantonio, M. (2010). A case of Cotard's syndrome successfully treated with aripiprazole monotherapy. Progress In Neuro-
Psychopharmacology & Biological Psychiatry , 34 (7), 1347-1348. doi:10.1016/j.pnpbp.2010.06.015
Chan, J., Chen, C., Robson, D., & Tan, H. (2009). Case report: Effective treatment of Cotard's syndrome:
Quetiapine in combination with venlafaxine. doi:10.1111/j.1440-1819.2008.01891.x
Psychiatry And Clinical Neurosciences , 63 (1), 125-126.
Consoli, A., Soultanian, C., Tanguy, M., Laurent, C., Perisse, D., Luque, R., & ... Cohen, D. (2007).
Cotard's syndrome in adolescents and young adults is associated with an increased risk of bipolar
Shiraishi, H., Ito, M., Hayashi, H., & Otani, K. (2004). Sulpiride treatment of Cotard's syndrome in schizophrenia. disorder. Bipolar Disorders , 9 (6), 665-668. doi:10.1111/j.1399-5618.2007.00420.x
Neuropsychopharmacology , 29 (4), 607-609.
2. WINDIGO PSYCHOSIS AND OTHER MADE UP DISORDERS
-This project would be a compilation of misunderstood "disorders" such as a Windingo Psychosis, where the individual believes he or she is an ancient monster and becomes cannibalistic. This is still cited as a disorder although there are no reported cases.
-I would link this project to reports of out-of-body experiences and other delusions. I want to understand the physiological basis that makes one perceive such things.
-What parts of the brain can be stimulated to make people perceive an out-of-body experience?
-What part of the brain is active when we decide if our experiences were real or a delusion?
-Are certain people more susceptible to believe such experiences as reality?
-Can understanding these brain parts help us piece together a definition for consciousness?
-Are the reported cases of brain stimulation producing an "out-of-body" experience accurate?
References:
Marano, L. (1982). Windigo psychosis: The anatomy of an emic–etic confusion. Current Anthropology ,
23 (4), 385-412. doi:10.1086/202868
Salley, R. D. (1982). REM sleep phenomena during out-of-body experiences. Journal Of The American
Society For Psychical Research , 76 (2), 157-165.

Braithwaite, J. J., Broglia, E., Bagshaw, A. P., & Wilkins, A. J. (2013). Evidence for elevated cortical hyperexcitability and its association with out-of-body experiences in the non-clinical population: New findings from a pattern-glare task. Cortex: A Journal Devoted To The Study Of The Nervous System And
Behavior , 49 (3), 793-805. doi:10.1016/j.cortex.2011.11.013
Braithwaite, J. J., Samson, D., Apperly, I., Broglia, E., & Hulleman, J. (2011). Cognitive correlates of the spontaneous out-of-body experience (OBE) in the psychologically normal population: Evidence for an increased role of temporal-lobe instability, body-distortion processing, and impairments in own-body transformations. Cortex: A Journal Devoted To The Study Of The Nervous System And Behavior , 47 (7),
839-853.
Heydrich, L., & Blanke, O. (2013). Distinct illusory own-body perceptions caused by damage to posterior insula and extrastriate cortex. Brain: A Journal Of Neurology , 136 (3), 790-803. doi:10.1093/brain/aws364
De Ridder, D., Van Laere, K., Dupont, P., Menovsky, T., & Van de Heyning, P. (2007). Visualizing out-ofbody experience in the brain. doi:10.1056/NEJMoa070010
The New England Journal Of Medicine , 357 (18), 1829-1833.
3. AGNOSIA AND ANOSOGNOSIA
-How is agnosia linked with anosognosia?
-What parts of the brain are involved with the meshing of these two phenomenon?
-What parts of the brain are responsible for the transdermal interference with these disorders?
-Why do these disorders seem to occur in a single brain hemisphere?
-What areas do lesions destroy to induce asnosia and agnosognosia, and can they be induced in other ways?
References:
Welman, A. J. (1969). Right-sided unilateral visual spatial agnosia, asomatognosia and anosognosia with left hemisphere lesions. Brain: A Journal Of Neurology , 92 (3), 571-580. doi:10.1093/brain/92.3.571
Spillane, J. D. (1942). Disturbances of the body scheme: anosognosia and finger agnosia.
242 42-44. doi:10.1016/S0140-6736(00)70248-0
The Lancet ,
Starkstein, S. E., Vázquez, S., Migliorelli, R., Tesón, A., Sabe, L., & Leiguarda, R. (1995). A single-photon emission computed tomographic study of anosognosia in Alzheimer's disease. Archives Of Neurology ,
52 (4), 415-420. doi:10.1001/archneur.1995.00540280105024
Cutting, J. (1978). Study of anosognosia.
555. doi:10.1136/jnnp.41.6.548
Journal Of Neurology, Neurosurgery & Psychiatry , 41 (6), 548-

10 Topic Areas for Adv Bio Psy
1.Mirror Neurons-true or not
2.Lateral inhibition of brain systems
3.The role of glial cells*
4.Palinopsia - can't unsee things
5. Anhedonia - can't feel pleasure in anything
6.Psychoneuroendrocrinology- diet, exercise, memory, hormones and mood* 7. Brain
Gut Connection - how body effects mind 8. Grid Cells and the brains GPS
9.Neuracircuits and pattern generators 10.Neural basis of Simple learning*
*favorites
Bests,
Jcapps
Sent from my iPad
Emily Ann Olds
Hakan 456
Topics of Interest
1.
How has the brain evolved in mammals? a.
Due to the vast amount of mammals, this topic has been limited to how the brain has evolved in human and non-human primates. Some studies researched were on the topic of oceanic mammals, so this information may be included in a potential lecture. Aside from looking into the anatomical evolution of the brain, some potential research will be on the evolution of social interactions and intelligence.
2.
Can we use research on individuals with Down Syndrome to find further knowledge on
Alzheimer’s Disease? a.
Many individuals with down syndrome eventually develop Alzheimer’s disease. These individuals often don’t live past forty at best, yet develop early Alzheimer’s disease.
While focusing on the neurobiology of the disease in both non-down syndrome and down syndrome individuals, one could potentially find similarities or clues to help further research on Alzheimer’s disease. Furthermore, some genetic research will be looked at based on the chromosomal differences being potential indicators. Lastly, the effects of Alzheimer’s Disease, Down Syndrome, and other side effects (ie. Siezures) will be looked into. There were numerous articles on the link between these individuals and aging development in “normal” individuals; in addition to imaging studies, brain pathology, and cognitive side effects.
3.
How does our brain react to hallucinogenic drugs, particularly LSD, Psilocybin, MDMA, and
DMT?

a.
While drug research is limited on these substances, expanding the research to more than one drug allowed me to find a plethora of articles. The focus of this research would be on hippocampal neurogenesis, as well as the effects of substances on neural response and interactions (ie. Rate, receptor ability, memory function, elasticity).
Studies included the effects of LSD on animal subjects, Psilocybin Hippocampal research,
MDMA’s effect on memory function, and the effect of DMT on elasticity. The effects of each substance on their primary receptors will be looked at closely in order to try and make connections and hypotheses about these drugs being used in a pharmaceutical manner.
Advance Bio Psych TopicsJohn Capps 8/25/13
Role of Glial Cells-
The role of glial cells in the brain is currently being updated with much more information. Glial cells are thought of as support cells for neurons, helping keep neurons together, insulate neurons, supply nutrients and oxygen to neurons, destroy pathogens and remove dead neurons.
Recent research indicates the existing neuron doctrine, which states neurons to be the primary communication cells of brain biology. May not be completely correct. When K+ is added to astrocytes, they exhibited a electrical-chemical potential similar to neurons. K+ is released after a action potential is fired down a neuron. This added to research of the 80s and 90s where it was found that glial cells responded to and release “neuro” transmitters. Astrocytes also communicate within their own communities and local neuronal networks using Ca+ waves.
Neurons are tied to muscular action and external senses, astrocytes have been seen to monitor neurons for information and modulate neuronal behavior. Neuronal activity that doesn’t involve glial cells are seen to be simple reflex. More complex processes may involve glial cells communication and modulation. This may point to why humans’ brain composition has the largest amount of astrocytes in the animal kingdom.
 Emerging roles of p53 in glial cell function in health and disease
 The role of glial cells in synapse elimination
Pacemaker Cells and Circadian Rhythm
Pacemaker networks can be observed in many neuronal networks of many animal and human nervous systems. These cells can cause involuntary muscles and tissues to contract or dilate. The properties of the cell membrane give these neurons their pacemaker ability by

allowing Na+ and K+ to leak in and cause a beating action potential. Pacemaker cells are linked to other pacemaker cells and can be primary pacemakers, or secondary pacemakers.
Pacemaker cells function can be easily demonstrated by the beating rhythm of cardiac cells but recent research indicates that they regulate much more within the body. These affect behavior, sleeping cycles, and information perception. They also effect peristalsis of digestive system and involuntary contraction and dilation of blood vessels. Changes in metabolism have been seen to can lead to a dis-syncing of the peripheral pacemakers with the central pacemaker system. Showing that diet and sleep wake cycles can affect circadian gene expression and sudden large changes in photoperiod and feeding time can reset the phase of rhythmic gene expression.
 Restricted feeding uncouples circadian oscillators in peripheral tissues from the central pacemaker in the suprachiasmatic nucleus.
 A Web of Circadian Pacemaker
Neural Basis of Simple Learning
Learning can be seen on a physical level by changes seen in the brain, size and shape, number of synapses, and the amount of supporting biological architecture. Hebb’s law states that neurons that fire together wire together, but how is simple learning stored. Long-term
Potentiation explains the complexes of neuron communication and learning can take place. Low level firing neuron 1 cause low level firing of neuron 2, as the same for high frequency firing of the pair. However, high frequency firing can cause long term effects on neuron 2 such that later low frequency firing of 1 cause high frequency firing of neuron 2.
The major brain systems affected by classical conditioning include the amygdala, cerebellum and the hippocampus. Operant conditioning is seen more in the basal ganglion.
Motivation is also involved in learning and is when a stimulus activates a reinforcement system and both the stimulus and reinforcement converge on a motor response to increase the S-R association. The VTA and related systems have importance in learning having to do with reinforcement where dopamine is released.
 The neural basis of basic associative learning of discrete behavioral responses.
 The neural basis of perceptual learning.
 Hebbian Learning and the neural basis of learning.
Some researchers believe that Savant like skills exist in a typically developed brain, but are inaccessible due to normal brain function. Transcranial magnetic stimulation can be used to inhibit parts of the brain that would typically be damaged in someone considered a Savant. The outcomes of

the studies showed increases in areas like memory and artistic ability. Future research in this area could lead the ability to strengthen ones mental abilities.
Snyder AW, Mulcahy E, Taylor JL, Mitchell DJ, Sachdev P, Gandevia SC. Savant-like skills exposed in normal people by suppressing the left fronto-temporal lobe.
J Integr Neurosci. 2003 Dec;2(2):149-58.
PubMed PMID: 15011267.
Young RL, Ridding MC, Morrell TL. Switching skills on by turning off part of the brain.
Neurocase. 2004
Jun;10(3):215-22. PubMed PMID: 15788259.
Takahata K, Kato M. [Neural mechanism underlying autistic savant and acquired savant syndrome].
Brain
Nerve. 2008 Jul;60(7):861-9. Review. Japanese. PubMed PMID: 18646626.
Snyder A. Explaining and inducing savant skills: privileged access to lower level, less-processed information.
Philos Trans R Soc Lond B Biol Sci. 2009 May 27;364(1522):1399-405. doi:
10.1098/rstb.2008.0290. Review. PubMed PMID: 19528023; PubMed Central PMCID: PMC2677578.
Chi RP, Fregni F, Snyder AW. Visual memory improved by non-invasive brain stimulation.
Brain Res. 2010
Sep 24;1353:168-75. doi: 10.1016/j.brainres.2010.07.062. Epub 2010 Aug 2. PubMed PMID: 20682299.
Mild traumatic brain injury, concussions, and postconcussive syndrome research has become increasingly popular due to issues of sports injuries and injuries of war. Many researchers have looked at the long-term effects of single and multiple concussions, noting changes in mood, memory, cognitive performance, anxiety, depression. Because mTBI is difficult to diagnose, current research is focused on mapping different biomarkers that would aid in its diagnosis.
Auxéméry Y. [Mild traumatic brain injury and postconcussive syndrome: a re-emergent questioning].
Encephale. 2012 Sep;38(4):329-35. doi: 10.1016/j.encep.2011.07.003. Epub 2011 Aug 31. Review.
French. PubMed PMID: 22980474.

Kontos AP, Covassin T, Elbin RJ, Parker T. Depression and neurocognitive performance after concussion among male and female high school and collegiate athletes.
Arch Phys Med Rehabil. 2012
Oct;93(10):1751-6. doi: 10.1016/j.apmr.2012.03.032. Epub 2012 Apr 10. PubMed PMID: 22503738.
Covassin T, Moran R, Wilhelm K. Concussion Symptoms and Neurocognitive Performance of High School and College Athletes Who Incur Multiple Concussions.
Am J Sports Med. 2013 Aug 19. [Epub ahead of print] PubMed PMID: 23959963.
Borich MR, Cheung KL, Jones P, Khramova V, Gavrailoff L, Boyd LA, Virji-Babul N. Concussion: current concepts in diagnosis and management.
J Neurol Phys Ther. 2013 Sep;37(3):133-9. doi:
10.1097/NPT.0b013e31829f7460. PubMed PMID: 23872682.
Di Battista AP, Rhind SG, Baker AJ. Application of blood-based biomarkers in human mild traumatic brain injury.
Front Neurol. 2013 May 1;4:44. doi: 10.3389/fneur.2013.00044. PubMed PMID: 23641234;
PubMed Central PMCID: PMC3640204
Mondello S, Schmid K, Berger RP, Kobeissy F, Italiano D, Jeromin A, Hayes RL, Tortella FC, Buki A. The
Challenge of Mild Traumatic Brain Injury: Role of Biochemical Markers in Diagnosis of Brain Damage.
Med Res Rev. 2013 Jun 28. doi: 10.1002/med.21295. [Epub ahead of print] PubMed PMID: 23813922.
The use of ‘bath salts,” a group of synthetic cathinone derivatives, has become increasingly popular over the last few years. Because the chemicals are not sold for human consumption, they don't need to be regulated by the FDA, and can be bought locally and online. Many recent studies have examined the effects that abuse potentials of what seems to be a constantly growing list of chemicals.
Aarde SM, Huang PK, Creehan KM, Dickerson TJ, Taffe MA. The novel recreational drug 3,4methylenedioxypyrovalerone (MDPV) is a potent psychomotor stimulant: self-administration and locomotor activity in rats.
Neuropharmacology. 2013 Aug;71:130-40. doi:
10.1016/j.neuropharm.2013.04.003. Epub 2013 Apr 15. PubMed PMID: 23597511; PubMed Central
PMCID: PMC3681807.

German CL, Fleckenstein AE, Hanson GR. Bath salts and synthetic cathinones: An emerging designer drug phenomenon.
Life Sci. 2013 Aug 2. doi:pii: S0024-3205(13)00424-4. 10.1016/j.lfs.2013.07.023. [Epub ahead of print] PubMed PMID: 23911668.
Bonano JS, Glennon RA, De Felice LJ, Banks ML, Negus SS. Abuse-related and abuse-limiting effects of methcathinone and the synthetic "bath salts" cathinone analogs methylenedioxypyrovalerone (MDPV), methylone and mephedrone on intracranial self-stimulation in rats.
Psychopharmacology (Berl). 2013
Aug 15.
Watterson LR, Kufahl PR, Nemirovsky NE, Sewalia K, Grabenauer M, Thomas BF, Marusich JA, Wegner S,
Olive MF. Potent rewarding and reinforcing effects of the synthetic cathinone 3,4methylenedioxypyrovalerone (MDPV).
Addict Biol. 2012 Jul 11.