Science topic
Prefrontal Cortex - Science topic
The rostral part of the frontal lobe, bounded by the inferior precentral fissure in humans, which receives projection fibers from the mediodorsal nucleus of the thalamus. The prefrontal cortex receives afferent fibers from numerous structures of the diencephalon, mesencephalon, and limbic system as well as cortical afferents of visual, auditory, and somatic origin.
Questions related to Prefrontal Cortex
For researchers who have conducted transcriptomics using the adult rat prefrontal cortex, is it necessary to optimize the RNA extraction method? Additionally, what is the average weight of the rat prefrontal cortex, and how much RNA can typically be extracted from it?
Dear all, I am trying to do a synaptosomes preparation from Postmortem Human Prefrontal Cortex (frontal). I read few articles, they used 1 to 5 gram at the beginning. I started with low amount of frozen brain, around 300 mg (PMI < 4 hours). From 300 mg weight of prefrontal cortex, I generally obtain ~25 micrograms of total protein from isolated synaptosomes.
Is anyone have any idea to increase the yield at the end (beside increasing the weight of the brain)? I do not have a high amount (weight) of human brain.
Each minced prep is immediately homogenized by applying 20 slow stokes using a teflon-glas tissue grinder (grinding chamber clearance is 0.15 mm). Then I use layering of discontinuous sucrose gradient.
I am thinking to use a glas-glas tissue grinder (grinding chamber clearance is 0.025 - 0.076 mm).
I welcome any idea.
Cheers,
Stella
In a recent study published in the journal "Brain Stimulation," researchers found that transcranial direct current stimulation (TDCS) applied to the prefrontal cortex of the brain can help reduce symptoms of depression in people with mild to moderate depression. In the study, participants received TDCS for two weeks, five days a week, for 20 minutes each session. Results showed that participants who received TDCS had greater reductions in depression symptoms than participants who received a placebo.
However, other studies have shown that the effectiveness of TDCS for treating depression is limited. In a recent study published in the journal "The Lancet Psychiatry," researchers found that TDCS applied to the prefrontal cortex did not produce any difference in depression symptoms between participants who received TDCS and participants who received a placebo.
My experimental design requires the isolation of the medial prefrontal cortex and amygdala from the mouse brain, but these brain regions are difficult to distinguish with the naked eye, even with the help of the atlas. How do you complete similar experiments?
Below are a few early questions I am curious about understanding in the field of neurofeedback and brain activity.
1. So how *do* you actually create a control for neurofeedback?
2. Why is it easier for brain states to enter hallucinatory ones rather than high intelligence ones? May neurofeedback facilitate entering "high intelligence" ones, as in those, correlated with latent g?
3. How do you detect if someone's emotion is feigned or reptilian--what is the difference in neural signature, and can it be detected in neurofeedback and even trained to be selectively feigned or reptilian depending on the stimuli? A good example would be to create emotional distance, in other words, have a brain state correlated with feigning an emotion, about one's trauma, once they have processed it over and over again. An example where it may apply in the opposite is to learn empathy and collaborative skills with other people. I've heard of the Duchenne vs Pyramidal smile but I'm curious if there are other ways of differentiating emotions, especially non-outwardly expressed ones.
4. What were the seminal papers leading to the fitting of the PING (pyramidal interneuron network gamma synchrony) model to the neural circuitry in the DLPFC? Is anyone aware of this model and how to train the relevant brain regions exhibiting this pattern, namely like in the DLPFC, to have higher power during working memory tasks?
5. Is the fact that individuals with ADHD exhibit gamma-band responses during stimulus encoding, that are uncorrelated with task performance, compared to controls, correlated to autistic traits?
6. What is the “auditory oddball task” and why is it important for comparing gamma oscillation differences in SZ and control patients?
7. What is the action of the medial prefrontal cortex vs dorsolateral prefrontal cortex and are the deficits more easily reversible in one region vs another? Which is more strongly implicated in SZ? Which in OCD?
8. What is the significance of 40 Hz activity in the human brain and why is activity in this band during working memory tasks correlated to increased performance?
9. Why are SZ brains showing high gamma band oscillations for “simple tasks” compared to controls?
10. Why is there late theta response in SZ compared to controls in tasks involving significant WM and rule-switching tasks?
I have seen this black spot so many times while isolating the brain of B6 mice, but I still don't know exactly what it is or which specific region it is. It seems to be B6 specific or at least, it is absent from SJL brains.
Dear colleagues- we routinely record local field potentials in freely moving mice from hippocampal CA1 and prefrontal cortex with ~ 125um depth electrodes, but would like to record multi neuronal single unit activity (and LFP's) in lightly restrained or freely moving animals. We would like to use silicon based shank electrodes with 16 to 32 recording sites, with one and sometimes two shanks- we have Intan recording systems. We have found some possible commercial solutions, but they are quite expensive and seem to be single use only. I was wondering if anyone had come across some more "reasonably priced" silicon or similar arrays? I am aware of tetrode methods and the more advanced CMOS based electrodes, but think the silicon array would be best suited to our current studies.
We have found some evidence for behavioral habituation to repeated muscimol microinjections into the orbitofrontal cortex during an aversive operant procedural task. The effect seems to wear off after 2-3 injections (given every other day).
Has anyone seen this? Any potential explanations?
Thank you!
Currently we are working on a review that surveys the cognitive/neural mechanisms of tactile working memory. We propose a sensory recruitment model, which suggests that prefrontal regions interact with somatosensory cortex to encode, maintain and retrieve tactile working memory. Please leave your email address if of interests.
Thanks,
Hello,
My friend is preparing for a systmatic review in the neural basis of instruction-based learning. Instruction-based learning (IBL) refers to learning to perform tasks based on instruction rapidy. You will be responsible for part of the writting and editing (specifically the role of ACC and IFS). Leave your email address if you are interested.
Best
I don't believe there's much research in this area in humans. There are mice and primate studies
For equipment testing purposes my research group wants to acquire an fMRI data set with frontal cortex activation, as anterior as possible.
What would be the most reliable (yet simple) task to achieve this in a single participant? Basically, I'm looking for the prefrontal equivalent of a rotating checkerboard.
I am looking for a skilled personnel in Kuwait University that is familiar with antioxidant studies using ELISA kit or other techniques on rat's brain homogenate, particularly the hippocampal and anterior cortex regions.
Hi All,
I need to specify a few Regions of Interest (ROI) in the human brain providing their coordinates (x,y,z). What I am interested in at this point are anterior cingulate cortex, dorsolateral prefrontal cortex, posterior parietal (in or near the intraparietal sulcus) motor cortex, bilateral primary motor, cerebellar cortex, cerebellar dentate, left putamen, left thalamus, premotor cortex, ventral lateral nucleus, striatum, precentral gyri, postcentral gyri, primary sensorimotor cortex and some other.
Is there a publication (preferably one and online?) I can check these cooridnates in?
Hello everyone,
I wanted to label up serotonin fibers within CPF and AMG as target regions of raphe nucleus. I started an immunohistochemistry using anti-5-HT antibody, and I got a good staining of cell bodies in raphe nucleus, however, I was unable to detect the projections within the regions of interest.
For more information, I used:
* coronal sections of mice brain with a thickness of 40µm
* anti 5-HT antibody: 1:5000
* the activity was visualized with DAB
Please, let me know if you need further info.
Thank you in advance
Hello everyone, I wanted to ask you if you know any good paper that dig into the connection between medial Prefrontal Cortex and the Dorsal Hippocampus. Also if you knew some paper related to shizofrenia would be great.
Thank you :-)
Hello everyone! I need to label mouse PV inhibitory neurons in the medial prefrontal cortex at an early post-natal time point (P7). However, I am experiencing some problems finding a good antibody to achieve this purpose, since these neurons still do not express PV at this time point (they only start expressing around P14) and I require a strong and, preferably, a nuclear labeling. Can you point me to good antibody for immunohistochemistry in frozen slices?
Thank you in advance for your help.
Hello;
In terms of learning and memory, do you think that proinflammatory cytokines such as TNF-alpha, IL-1beta, and IL-6 may act differently in the prefrontal cortex and hippocampus?
I've some data that shows TNF-alpha and IL-1beta are reduced in the prefrontal cortex but increased in the hippocampus in the animals with impaired learning and memory scores in Morris Water Maze and Novel Object Recognition tests. In my opinion, it may possible that the neurotoxin that I used may reduce live cells and cause to detect a lower amount of proinflammatory cytokines. However, since the level of them are higher in the hippocampus (as expected) I can not make any connection with that difference between prefrontal cortex and hippocampus.
Of course, there are some papers reporting the diverse role of those cytokines in different conditions, however, I could not find the proper and clear answer for my case.
Thank you for your help.
Kind Regards.
how can I download a free version of the book with this title:
Paxinus and franklin's the mouse brain in stereotaxic coordination
Has someone heard about unexpected effects of sham when using tDCS? We are observing what seems to be a systematic inhibitory effect of 2 mA (30 sec ramp up + 30 sec ramp down) cathodal sham stimulation. We are stimulating the right ventrolateral prefrontal cortex. I did not believe this putative effect at the very begining of the experiment, but after running a lot of participants with an experimental task I know very very well, I am now about to claim that our sham condition is playing a role...
I'm interested in isolating RNA from mouse hippocampus and prefrontal cortex. My lab routinely uses the Trizol method for large pieces of tissue (eg, liver and intestine), ending with dissolving the RNA pellet in 200 uL DEPC water. For hard-to-extract tissues (eg, adipose) we reduce the final step to 20-50 uL DEPC water. Is this an acceptable modification for hippocampus, or should I reduce the volume even more? We usually aim to get at least 250 ng/uL RNA for reverse transcription but I'm wondering if this is possible with such a small piece of tissue. Are there any other modifications to help with yield?
What areas of the brain can be measured using EEG? What functions are appropriate and not appropriate to study with this method? Can the EEG record accurately activity in deeper brain structures and cortical areas along the midline (MPFC, Precuneus, ACC, subcortical structures)? What are the main advantages and disadvantages of this method?
I am trying to do some molecular analyses from brain tissue activated with DREADDs, and I am wondering how large is the spread of a single stereotaxic injection of the AAV-DREADD. For example, if I target the infralimbic or prefrontal cortex, what kind of volume am I expected to have DREADD expression in?
To assay changes in synaptic protein complement, we want to harvest microdissected CA1 and prefrontal cortex slices from young (P5-P12) mice for Western Blotting (WB) of isolated synaptic fractions. We want to quantify total and synaptic GluA1, GluA2, NR2A and NR2B receptor expression.
It seems like it would be hard to get enough CA1 tissue. If you've had success doing this, could you please add a reference citing ug yield per P5-P12 CA1 and amount needed for Westerns.
We would obviously need synaptosomes but again, unsure of the feasibility for CA1, and even we get a usable yield, will it work on immature synapses and give enough yield at particularly young ages (P5-P7)?
I am trying to inject MW 10,000 dextran into the orbitofrontal cortex. I am using a 13 microns glass pipette. I am injecting just with a regular syringe and a tubing, which is connected to the pipette. I fixed the brain in PFA, cut on the freezing microtome and I don't see any fluorescence. What could be the problem? Old dextran, need antibodies to amplify the signal or I have to image slides in any special way? Note: I am doing this for the first time! Thank you for your answers.
Does Deep Brain Stimulation work on the Amygdala itself or on connection between amygdala and medial Prefrontal Cortex too?
Hi, I'm looking for non-surgical, non-traumatic models of prefrontal lesion in rat. I'm aware of rotenone, but because of peripheral issues I can't use this substance. I thought of 6-OHDA, but I'm not sure about prefrontal damage. Any help would be appreciated. Thanks!
Dear Colleagues,
Are cognitive control and cognitive effort the same thing?
I am confused. In the neuroscientific literature on second language learning, the neural organization of cognitive control and cognitive effort seems to overlap (e.g., the anterior cingulate, dorsolateral prefrontal cortex, inferior parietal regions). At the same time, I have come across some results that make me think that cognitive control and cognitive effort are not the same thing.
For instance, I have found fMRI studies that reported increased "cognitive effort" (and therefore more widespread fMRI activation) in less proficient speakers of a second language (e.g., Abutalebi et al. 2018). At the same time, several ERP studies have suggested more "cognitive/language control" in highly proficient second language users. For example, Fernandez et al. (2013) have shown that higher second language proficiency was associated with a greater mean N2 amplitude (greater inhibition) on an executive function test. Another example: Rossi et al (2018) concluded that individuals with high second language proficiency require more cognitive/language control for their first language, even before they speak their second language.
I will greatly appreciate your help.
With my best wishes,
Monika
Friends,
The difficulty to form and execute plans of action is diagnostic of large prefrontal lesions. The expectancy of reward activates many neurons, especially in orbital prefrontal cortex. All four major executive functions of the lateral prefrontal cortex (planning, executive attention, working memory, and decision-making) are prospective, “look” to a more or less distant future. The prefrontal cortex is rightfully called the “organ of creativity,” as it is capable of organizing novel actions and speech (it has “memory of the future,” Ingvar 1985). It is also capable of “imagining” what’s to come, and to estimate future risks and benefits. The stock market is moved up or down by the collective prefrontal cortex of countless investors. In sum, here is a brain structure that is literally driven by the future, eminently teleological. Many seem to ignore such an obvious fact. A bit of reflection is here in order, however.
For the self-respecting scientist, teleology is anathema and intolerable absurdity, because it reverses the natural temporal order between cause and effect. That reversal in the prefrontal cortex is only apparent, however, because for that cortex, as for the rest of nature, there is “nothing entirely new under the sun.” Thus, all new planning, all new creation, all new imagination, and all new decisions are based on history and prior experience. All of them are simply re-creations of the past.
Thus the absurdity is gone. But think of how dull, how witless, how plain and how barren would be a world without the prefrontal cortex!
Cheers,
Joaquín
J.M. Fuster and S.L Bressler – Past makes future: Role of pFC in prediction. J. Cogni. Neuroscience, 27: 639-654, 2015.
Hi,
I would be thankful for any piece of literature introducing short, accessible and uncomputerised psychological tests for executive functioning and visual-motor processing. I am most interested in assessment of spatial and hierarchical planning.
Thank you
Hello, we are analyzing inflammatory markers (such as TNF-alpha, IL1B, IL6 and INF-gamma) in brain samples (hippocampus and prefrontal cortex) after an intra-peritoneal injection of LPS in C57BL/6 mice.
Despite the high increments of these markers described in the literature using this method, we obtain very low increments or no changes. We suspect that maybe the fact that our animals are housed in a SPF facility could be interfering. Has anyone using SPF animals had the same problem? Could you give us some advice?
I am doing experiments with rats and want to stain brains so that I can distinguish layers of the cortex.
In the my project miR-516b-5p is my choice for study. There is a problem in this project and it is: miR-516b-5p has low expression in peripheral blood mononuclear cells of Parkinson patients! what is the reason????
It is commonly stated that the prefrontal cortex typically is not fully functional until as late as age 24. If true, this must be an average figure.
If one considers young children that, due to circumstances, are required to act responsibly and independently, far beyond their chronological age, and how they continue through their adulthood to being very responsible and independent.
On the other hand, consider the child who has a "helicopter" mom or other overindulgent caregivers, and how everything is done for them so they often do not act responsibly or independent. This lack of character building then results in an adult who continues acting like a child who is undisciplined, unethical, and irresponsible.
Of course, a middle ground is needed for child development to result in an adult who is well-balanced.
Are my impressions supported by empirical evidence or well-founded theory? Is there a neuroscientific explanation re. the plasticity of the brain?
To define it as spontaneous production, the selection and the execution of new auditory-motor sequences appears insufficient. On the other hand, compared to numerous brain imaging studies on musical cognition, perception and musical development, there are few of them on musical invention which are, for the most part, confined to the study of already memorised performances and very few on musical improvisation in real time. In a brilliant work, a number of years ago Limb (2008) asked ten pianists to memorise a melody and, after having them lie in the tube of a suitably modified magnetic resonance machine and connected to a keyboard, he managed to have them reproduce a melody they had just learned, make a simple scale and, finally, improvise. Limb saw that the improvisation was correlated to the activation of a nerve network that included, among other things, structures such as the inferior left frontal gyrus, the anterior cingulated cortex and the medial prefrontal cortex. The most interesting evidence was the widespread ‘turning-off’ of the prefrontal areas, which are generally correlated to the conscious control of the activities in progress and responsible for interference in the capacity to concentrate. This experience of ‘turning-off’ is not yet sensorial and not yet perceptive; it is not an experience of emptiness, but corresponds to the activation of mental images that anticipate the specific action that leads to an internal emulation of the planned motor actions, very similar to what takes place in reality. As has been shown recently by Ridderinkhof and Brass, (2015), also with reference to the sphere of football, the comparison between the effects of the anticipated action and those of the internal emulation may generate an error signal that may encourage the improvement of the motor performance, even without the execution of the real movement.
Hi all,
I recently ran a western blot using medial prefrontal cortex samples from PN17 rats. I followed the same protocol that other students have used in our lab (we prepare samples with RIPA buffer + phosphatase and protease inhibitor), and I see this weird double band where spinophilin (green) should be. I loaded 20ug of protein, and my primary antibody concentration for spinophilin was 1:1000. The red is stained for GAPDH at 1:3000. It's weird because with the same amount of protein loaded (and same protocol), in the cerebellum and POA, we don't see the double band. But we also see this double band in the amygdala as well.
Is this simply a regional difference and therefore I need to change the amount of protein loaded? If not, does anyone know why this might be the case. I'd also appreciate any suggestions to improving the method.
Thank you!
What do you think about a combination of four pharmacological agents from four different classes to ameliorate the negative/cognitive/pseudonegative symptoms of a schizophrenic psychosis, particularly the following combination: olanzapine (antipsychotic/neuroleptic), valproate (anticonvulsant/mood stabilizer), fluoxetine (SSRI) and modafinil (psychostimulant), leading to a net increase in prefrontal dopaminergic and noradrenergic, as well as serotoninergic, histaminergic and GABAergic neurotransmissions?
Hi everyone,
I am performing stereotactic surgery for mPFC in CD1 mice. The coordinates that I am trying to use is AP: +1.9, ML: +/- 0.3, DV: -2.5. Apart from this antero-posterior coordinates, I have also tried +1.6, +1.7 and +1.8. But in all these cases, I see enormous blood while inserting the cannula or even the injector. I see so many papers injecting drugs, lentivirus etc in mPFC using same coordinates, but none say a word about the blood. If anyone has experience on this, please share your experience here. Thanks!
From a neurobiological perspective, creativity is generated by a huge and intricate variety of cortical and subcortical activity, concentrated primarily in the ventral striatum and in the prefrontal cortex. If the basal ganglia produce continuous novelty, the prefrontal cortex transforms the latest news in creative behaviors explicit. In this workspace, countless expressions of harmony and disharmony neural accompany the emergence of phenomena of thought and behavior original. A multitude of intra-cognitive process scattered competing for access to a conscious workspace for filtering, communicate and exchange information.
In order to perform a fMRI ROI analysis we need some prefrontal cortex region masks. Particularly, we are interested in the vmPFC, dmPFC, dLPFC and vlPFC. It seems that are a lot of different definitions for the same region. So, does anyone know how we can get it from the commonly used atlas (Harvard-Oxford or AAL), combining different labels? Or if anyone has already some of these masks, could it be possible to send to us?
Thanks very much in advance,
Fernanda
The motor cortex is in the frontal lobe; the prefrontal cortex controls the main executive functions (executive attention, working memory, decision-making, inhibitory control); patients with substantial frontal lesions lack the will and capacity to formulate and carry out plans of action; certain actions are preceded by electrical signals in frontal cortex, even before the conscious experience of the intention to move. All of this seems to justify calling the cortex of the frontal lobe, as a whole, “the executive of the brain” (I believe Pribram was the first to use the term). I know, it is a metaphor, but has interesting connotations with regard to free will and the generation of willed action. Further, it keeps misguided dualism at bay.
The rats will be subjected to chronic alcohol vs controls. The brains will be collected, RNA extracted and the levels of candidate genes will be analyzed by RT PCR.
Which areas of the brain are most promising to see the meaningful differences.
Factors to consider:
Some important areas don't contain cell nuclei. Some important areas are small and hard to locate and collect. Shall we first separate brain areas and then freeze? Or freeze, then cut and cut out frozen areas?
So the question is: among the areas related to chronic alcoholism, which ones are easy to locate and collect?
I think cerebellum, striatum,, hippocampus and prefrontal cortex, but my knowledge of brain areas and of alcohol research is limited. Please help!
I am trying to induce LTD in the prefrontal cortex of anesthetized rats (300-350g). The stimulus protocol I found suggests applying a 900 pulse train at 1Hz frequency using 70% maximal amperage. For some reason, this paradigm has produced a depressed stimulus evoked LFP in some rats, or a potentiated LFP in other rats. Any suggestions???
Dear Researchers,
I have to use the nuclear, cytoplasmic and mitochondrial extract for my studies involving m-RNA and protein in brain isolated parts (striatum, substantia nigra, hippocampus, prefrontal cortex).
I have no much budget to purchase kits for the same like of Thermo scientific (http://www.thermofisher.com/order/catalog/product/78835?ICID=search-78835)
I wish to prepare chemical solutions for extracting them.
Kindly tell me the exact good and short reliable protocol to perform that involving ease and reproducible results...
Thanking you
I need to implant my electrodes in the mPFC. After removing the skull and dura, there is a big vessel in the place where I have to implant my electrodes. I know if my electrodes damage the vessel, it will cause bleeding, but there is no space for me to cross the vessel. So what I do stupidly is that I remove the vessel on purpose and wait for several minutes until it stops bleeding, then I implant my electrodes.
My question is whether someone knows if during implantation there is no bleeding, whether during the rat's recovery, the bleeding could happen again and clot and block my electrodes. Also, whether the vessel I damaged could grow back along my electrodes.
The third question is three days after surgery I find there is yellow liquid coming from the brain. And the rat doesn't move too much. Does that mean the rat has inflammation? What should I do?
Thanks for your reply!
I'd like to fluorescently stain for activation of GABAergic neurons in the mPFC- but have a few questions.
1) When looking at the mPFC, would it be best to use antibodies for FOS and GABA, or FOS and GAD67? What are the advantages or disadvantages to each?
2) Are there any particular antibodies you would recommend for this?
3) Any tips and tricks as far as staining goes? TBS or PBS? Dilutions?
Thank you in advance!
I found three major approaches of the neurological mechanism of attention:
a)mirror neurons related with association areas and the develop of a specific task,
b) lateral intraparietal cortex on forced decision task
c) dorsal prefrontal cortex in taks related with working memory
Is there another important approach? Are these systems related? Is there a better paradigm to understand attention process on a neuroscientific poinf of view?
If I want to lesion serotonergic neurons by this method to check DRN role in effects of amygdala stimulation in prefrontal cortex activity. How long should I wait from the 5,7-DHT injection until the second part of the experiment?
Thanks!
I am currently in my Honours year and my project used TMS on the right Temporal-parietal junction and right dorsolateral prefrontal cortex and observed it's effects on social cognition. We did not find significant results and I am just trying to explain why in my discussion. One of the reasons why I believe we did not achieve significant results is because the left hemisphere also is involved in social cognition and compensated for the disruption in the right hemisphere. My literature search has not yielded any studies that investigate lateralisation with TMS and was wondering if any actually existed??
Any help at all would be greatly appreciated!
Regards,
Kerman
Who knows how to induce epileptiform activity in prefrontal cortex slice using field recording? I tried Mg-free ACSF but did not see any spike.
I'm looking for an antibody that nicely identifies GABAergic neurons (of all types). We have been using an anti-GAD67 (Millipore) or an anti-GABA (Sigma) antibodies with results leaving a little to desire. I'd be very thankful if you can help me find a good one. Our mouse brains are perfused in 4% PFA.Thanks a lot! Anne.
I would need a paper or video that it shows me to dissect with accuracy the prefrontal cortex of mice for synaptosomes
Can anyone elaborate upon the left prefrontal cortex retrieving simple information encoded whereas the right pre frontal lobe is able to retrieve difficult encodings. suggesting that the left side of the brain is suited to recollecting memories whereas the right side of the brain is more specialised in the area for familiarity-based traces that contain less detailed information.
I want to provide a picture of which are the areas of prefrontal cortex I am mentioning to the readers of my review. However, google-ing (even on google.scholar or pubmed) could not help me find official coordinates or location discriptions of the vmPFC, dlPFC, orbitofrontal cortex etc.
I would think there should be an official map of this, how else can people state that they find something in e.g. the vmPFC?
Thank you very much for reading my question. I'd very much like to hear your advice/opinion!
I have found several imaging studies, but I am looking for more information on how this specific neurotransmitter could mediate PFC activity.
We all know that PFC is affected due to Major Depression. But i want to know which region of PFC is majorly affected? Is it the VMPFC or the DLPFC? Because, most of the literature has focused up on DLPFC? Is that more correlated to depression than VMPFC?
In Descartes' Error -- Antonio Damasio cites a study by Fulton and Jacobsen and evidence that certain kinds of damage to the ventromedial prefrontal areas can result in markedly reduced social interactions and indifference to one's future. What about the immediate present? Does the spontaneous sensory perimeter also lose its affective appreciation? Or is this mainly about projected future moments and directed behavior?
Greg Miller " Many details of the process of memory recall are not known (or are disputed). Even so, some researchers say it's time to revise some aspects of the standard view—such as the notion that the hippocampus is not involved in retrieving older episodic memories, and that memories become fixed and unchangeable once transferred to the neocortex. Newer work suggests a far more fluid role of memory, and one in which retrieval plays a crucial role in shaping memory over time"
Damasio et al. propose that somatic markers (feedback signals representing homoeostatic and other bodily states) play a pivotal role in our decision-making processes. The ventromedial prefrontal cortex (VMPFC) is identified as the cerebral module of most relevance to the somatic system. Emotions are understood by SMH advocates as the feeling of the bodily states reported by the markers. Sufferers of damage to the VMPFC have consistently demonstrated anomalous emotional dispositions accompanied by poor decision making (both time-costly and poor outcomes), in the absence of further detrament (no loss of iq, working memory...). The role of emotions in decision making is proposed to be that of restricting the options put up for conscious consideration, based on biasing signals from the body. There is here a suggesting of tacit learning by the body, prior to conscious knowledge. (See the Iowa gambling task)
Smith and Elsworth (1985) and apparently others since then have identified six "cognitive appraisal dimensions" that can help distinguish emotions. Certainty, pleasantness, attentional activity, control, anticipated effort, and responsibility are all features of appraisal patterns underlying distinct emotions, and helping to define them.
Thus, we may find that certain emotions such as happiness and anger may share more relevant features than two emotions of the same valence (positive/negative). Since happiness and anger both construe appraisals of certainty and a sense of individual control over the situation, such cognitive dimensions might play a bigger part in determining the nature of the decisions made than the simple positive/negative valence distinction alone.
Do such considerations necessary undercut the Somatic Marker Hypothesis? Is there room for it to accept such dimensions to our emotions, without selling itself short?
Many thanks
Adam
Hello,
I would like to know what housekeeping genes one can use to discern gene expression changes in prefrontal cortex of Alzheimer's patients by qRT-PCR.
Many thanks.
I found strong prefrontal projections to the lateral habenula in humans, with high fibre tract density around AM. It is possible that the PFC-LHb projections form collaterals in AM. AM is known for reciprocal connections with hippocampus, prefrontal cortex and retrosplenial cortex. What is its role?
There seems to be a conflict, or at least confusion, in the literature whether the vmPFC and OFC are, in fact, separate areas. Additionally, the exact, or at least popularly accepted, location of these areas, seems quite elusive. Is this really a topic of contention, and is there any literature attempting to reconcile the many definitions and locations?
Thank you.
I am confused about the long-distance expression of ChR2. Recently, I injected AAV-ChR2 in ventral hippocampus of mice, After 4-6 weeks, I recorded the light-stimulated EPSC from prefrontal cortical slices. The ChR2 expression is good in vHIP, however, I had few fibers labelled to evoke blue light induced responses in prefrontal cortical slices~ Could someone help me?
I want to micro dissect the brain of rats and mice to isolate hippocampus, prefrontal cortex and other brain parts. Can help me out to find the best video on micro dissection of brain either in youtube or any other website? Thank you.
It is now well established that rodents exposed to chronic stress display apical dendritic shrinking in prefrontal cortex and hippocampus as well with no change in basal dendritic arborisation. I read numerous articles showing this neuronal specificity but nobody discuss it. So why such a specificity?
Or in other words at what sampling rate can I equate blood in a volume of tissue containing capillaries to be stationary?
Based on what I found on web pages, it seems it's not. But since mPFC has intensive neural connectivities with limbic structures, it involved in functions (e.g. cognitive control, memory, emotional regulation etc.) that are usually related to limbic system, and often to be found to have structural/functional abnormalities in psychiatric disorders along with limbic structures. However, generally speaking, it's not a part of limbic system. Can I say that?
Anyone tried DARPP-32(Thr34 and Thr75) on mPFC tissue? Does frozen tissue from fresh decap work for these assays?
