scholarly journals Evolution of Neuroaesthetic Variables in Portrait Paintings throughout the Renaissance

Entropy ◽  
2020 ◽  
Vol 22 (2) ◽  
pp. 146 ◽  
Author(s):  
Ivan Correa-Herran ◽  
Hassan Aleem ◽  
Norberto Grzywacz
Keyword(s):  
Neural Function ◽  
Aesthetic Value ◽  
15Th Century ◽  
Sensory Evaluations ◽  
The Brain

To compose art, artists rely on a set of sensory evaluations performed fluently by the brain. The outcome of these evaluations, which we call neuroaesthetic variables, helps to compose art with high aesthetic value. In this study, we probed whether these variables varied across art periods despite relatively unvaried neural function. We measured several neuroaesthetic variables in portrait paintings from the Early and High Renaissance, and from Mannerism. The variables included symmetry, balance, and contrast (chiaroscuro), as well as intensity and spatial complexities measured by two forms of normalized entropy. The results showed that the degree of symmetry remained relatively constant during the Renaissance. However, the balance of portraits decayed abruptly at the end of the Early Renaissance, that is, at the closing of the 15th century. Intensity and spatial complexities, and thus entropies, of portraits also fell in such manner around the same time. Our data also showed that the decline of complexity and entropy could be attributed to the rise of chiaroscuro. With few exceptions, the values of aesthetic variables from the top of artists of the Renaissance resembled those of their peers. We conclude that neuroaesthetic variables have flexibility to change in brains of artists (and observers).

scholarly journals Effect of Xenon Treatment on Gene Expression in Brain Tissue after Traumatic Brain Injury in Rats

2021 ◽  
Vol 11 (7) ◽  
pp. 889
Author(s):  
Anton D. Filev ◽  
Denis N. Silachev ◽  
Ivan A. Ryzhkov ◽  
Konstantin N. Lapin ◽  
Anastasiya S. Babkina ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Target Genes ◽  
Neural Function ◽  
Stress Genes ◽  
Expression Of Genes ◽  
Delayed Recovery ◽  
The Brain ◽  
Lower Expression

The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.

scholarly journals Culture Wires the Brain

2010 ◽  
Vol 5 (4) ◽  
pp. 391-400 ◽  
Author(s):  
Denise C. Park ◽  
Chih-Mao Huang
Keyword(s):  
Brain Structure ◽  
Cultural Psychology ◽  
Structure And Function ◽  
Neural Function ◽  
Limited Evidence ◽  
Neural Structure ◽  
Cultural Experiences ◽  
Brain Structure And Function ◽  
And Function ◽  
The Brain

There is clear evidence that sustained experiences may affect both brain structure and function. Thus, it is quite reasonable to posit that sustained exposure to a set of cultural experiences and behavioral practices will affect neural structure and function. The burgeoning field of cultural psychology has often demonstrated the subtle differences in the way individuals process information—differences that appear to be a product of cultural experiences. We review evidence that the collectivistic and individualistic biases of East Asian and Western cultures, respectively, affect neural structure and function. We conclude that there is limited evidence that cultural experiences affect brain structure and considerably more evidence that neural function is affected by culture, particularly activations in ventral visual cortex—areas associated with perceptual processing.

scholarly journals Remote control of neural function by X-ray-induced scintillation

2019 ◽  
Author(s):  
Takanori Matsubara ◽  
Takayuki Yanagida ◽  
Noriaki Kawaguchi ◽  
Takashi Nakano ◽  
Junichiro Yoshimoto ◽  
...  
Keyword(s):  
Dopamine Neurons ◽  
Neural Function ◽  
X Rays ◽  
Cellular Functions ◽  
X Ray ◽  
Functional Studies ◽  
Clinical Dose ◽  
Visible Luminescence ◽  
Midbrain Dopamine ◽  
The Brain

Scintillators emit visible luminescence when irradiated with X-rays. Given the unlimited tissue penetration of X-rays, the employment of scintillators could enable remote optogenetic control of neural functions at any depth of the brain. Here we show that a yellow-emitting inorganic scintillator, Ce-doped Gd3(Al,Ga)5O12 (Ce:GAGG), could effectively activate red-shifted excitatory and inhibitory opsins, ChRmine and GtACR1, respectively. Using injectable Ce:GAGG microparticles, we successfully activated and inhibited midbrain dopamine neurons in freely moving mice by X-ray irradiation, producing bidirectional modulation of place preference behavior. Ce:GAGG microparticles were non-cytotoxic and biocompatible, allowing for chronic implantation. Pulsed X-ray irradiation at a clinical dose level was sufficient to elicit behavioral changes without reducing the number of radiosensitive cells in the brain and bone marrow. Thus, scintillator-mediated optogenetics enables less invasive, wireless control of cellular functions at any tissue depth in living animals, expanding X-ray applications to functional studies of biology and medicine.

Summing Up

2019 ◽  
pp. 145-158
Author(s):  
Dale Purves
Keyword(s):  
Nervous System ◽  
Cardiovascular System ◽  
Digestive System ◽  
Neural Function ◽  
Empirical Basis ◽  
Organ Systems ◽  
The World ◽  
Survival And Reproduction ◽  
Successful Behavior ◽  
The Brain

A major challenge in neuroscience today is to decipher the operating principle of the brain and the rest of the nervous system in the same straightforward way that biologists have come to understand the functions of other organs and organ systems (e.g., the cardiovascular system, the digestive system, and so on). The argument here has been that the function of nervous systems is to make, maintain, and modify neural associations that ultimately promote survival and reproduction in a world that sensory systems can’t apprehend. In this way, we and other animals can link the subjective domain of perception to successful behavior without ever recovering the properties of the world. Neural function on a wholly empirical basis may be the key to understanding how brains operate.

scholarly journals Functional neuroimaging as a direct probe of the effects of gonadal steroid hormones on the brain

2002 ◽  
Vol 4 (2) ◽  
pp. 192-195
Keyword(s):  
Steroid Hormones ◽  
Animal Studies ◽  
Functional Neuroimaging ◽  
Functional Brain Imaging ◽  
Neural Function ◽  
Gonadal Steroid Hormones ◽  
Gonadal Steroid ◽  
Neurophysiological Data ◽  
Health And Disease ◽  
The Brain

There is considerable evidence from animal studies dial gonadal steroid hormones modulate neuronal activity and affect behavior. In humans, however, the behavioral and cognitive evidence has not been conclusive, and, until recently, there have been few direct neurophysiological data. Functional brain imaging offers unique opportunities to characterize in humans the effects of gonadal steroid hormones on basic neurobiological parameters, such as neuronal metabolism and neurochemical systems, and to clarify the interactions between these hormones and cognition and mood regulation in health and disease. The most commonly used tools within the considerable armamentarium available for such research and the parameters of neural function that they can access are briefly reviewed here.

scholarly journals Kynurenines increase MRS metabolites in basal ganglia and decrease resting-state connectivity in frontostriatal reward circuitry in depression

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiangchuan Chen ◽  
Diana J. Beltran ◽  
Valeriya D. Tsygankova ◽  
Bobbi J. Woolwine ◽  
Trusharth Patel ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Functional Connectivity ◽  
Resting State ◽  
Kynurenine Pathway ◽  
Self Report ◽  
Resonance Spectroscopy ◽  
Neural Function ◽  
Brain Chemistry ◽  
The Impact ◽  
The Brain

AbstractInflammation is associated with the development of anhedonia in major depression (MD), but the pathway by which inflammatory molecules gain access to the brain and lead to anhedonia is not clear. Molecules of the kynurenine pathway (KP), which is activated by inflammation, readily influx into the brain and generate end products that alter brain chemistry, disrupt circuit functioning, and result in the expression of inflammatory behaviors such as anhedonia. We examined the impact of plasma and CSF KP metabolites on brain chemistry and neural function using multimodal neuroimaging in 49 depressed subjects. We measured markers of glial dysfunction and distress including glutamate (Glu) and myo-inositol in the left basal ganglia using magnetic resonance spectroscopy (MRS); metrics of local activity coherence (regional homogeneity, ReHo) and functional connectivity from resting-state functional MRI measures; and anhedonia from the Inventory for Depressive Symptoms-Self Report Version (IDS-SR). Plasma kynurenine/tryptophan (KYN/TRP) ratio and cerebrospinal fluid (CSF) 3-hydroxykynurenine (3HK) were associated with increases in left basal ganglia myo-inositol. Plasma kynurenic acid (KYNA) and KYNA/QA were associated with decreases and quinolinic acid (QA) with increases in left basal ganglia Glu. Plasma and CSF KP were associated with decreases in ReHo in the basal ganglia and dorsomedial prefrontal regions (DMPFC) and impaired functional connectivity between these two regions. DMPFC-basal ganglia mediated the effect of plasma and CSF KP on anhedonia. These findings highlight the pathological impact of KP system dysregulation in mediating inflammatory behaviors such as anhedonia.

The cranial nerves

2013 ◽  
Author(s):  
Martin E. Atkinson
Keyword(s):  
Head And Neck ◽  
Cranial Nerves ◽  
Dental Students ◽  
The Body ◽  
Neural Function ◽  
Nerve Supply ◽  
Spinal Nerves ◽  
Complete Detail ◽  
And Function ◽  
The Brain

The cranial nerves are the most important neural structures relevant to dental students and practitioners. The cranial nerves are the nerve supply to all the structures in the head and neck and underpin of the anatomy and function of these regions—the head and neck will not work without them. In a wider context, correct functioning of the cranial nerves is a very good indicator of the health or otherwise of the CNS; it may be necessary to test the function of some, or even all, of the cranial nerves at times to assess neural function. In addition, many of the cranial nerves may be involved in various diseases of the head and neck. As outlined in Chapter 3, 12 pairs of cranial nerves arising from the brain form one major component of the peripheral nervous system, the 31 pairs of spinal nerves forming the other. Each pair of cranial nerves has a name and number. Conventionally, they are numbered using the Roman numerals I to XII. The nerves are numbered from one to 12, according to their origin from the brain; nerves with the lowest numbers arise from the most anterior aspect of the brain (the forebrain) whereas those with highest numbers arise from the lowest part (the medulla). Several aspects of any nerve anywhere in the body are required to d escribe its anatomy and function in complete detail: • Its origins and terminations in the CNS; • Its neuronal components—are they motor, sensory, or autonomic? • Its course to and from its target tissues; • Its distribution to specific areas and structures through specific branches; • Its overall functions and specific functions of its component parts. In addition, if the clinical significance is going to be appreciated, we w ill also need to consider: • The effects of damage or disease on the nerve; • Its important relationships to other structures; • How to test whether the nerve is functioning correctly. Given that there are 12 pairs of nerves, does a competent dentist need to know everything in the two lists about every cranial nerve? The answer, you will be relieved to hear, is ‘no’.

scholarly journals Interdependence of oestrogen and insulin-like growth factor-I in the brain: potential for analysing neuroprotective mechanisms

2005 ◽  
Vol 185 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Pablo Mendez ◽  
Iñigo Azcoitia ◽  
Luis Miguel Garcia-Segura
Keyword(s):  
Growth Factor ◽  
Glycogen Synthase ◽  
Reproductive Behaviour ◽  
Mitogen Activated Protein Kinase ◽  
Neural Function ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
The Brain

The actions of oestradiol in the brain involve interaction with growth factors, such as insulin-like growth factor-I (IGF-I). Many cells in the brain co-express receptors for oestradiol and IGF-I and both factors interact to regulate neural function. The relationship of oestrogen receptor α with IGF-I receptor through the mitogen-activated protein kinase and the phosphoinositide 3-kinase signalling pathways may represent the point of convergence used by these two factors to cooperatively modulate neuritic growth, synaptic plasticity, neuroendocrine events, reproductive behaviour and neuronal survival. In addition, Akt and glycogen synthase kinase 3β are key molecular targets to explain the interaction of oestrogen and IGF-I receptor signalling in the promotion of neuroprotection.

Sign in / Sign up

Export Citation Format

Share Document