Evolution of the Prefrontal Cortex in the Hominins

2021 ◽  
pp. 333-371
Author(s):  
Richard E. Passingham
Keyword(s):  
Body Weight ◽  
Prefrontal Cortex ◽  
Climatic Change ◽  
Frontal Lobe ◽  
Rapid Expansion ◽  
Stone Tool ◽  
Cultural Environment ◽  
Selection Pressures ◽  
The Brain ◽  
Rapid Transfer

When body weight is taken into account, there was a rapid expansion of the brain during the evolution of the hominins, with the greatest increase occurring from around 400,000 years ago. After this time there is evidence of the bulging of the frontal lobe indicating the further expansion of the prefrontal (PF) cortex. Many selection pressures could have influenced these changes, but all of them involve a change in environment. This could occur via climatic change, via changes in the ecosystem, by migration, or by changes in the cultural environment. The cultural environment includes technology such as stone tool making, cooperation in hunting, and the improvements in communication that this required. The adaptation to new environments requires the solution of new problems, and this was aided by the ability of the PF cortex to support rapid transfer from one problem to another.

Editorial introduction to Greenwood/West dialogue

2000 ◽  
Vol 6 (6) ◽  
pp. 704-704
Author(s):  
JASON BRANDT
Keyword(s):  
Anorexia Nervosa ◽  
Prefrontal Cortex ◽  
Pathological Gambling ◽  
Frontal Cortex ◽  
Frontal Lobe ◽  
Editorial Introduction ◽  
Frontal Lobe Dysfunction ◽  
The Brain ◽  
Artistic Skill

Although a U.S. Presidential Proclamation designated the 1990s “The Decade of the Brain,” not all cerebral constituents shared equally in the limelight. By anyone's accounting, the prefrontal cortex was the darling of clinicians and neuroscientists throughout the '90s, with everything from schizophrenia and anorexia nervosa to pathological gambling and the emergence of artistic skill attributed to “frontal lobe dysfunction” (David, 1992; Miller et al., 1998; Rugle & Melamed, 1993). It should come as no surprise, then, that that most universal of cognitive afflictions, aging, should be linked to changes in frontal cortex.

Ontogeny of the brain in oval squid Sepioteuthis lessoniana (Cephalopoda: Loliginidae) during the post-hatching phase

2013 ◽  
Vol 93 (6) ◽  
pp. 1663-1671 ◽  
Author(s):  
Shiori Kobayashi ◽  
Chitoshi Takayama ◽  
Yuzuru Ikeda
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Body Size ◽  
Embryonic Development ◽  
Frontal Lobe ◽  
Optic Lobe ◽  
Relative Volume ◽  
Mantle Length ◽  
Sepioteuthis Lessoniana ◽  
The Brain

Among invertebrates, cephalopods have one of the most well-organized nervous systems. However, with respect to the ontogeny of the nervous system, the post-embryonic development of the cephalopod brain has only been documented for a few species. Here, we investigated the development of the brain of captive oval squid Sepioteuthis lessoniana during the post-hatching phase. The central part of the brain of the oval squid is divided into four main regions, namely, the supraoesophageal, anterior suboesophageal, middle suboesophageal, and posterior suboesophageal masses, each consisting of several lobes. At various ages in juvenile squid, the total volume of the central part of the brain (except the optic lobe) is significantly correlated with its body size, indicated by mantle length and wet body weight. The vertical lobe, superior frontal lobe, and anterior subesophageal mass drastically increase in relative volume as the squid grows. In contrast, the middle suboesophageal mass and posterior suboesophageal mass do not increase in volume with increasing squid age and body size. The effects of these results have been discussed in relation to the onset of squid behaviours during post-hatching.

Set-maintenance and set-shifting problems in schizophrenic subtypes: relationship to dysfunctions of the fronto-striatal loops

2000 ◽  
Vol 12 (1) ◽  
pp. 32-38
Author(s):  
M.G. Lanser ◽  
B.A. Ellenbroek ◽  
A.R. Cools ◽  
F.G. Zitman
Keyword(s):  
Parkinson’S Disease ◽  
Prefrontal Cortex ◽  
Frontal Lobe ◽  
Neuropsychological Tests ◽  
Set Shifting ◽  
Frontal Lobe Lesions ◽  
Core Symptom ◽  
Schizophrenic Patients ◽  
Information Set ◽  
The Brain

SUMMARYResearch with patients suffering from Parkinson's disease and frontal lobe lesions has shown that disturbances in the fronto-striatal loops in the brain can cause perseveration. Perseveration is a core symptom of schizophrenia, yet the cause is not known. For schizophrenic patients disorders of many parts of the fronto-striatal loops are found, for example disturbances of the prefrontal cortex and the striatum. Perseveration in schizophrenia can be explained with set-maintenance problems, related to dysfunction of the prefrontal cortex, or with set-shifting problems that are related to disorders in the striatum. These set-maintenance and set-shifting problems can be distinguished with neuropsychological tests. Regarding the bloodflow patterns for the different subtypes of schizophrenia three problems are expected as explanations for perseveration: set-maintenance problems concerning abstract information, set-maintenance problems shifting between stimuli and enhanced set-shifting with cues.

scholarly journals Khat distorts the prefrontal cortex histology and function of adult Wistar rats

2018 ◽  
Vol 7 (1) ◽  
pp. 1121-1131
Author(s):  
Isaac Echoru ◽  
Edmund E.M. Bukenya ◽  
Godfrey Masilili ◽  
Elna Owembabazi ◽  
Ann Monima Lemuel ◽  
...  
Keyword(s):  
Working Memory ◽  
Body Weight ◽  
Prefrontal Cortex ◽  
Selective Attention ◽  
Wistar Rats ◽  
Weight Ratio ◽  
Dependent Manner ◽  
Body Weight Ratio ◽  
Pharmacological Significance ◽  
The Brain

Khat is a psychoactive herbal drug of pronounced ethno-pharmacological significance often abused due to its unregulated use. It affects many brain centers including the prefrontal cortex which is the anterior most part of the frontal lobe. The prefrontal cortex modulates working memory, planning complex cognitive behaviors however; it is linked to many psychological disorders such as depression, schizophrenia and memory loss. We studied the effects exerted by khat on the PFC cytoarchitecture and functions since this part of the brain is highly interconnected with various cortical regions. This was an experimental study of 6 weeks. A total of 24 male adult wistar rats of 130g-155g were divided into four groups of 6 animals that received respective khat doses of 2000mg/kg, 1000mg/kg, 500mg/kg and 10ml/kg of distilled water for the controls. Brain to body weight ratio was determined at week 6 using an analytical balance (Fisher Science Education™, RS232C; USA). Histology of the brain was determined using H and E and Kulvers staining technique. Khat exhibited features of prefrontal cortex disorientation such as necrosis, vacuolations, chromatolysis, demyelination, cortical degeneration and hemorrhage in a dose dependent manner. Selective attention and working memory were impaired well as brain to body weight ratio was reduced significantly (P ≤ 0.05). Repeated exposure to khat distorts the prefrontal cortex cytoarchitecture and impairs selective attention and working memory accuracy due to ischemia and cell exhaustion by khat toxicity.Keywords: Khat, prefrontal cortex histology, working memory, selective attention

scholarly journals Causal inference in the multisensory brain

2018 ◽  
Author(s):  
Yinan Cao ◽  
Christopher Summerfield ◽  
Hame Park ◽  
Bruno L. Giordano ◽  
Christoph Kayser
Keyword(s):  
Prefrontal Cortex ◽  
Causal Inference ◽  
Frontal Lobe ◽  
Multisensory Integration ◽  
Multisensory Perception ◽  
Adaptive Behaviour ◽  
Sensory Fusion ◽  
Spatio Temporal ◽  
The Brain ◽  
Combining Information

When combining information across different senses humans need to flexibly select cues of a common origin whilst avoiding distraction from irrelevant inputs. The brain could solve this challenge using a hierarchical principle, by deriving rapidly a fused sensory estimate for computational expediency and, later and if required, filtering out irrelevant signals based on the inferred sensory cause(s). Analysing time- and source-resolved human magnetoencephalographic data we unveil a systematic spatio-temporal cascade of the relevant computations, starting with early segregated unisensory representations, continuing with sensory fusion in parietal-temporal regions and culminating as causal inference in the frontal lobe. Our results reconcile previous computational accounts of multisensory perception by showing that prefrontal cortex guides flexible integrative behaviour based on candidate representations established in sensory and association cortices, thereby framing multisensory integration in the generalised context of adaptive behaviour.

SPECIFIC PROPERTIES OF TUBULIN IN THE PREFRONTAL CORTEX IN CONTROL, SCHIZOPHRENIA AND VASCULAR DEMENTIA

2020 ◽  
pp. 65-71
Author(s):  
Burbaeva G.Sh. ◽  
Androsova L.V. ◽  
Vorobyeva E.A. ◽  
Savushkina O.K.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Vascular Dementia ◽  
Binding Activity ◽  
Nephelometric Method ◽  
Rate Of Polymerization ◽  
Mental Diseases ◽  
And Control ◽  
The Brain

The aim of the study was to evaluate the rate of polymerization of tubulin into microtubules and determine the level of colchicine binding (colchicine-binding activity of tubulin) in the prefrontal cortex in schizophrenia, vascular dementia (VD) and control. Colchicine-binding activity of tubulin was determined by Sherlinе in tubulin-enriched extracts of proteins from the samples. Measurement of light scattering during the polymerization of the tubulin was carried out using the nephelometric method at a wavelength of 450-550 nm. There was a significant decrease in colchicine-binding activity and the rate of tubulin polymerization in the prefrontal cortex in both diseases, and in VD to a greater extent than in schizophrenia. The obtained results suggest that not only in Alzheimer's disease, but also in other mental diseases such as schizophrenia and VD, there is a decrease in the level of tubulin in the prefrontal cortex of the brain, although to a lesser extent than in Alzheimer's disease, and consequently the amount of microtubules.

Activation of Melanocortin-4 Receptor by a Synthetic Agonist Inhibits Ethanolinduced Neuroinflammation in Rats

2020 ◽  
Vol 25 (45) ◽  
pp. 4799-4805 ◽  
Author(s):  
Osvaldo Flores-Bastías ◽  
Gonzalo I. Gómez ◽  
Juan A. Orellana ◽  
Eduardo Karahanian
Keyword(s):  
Prefrontal Cortex ◽  
Alcohol Consumption ◽  
Ethanol Intake ◽  
Neuroinflammatory Response ◽  
Agonist Peptide ◽  
Melanocortin 4 Receptor ◽  
Tnf Α ◽  
Cord Injury ◽  
High Ethanol ◽  
The Brain

Background: High ethanol intake induces a neuroinflammatory response resulting in the subsequent maintenance of chronic alcohol consumption. The melanocortin system plays a pivotal role in the modulation of alcohol consumption. Interestingly, it has been shown that the activation of melanocortin-4 receptor (MC4R) in the brain decreases the neuroinflammatory response in models of brain damage other than alcohol consumption, such as LPS-induced neuroinflammation, cerebral ischemia, glutamate excitotoxicity, and spinal cord injury. Objectives: In this work, we aimed to study whether MC4R activation by a synthetic MC4R-agonist peptide prevents ethanol-induced neuroinflammation, and if alcohol consumption produces changes in MC4R expression in the hippocampus and hypothalamus. Methods: Ethanol-preferring Sprague Dawley rats were selected offering access to 20% ethanol on alternate days for 4 weeks (intermittent access protocol). After this time, animals were i.p. administered an MC4R agonist peptide in the last 2 days of the protocol. Then, the expression of the proinflammatory cytokines interleukin 6 (IL-6), interleukin 1-beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) were measured in the hippocampus, hypothalamus and prefrontal cortex. It was also evaluated if ethanol intake produces alterations in the expression of MC4R in the hippocampus and the hypothalamus. Results: Alcohol consumption increased the expression of MC4R in the hippocampus and the hypothalamus. The administration of the MC4R agonist reduced IL-6, IL-1β and TNF-α levels in hippocampus, hypothalamus and prefrontal cortex, to those observed in control rats that did not drink alcohol. Conclusion: High ethanol consumption produces an increase in the expression of MC4R in the hippocampus and hypothalamus. The administration of a synthetic MC4R-agonist peptide prevents neuroinflammation induced by alcohol consumption in the hippocampus, hypothalamus, and prefrontal cortex. These results could explain the effect of α-MSH and other synthetic MC4R agonists in decreasing alcohol intake through the reduction of the ethanol-induced inflammatory response in the brain.

025 Sleep Disruption on an Orbital Shaker alters Glutamate in Prairie Vole Prefrontal Cortex

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A11-A12
Author(s):  
Carolyn Jones ◽  
Randall Olson ◽  
Alex Chau ◽  
Peyton Wickham ◽  
Ryan Leriche ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Prefrontal Cortex ◽  
Early Life ◽  
Autism Spectrum ◽  
Prairie Vole ◽  
Sleep Disruption ◽  
Glutamatergic Synapses ◽  
The Brain ◽  
Orbital Shaker

Abstract Introduction Glutamate concentrations in the cortex fluctuate with the sleep wake cycle in both rodents and humans. Altered glutamatergic signaling, as well as the early life onset of sleep disturbances have been implicated in neurodevelopmental disorders such as autism spectrum disorder. In order to study how sleep modulates glutamate activity in brain regions relevant to social behavior and development, we disrupted sleep in the socially monogamous prairie vole (Microtus ochrogaster) rodent species and quantified markers of glutamate neurotransmission within the prefrontal cortex, an area of the brain responsible for advanced cognition and complex social behaviors. Methods Male and female prairie voles were sleep disrupted using an orbital shaker to deliver automated gentle cage agitation at continuous intervals. Sleep was measured using EEG/EMG signals and paired with real time glutamate concentrations in the prefrontal cortex using an amperometric glutamate biosensor. This same method of sleep disruption was applied early in development (postnatal days 14–21) and the long term effects on brain development were quantified by examining glutamatergic synapses in adulthood. Results Consistent with previous research in rats, glutamate concentration in the prefrontal cortex increased during periods of wake in the prairie vole. Sleep disruption using the orbital shaker method resulted in brief cortical arousals and reduced time in REM sleep. When applied during development, early life sleep disruption resulted in long-term changes in both pre- and post-synaptic components of glutamatergic synapses in the prairie vole prefrontal cortex including increased density of immature spines. Conclusion In the prairie vole rodent model, sleep disruption on an orbital shaker produces a sleep, behavioral, and neurological phenotype that mirrors aspects of autism spectrum disorder including altered features of excitatory neurotransmission within the prefrontal cortex. Studies using this method of sleep disruption combined with real time biosensors for excitatory neurotransmitters will enhance our understanding of modifiable risk factors, such as sleep, that contribute to the altered development of glutamatergic synapses in the brain and their relationship to social behavior. Support (if any) NSF #1926818, VA CDA #IK2 BX002712, Portland VA Research Foundation, NIH NHLBI 5T32HL083808-10, VA Merit Review #I01BX001643

scholarly journals Glia Not Neurons: Uncovering Brain Dysmaturation in a Rat Model of Alzheimer’s Disease

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 823
Author(s):  
Ekaterina A. Rudnitskaya ◽  
Tatiana A. Kozlova ◽  
Alena O. Burnyasheva ◽  
Natalia A. Stefanova ◽  
Nataliya G. Kolosova
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Brain Structures ◽  
Time Frame ◽  
Oxys Rats ◽  
Unknown Etiology ◽  
Suitable Model ◽  
Model Of Alzheimer’S Disease ◽  
The Brain

Sporadic Alzheimer’s disease (AD) is a severe disorder of unknown etiology with no definite time frame of onset. Recent studies suggest that middle age is a critical period for the relevant pathological processes of AD. Nonetheless, sufficient data have accumulated supporting the hypothesis of “neurodevelopmental origin of neurodegenerative disorders”: prerequisites for neurodegeneration may occur during early brain development. Therefore, we investigated the development of the most AD-affected brain structures (hippocampus and prefrontal cortex) using an immunohistochemical approach in senescence-accelerated OXYS rats, which are considered a suitable model of the most common—sporadic—type of AD. We noticed an additional peak of neurogenesis, which coincides in time with the peak of apoptosis in the hippocampus of OXYS rats on postnatal day three. Besides, we showed signs of delayed migration of neurons to the prefrontal cortex as well as disturbances in astrocytic and microglial support of the hippocampus and prefrontal cortex during the first postnatal week. Altogether, our results point to dysmaturation during early development of the brain—especially insufficient glial support—as a possible “first hit” leading to neurodegenerative processes and AD pathology manifestation later in life.

scholarly journals ICI 182,780 Penetrates Brain and Hypothalamic Tissue and Has Functional Effects in the Brain after Systemic Dosing

Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 5219-5226 ◽  
Author(s):  
Peter D. Alfinito ◽  
Xiaohong Chen ◽  
James Atherton ◽  
Scott Cosmi ◽  
Darlene C. Deecher
Keyword(s):  
Body Weight ◽  
Skin Temperature ◽  
Ethinyl Estradiol ◽  
Ovariectomized Rats ◽  
Ici 182,780 ◽  
Hot Flush ◽  
Hypothalamic Tissue ◽  
Dependent Model ◽  
The Brain ◽  
Neuroendocrine Functions

Previous reports suggest the antiestrogen ICI 182,780 (ICI) does not cross the blood-brain barrier (BBB). However, this hypothesis has never been directly tested. In the present study, we tested whether ICI crosses the BBB, penetrates into brain and hypothalamic tissues, and affects known neuroendocrine functions in ovariectomized rats. Using HPLC with mass spectrometry, ICI (1.0 mg/kg·d, 3 d) was detected in plasma and brain and hypothalamic tissues for up to 24 h with maximum concentrations of 43.1 ng/ml, and 31.6 and 38.8 ng/g, respectively. To evaluate antiestrogenic effects of ICI in the brain after systemic dosing, we tested its ability to block the effect of 17 α-ethinyl estradiol (EE) (0.3 mg/kg, 8 d) on tail-skin temperature abatement in the morphine-dependent model of hot flush and on body weight change. In the morphine-dependent model, EE abated 64% of the naloxone-induced tail-skin temperature increase. ICI pretreatment (1.0, 3.0 mg/kg·d) dose dependently inhibited this effect. ICI (3.0 mg/kg·d) alone showed estrogenic-like actions, abating 30% the naloxone-induced flush. In body weight studies, EE-treated rats weighed 58.5 g less than vehicle-treated rats after 8 d dosing. This effect was partially blocked by ICI (3.0 mg/kg·d) pretreatment. Similar to EE treatment, rats receiving 1.0 or 3.0 mg/kg·d ICI alone showed little weight gain compared with vehicle-treated controls. Thus, ICI crosses the BBB, penetrates into brain and hypothalamic tissues, and has both antiestrogenic and estrogenic-like actions on neuroendocrine-related functions.

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