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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Feb 4, 2014

 

The study highlights that consuming Cannabis during pregnancy clearly results
in defective development of nerve cells of the cerebral cortex, the part of the brain
that orchestrates higher cognitive functions and drives memory formation. .






WHO Child Growth Charts

 

 

 

Cannabis endangers fetal brain development

An increasing number of children suffer from the consequences of maternal drug exposure during pregnancy, and Cannabis is one of the most frequently used substances.

This motivated a study conducted on mice and human brain tissue, to decipher the molecular basis of how the major psychoactive component from Cannabis — delta-9-tetrahydrocannabinol or THC — affects fetal brain development. The results of the study are published in the EMBO Journal.

The study highlights that consuming Cannabis during pregnancy clearly results in defective development of nerve cells of the cerebral cortex, the part of the brain that orchestrates higher cognitive functions and drives memory formation.


In particular, THC negatively impacts when, how and if synapses and axons will develop and function.

Researchers identified Stathmin-2 as a key protein target of THC — and the loss of Stathmin-2 is behind errors in nerve growth.

It is stressed that Cannabis exposure in experimental models precisely coincided with the fetal period when nerve cells form connections with each other.


According to study leader Professor Tibor Harkany of Karolinska Institute and the Medical University of Vienna, Austria, these developmental deficits may generate life-long modifications to brain function in those children affected.

Even though not all children who have been exposed to Cannabis will suffer immediate and obvious deficits, Professor Harkany warns that relatively subtle damage can significantly increase the risk of delayed neuropsychiatric diseases.


"Even if THC only caused small changes, its effect may be sufficient to sensitize the brain to later stressors or diseases that provoke neuropsychiatric illnesses in the future for those affected.

"This also concerns the medical use of Cannabis, which should be avoided during pregnancy."

Tibor Harkany, professor, Karolinska Institute and the Medical University of Vienna, Austria


Abstract
Children exposed in utero to cannabis present permanent neurobehavioral and cognitive impairments. Psychoactive constituents from Cannabis spp., particularly Δ9-tetrahydrocannabinol (THC), bind to cannabinoid receptors in the fetal brain. However, it is unknown whether THC can trigger a cannabinoid receptor-driven molecular cascade to disrupt neuronal specification. Here, we show that repeated THC exposure disrupts endocannabinoid signaling, particularly the temporal dynamics of CB1 cannabinoid receptor, to rewire the fetal cortical circuitry. By interrogating the THC-sensitive neuronal proteome we identify Superior Cervical Ganglion 10 (SCG10)/stathmin-2, a microtubule-binding protein in axons, as a substrate of altered neuronal connectivity. We find SCG10 mRNA and protein reduced in the hippocampus of midgestational human cannabis-exposed fetuses, defining SCG10 as the first cannabis-driven molecular effector in the developing cerebrum. CB1 cannabinoid receptor activation recruits c-Jun N-terminal kinases to phosphorylate SCG10, promoting its rapid degradation in situ in motile axons and microtubule stabilization. Thus, THC enables ectopic formation of filopodia and alters axon morphology. These data highlight the maintenance of cytoskeletal dynamics as a molecular target for cannabis, whose imbalance can limit the computational power of neuronal circuitries in affected offspring.

Synopsis
Δ9-tetrahydrocannabinol (THC), the major psychoactive component from cannabis, is shown to activate a molecular cascade modulating SCG10/stathmin-2 availability and function, thus inducing cytoskeletal modifications in fetal neurons.

In vivo experiments demonstrate that THC disrupts endocannabinoid signaling and acts as a functional antagonist in the fetal brain.

C-Jun terminal kinase links CB1 cannabinoid receptor and SCG10/stathmin-2 phosphorylation and degradation.

Maternal cannabis smoking reduces SCG10/stathmin-2 mRNA and protein expression in human fetal brains, identifying SCG10/stathmin-2 as a key molecular effector mediating adverse cannabis effects.

In addition to researchrs from Sweden and Austria, researchers from the US, Germany, Finland and the UK took part in the study. The work was financed with grants from the Scottish Universities Life Science Alliance, the Swedish Research Council, Hjärnfonden, the Novo Nordisk Foundation, the Wellcome Trust, and the National Institutes of Health.

Publication: 'Miswiring the brain delta-9-tetra-hydro-cannabinol disrupts cortical development by inducing an SCG10/stathmin-2 degradation pathway', Giuseppe Tortoriello, Claudia V. Morris, Alan Alpar, Janos Fuzik, Sally L. Shirran, Daniela Calvigioni, Erik Keimpema, Catherine H. Botting, Kirstin Reinecke, Thomas Herdegen, Michael Courtney, Yasmin L. Hurd and Tibor Harkany, EMBO Journal, online 27 January 2014.

Contact the Press Office at Karolinska Institutet and download an image: ki.se/pressroom.

More about MedUni Vienna: http://cbr.meduniwien.ac.at.

Karolinska Institutet - a medical university: http://ki.se/english.