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PubMed1994

Development of cranial flexure and Rathke's pouch in the chick embryo.

Experiments were done to investigate the cause of the cranial (mesencephalic) flexure of the chick brain during stages 10 to 14. Measurements of the length and thickness of the roof and floor of the mesencephalon gave values similar to the values obtained previously by others. The labeling index was determined in the roof and floor of the prosencephalon, mesencephalon, and rhombencephalon as a preliminary measure of cell division. The labeling index was about the same in all regions, and was high enough to suggest that most of the cells were dividing. The labeling indices did not suggest that differential growth was caused by differential rates of cell division in the roof and floor of the mesencephalon. It was found through time lapse photography that the foregut and heart remained stationary along the rostrocaudal axis, whereas the prosencephalon moved rostrally and the mesencephalon underwent flexure. Measurements suggested that the neural tube cranial to the otic primordium grew in volume exponentially at a rate consistent with the labeling index. The rostral tip of the neural tube was observed to be linked to the rostral tip of the foregut by the ectoderm that formed Rathke's pouch at the neural tube and the pharyngeal membrane (prospective stomodeum) at the foregut. As the neural tube grew in length, the link between the neural tube and the foregut did not. We suggest that because of this link, the growing neural tube had to bend around the foregut, forming the cranial flexure, and the ectoderm folded where it attached to the prosencephalon, forming Rathke's pouch.

Animals↗

PubMed1985

Prosencephalic afferents to the mediodorsal thalamic nucleus.

The afferent projections from the prosencephalon to the mediodorsal thalamic nucleus (MD) were studied in the cat by use of the method of retrograde transport of horseradish peroxidase (HRP). Cortical and subcortical prosencephalic structures project bilaterally to the MD. The cortical afferents originate mainly in the ipsilateral prefrontal cortex. The premotor, prelimbic, anterior limbic, and insular agranular cortical areas are also origins of consistent projections to the MD. The motor cortex, insular granular area, and some other cortical association areas may be the source of cortical connections to the MD. The subcortical projections originate principally in the ipsilateral rostral part of the reticular thalamic nucleus and the rostral lateral hypothalamic area. Other parts of the hypothalamus, the most caudal parts of the thalamic reticular nucleus, the basal prosencephalic structures, the zona incerta, the claustrum, and the entopeduncular and subthalamic nuclei are also sources of projections to the MD. Distinct, but somewhat overlapping areas of the prosencephalon project to the three vertical subdivisions of MD (medial, intermediate, and lateral). The medial band of the MD receives a small number of prosencephalic projections; these arise mainly in the caudal and ventral parts of the prefrontal cortex. Cortical projections also arise in the infralimbic area, while subcortical projections originate in the medial part of the rostral reticular thalamic nucleus and lateral hypothalamic area. The intermediate band of the MD receives the largest number of fibers from the prosencephalon. These arise principally in the intermediate and dorsal part of the lateral and medial surface of the prefrontal cortex, the premotor cortex, and the prelimbic and agranular insular areas. Projections also originate in basal prosencephalic formations (preoptic area, Broca's diagonal band, substantia innominata, and olfactory tubercle), rostral reticular thalamic nucleus, and lateral hypothalamic area. A large number of prosencephalic structures also project to the lateral band of the MD. These are mainly the most dorsal and caudal parts of the lateral and medial surface of the prefrontal cortex, the premotor and motor cortices, and the prelimbic, anterior limbic, and insular areas. Projections arise also in the lateral rostral and caudal parts of the reticular thalamic nucleus, the zona incerta, the lateral and dorsal hypothalamic area, the claustrum, and the entopeduncular nucleus. These and previous results demonstrate a gradation in the afferent connections to the three subdivisions of the MD.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗

PubMed1986

Plasticity and rigidity of differentiation of brain vesicles studied in quail-chick chimeras.

Transplantation of a piece of the alar plate of the prosencephalon or of the rhombencephalon of quail embryos into the roof of the mesencephalon of chick embryos was carried out at 7-10 somite stage. Results obtained were: the transplanted alar plate of the prosencephalon differentiated into tissue closely resembling the tectum when the transplants were integrated into the host mesencephalon; in all the cases, the alar plate of the rhombencephalon did not differentiate into tectum-like structure, but into rhombencephalic descendants. We conclude that the alar plate of the prosencephalon at 7-10 stage is not definitively determined and may retain an ability to differentiate into the optic tectum, whereas the prospective fate of the rhombencephalon has already been determined at 7-10 stage.

Animals↗

PubMed1995

Morphological and GABA-immunoreactive development of the embryonic chick telencephalon.

The development of neurons utilizing gamma-aminobutyric acid (GABAergic neurons) in prosencephalon and telencephalon from chicken embryonic days 4-14 (E4-E14) was studied by means of immunohistochemistry. Furthermore, routine histology and transmission electron microscopy. respectively, were performed in order to study the morphological development in the designated area. The main finding is that development of GABAergic neurons in the chick telencephalon is rapid; the GABA neurons are appearing in bulk at day 8, being "overexpressed" at days 10-11, decreasing in numbers thereafter and achieving mature morphology on day 14, which is considerably faster than in the rodent. Morphological analysis revealed that the prosencephalon mainly consisted of a thin layer of undifferentiated neuroblasts in the E4 embryo. By E6, the prosencephalon had increased in thickness and occasional cells outside the neuroepithelium showed a more mature morphology with a few cells weakly staining positive for GABA. At E8, the prospective granular and subventricular layers had developed. At E14, the appearance of the telencephalon is approximating that of the adult since both ependymal cells and morphologically mature neurons can be seen.

Animals↗

PubMed1995

Ontogeny of GABA-immunoreactive neurons in the central nervous system in a teleost, gasterosteus aculeatus L.

The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is known to exert various neurotrophic actions in the developing nervous system, but little is known about its distribution in the central nervous system during early development. We have studied the development of GABA-immunoreactive (GABAir) neurons during embryogenesis of a teleost fish, the three-spined stickleback. As early as 51 h postfertilization (PF; hatching occurs 144-168 h PF, and the first monoaminergic neurons appear around 72 h PF) GABAir neurons appear in the ventral prosencephalon caudal to the optic recess, in the ventral mesencephalon, and in the spinal cord. Then, there is a gradual addition of GABAir cell groups in the rostral prosencephalon and ventral rhombencephalon (66 h PF), dorsal and caudal hypothalamus and pretectum (72 h PF), ventral hypothalamus (78 h PF), preoptic region, thalamus, and in the mesencephalon and rhombencephalon (96 h PF). GABAir axons appear in the spinal cord already at 51 h PF, and then gradually appear in the various tracts of the early axonal scaffold of pathfinding fibers, so that by 96 h PF the entire axonal scaffold contains GABAir fibers. It appears likely that GABAergic axons contribute a major population to the formation of the axonal scaffold. Moreover, in the prosencephalon GABAir neurons are arranged in clusters that may reflect a neuromeric organization with six prosencephalic neuromeres.

Animals↗

PubMed2004

An avian model of genetic reflex epilepsy.

The Fayoumi strain of chickens (Fepi) carries a recessive autosomal gene mutation in which homozygotes are afflicted with a photogenic and audiogenic reflex epilepsy. Seizures consist of stimulus-locked motor symptoms followed by generalized self sustained convulsions. EEG recordings show spikes and spike and waves patterns at rest which are suppressed during seizures and replaced by a desynchronized pattern of activity. Neurones of the prosencephalon discharge in bursts at rest, while neurones of the mesencephalon are bursting during seizures. Living neural chimeras were obtained by replacing specific embryonic brain vesicles in a normal chicken embryo with equivalent vesicles from a Fepi donor. These chimeras show that the epileptic phenotype can be totally or partially transferred from the Fepi to the normal chickens. Total transfer of photogenic and audiogenic seizures was obtained by substitution of both the prosencephalon and mesencephalon, while substitution of the prosencephalon alone resulted in transfer of interictal paroxysmal activity and substitution of the mesencephalon alone resulted principally in transfer of ictal motor symptoms. Increased expression of the c-fos protooncogene, as revealed by the western blot technique, confirmed the distinct encephalic localizations of the symptoms of the photogenic and audiogenic reflex epilepsy of the Fepi shown with the methods of electrophysiology and brain chimeras. We conclude that the Fepi is a good model of brain stem reflex epilepsy and suggest that the brain stem is a generator of some other animal and human genetic reflex "epileptic syndromes".

Action Potentials↗

PubMed2000

Magnetic resonance imaging volumes of the hippocampus and the amygdala in women with borderline personality disorder and early traumatization.

BACKGROUND: Based on findings of stress-induced neural disturbances in animals and smaller hippocampal volumes in humans with posttraumatic stress disorder), we hypothesized that patients with borderline personality disorders (BPD), who often are victims of early traumatization, have smaller volumes of the hippocampus and the amygdala. We assumed that volumes of these brain regions are negatively correlated with traumatic experiences and with neuropsychological deficits. METHODS: We studied 21 female patients with BPD and a similar group of healthy controls. We performed clinical assessments, a modified version of the Childhood Trauma Questionnaire, and magnetic resonance imaging volumetric measurements of the hippocampus, amygdala, temporal lobes, and prosencephalon. Neuropsychological testing included scales on which disturbances in BPD were previously reported. RESULTS: The patients with BPD had nearly 16% smaller volumes of the hippocampus (P<.001) and 8% smaller volumes of the amygdala (P<.05) than the healthy controls. The results for both hemispheres were nearly identical and were controlled for the volume of the prosencephalon and for head tilts. The volumes of the hippocampus were negatively correlated with the extent and the duration of self-reported early traumatization only when BPD and control subjects were considered together. Levels of neuropsychological functioning were associated with the severity of depression but not with the volumes of the hippocampus. CONCLUSION: In female patients with BPD, we found reduction of the volumes of the hippocampus (and perhaps of the amygdala), but the association of volume reduction and traumatic experiences remains unclear. Arch Gen Psychiatry. 2000;57:1115-1122.

Adult↗

PubMed2000

The vesicular forebrain (pseudo-aprosencephaly): a missing link in the teratogenetic spectrum of the defective brain anlage and its discrimination from aprosencephaly.

Two cases out of a sample of 41 fetuses and infants with prosencephalic malformation, observed at the Institute of Pathology and Department of Neuropathology of the University of Heidelberg, are described here in detail. These cases presented grossly with microcephaly and missing forebrain, appearing to be cases of aprosencephaly. However, in one of these cases glio-mesenchymal membranes with an ependymal outline, consistent with the microscopic appearance of the dorsal sac membrane in holoprosencephaly and obviously representing remnants of a collapsed primitive prosencephalic vesicle, could be demonstrated. In the other case only hindbrain structures, with the exception of the cerebellum, were present without any demonstrable remnants of a prosencephalon. We propose that the microscopic specification of a primitive prosencephalic vesicle in the first case and similar cases does not justify the diagnosis of atelencephaly/aprosencephaly because the prosencephalon was not really missing (pseudo-aprosencephaly). The prosencephalic anlage had been formed but remained vesicular without further differentiation of a holospheric brain mantle as in common holoprosencephaly ('vesicular forebrain'). We believe that pseudo-aprosencephaly represents the most primitive form of holoprosencephaly, in which the forebrain remains as a complete sac, linking classical holoprosencephaly with 'true' aprosencephaly, i.e., defective prosencephalic anlage due to developmental arrest. The 'vesicular forebrain' allows one to extend the classification of Probst by an additional category which might be termed complete sac category, intercalated between the dorsal sac category and 'true' atelencephaly/aprosencephaly.

Anencephaly↗

PubMed1992

Pattern of electroencephalographic activity during light induced seizures in genetic epileptic chicken and brain chimeras.

Genetic epilepsy was studied in Fayoumi epileptic (F.Epi) chickens and in neural chimeras obtained by selective substitution of embryonic brain vesicles of F.Epi donors in normal recipient chickens. Typical motor seizures accompanied by convulsions were evoked by intermittent light stimulation in F.Epi and in chimeras having embryonic substitution of the prosencephalon and the mesencephalon. The motor seizure was less severe in chimeras receiving only the prosencephalon. In the F.Epi, as well as in all the chimeras, the EEG during seizures was characterized by a desynchronized (or a flattening) pattern of activity. F.Epi and chimeras had a lower threshold to Metrazol induced seizures than control chickens. The experimental animals show that, in this model, large prosencephalic and mesencephalic areas are involved in the epileptic disease. The epileptic character of this genetic dysfunction is discussed.

Animals↗

PubMed1998

Demarcation of prosencephalic regions by CD15-positive radial glia.

A subpopulation of radial glial cells has been identified in the mouse prosencephalon during the second half of embryonic development. This subpopulation, specified by the putative cell adhesion molecule CD15 (LeX, FAL), is arranged in a segmented pattern within the telencephalon and diencephalon. Glial processes, spanning the prosencephalic wall, first appear at E10.5 and remain clearly visible until E19, when staining of discrete nuclei begins to appear. Registration of the correspondence between ventricular and pial surfaces, however, is still possible due to the persistence of individual CD15-positive fibres. These can be traced even when the initial simple linear (radial) orientation between ventricular and pial surfaces becomes complicated and distorted. After birth, CD15 immunoreactivity is distributed in a mosaic pattern in the forebrain. Because radial glial cells provide a scaffolding system for postmitotic neurones, the pattern of CD15-positive fibres in the embryonic prosencephalon may also demarcate future discrete regions of the postnatal brain.

Animals↗

PubMed2004

Chronic aluminum administration to old rats results in increased levels of brain metal ions and enlarged hippocampal mossy fibers.

The effect of chronic aluminium administration (2 g/L/6 months) was investigated in the central nervous system (CNS) of old rats. The content of Al(3+), Cu(2+), Zn(2+), and Mn(2+) was measured in prosencephalon + mesencephalon, pons-medulla, and cerebellum. The area occupied by the mossy fibers in the hippocampal CA3 zone was also measured. In Al-treated rats the contents of Al(3+), Cu(2+), Zn(2+), and Mn(2+) were significantly increased in prosencephalon + mesencephalon and pons-medulla, while no change was observed in the cerebellum except a Cu(2+) decrease. The area occupied by the mossy fibers in the CA3 field was significantly increased (+32%) in Al-treated rats. Taken together, the present findings document that the aging CNS is particularly susceptible to aluminum toxic effects that may be responsible for a consistent rise in the cell load of oxidative stress. This may contribute, as an aggravating factor, to the development of neurodegenerative events, as observed in Alzheimer disease.

Aluminum↗

PubMed2003

The effect of chronic aluminum(III) administration on the nervous system of aged rats: clues to understand its suggested role in Alzheimer's disease.

The effect of chronic aluminum intake has been investigated in the brain of aged male Wistar rats to assess the potential role of the accumulation of this metal ion on the development of neurodegenerative features observed in Alzheimer's disease. AlCl3 x 6 H2O (2g/L) was administered to experimental animals for 6 months in the drinking water. The total content of Al (microg/g fresh tissue) was measured by inductively coupled plasma atomic emission spectrometry (ICP-AES), while the content of Cu, Zn and Mn was determined by flame AAS in the prosencephalon + mesencephalon, pons-medulla and cerebellum of control and Al(III)-treated animals. The area occupied by mossy fibres in the CA3 field of the hippocampus was estimated by a computer-assisted morphometric method following Timm's preferential staining. In Al(III)-treated rats the concentration of Cu, Zn and Mn did not increase significantly (p < 0.5) in prosencephalon + mesencephalon, nor in pons-medulla (p < 0.5) except for Cu (p < 0.05) in pons-medulla. In the cerebellum the only significant increase was seen for Zn (p < 0.01) while no change was observed for Cu and Mn. The area occupied by the mossy fibres in the hippocampal CA3 field was significantly increased (+32%) in aged Al(III)-treated rats. Since Cu, Zn and Mn are essential components of the cytosolic and mitochondrial superoxide dismutases, it is possible that the increased content of these ions in aged Al(III)-treated rats represents an increased amount of genetic expression of these antioxidant enzymes. Considering that the positivity to Timm's reaction is based on the presence of free or loosely bound Zn2+ ions within synaptic terminals and that Zn2+ ions are reported to be accumulated by hippocampal neurons when tissue injury occurs, the increased area of the mossy fibres in CA3 field of Al(III)-treated rats could indicate increased hippocampal damage in these animals. Taken together, the present findings indicate that the aging CNS is particularly susceptible to Al(III) toxic effects which may increase the cell load of oxidative stress and may contribute, as an aggravating factor, to the development of neurodegenerative events as observed in Alzheimer's disease.

Aggression↗

PubMed1996

Early deletion of neuromeres in Wnt-1-/- mutant mice: evaluation by morphological and molecular markers.

The Wnt-1 gene is required for the development of midbrain and cerebellum; previous work showed that knockout of Wnt-1 causes the loss of most molecular markers of these structures in early embryos and deletion of these structures by birth. However, neither the extent of early neuronal defects nor any possible alterations in structures adjacent to presumptive midbrain and cerebellum were examined. By using a neuron-specific antibody and fluorescent axon tracers, we show that central and peripheral neuronal development are altered in mutants during initial axonogenesis on embryonic day 9.5. The absence of neuronal landmarks, including oculomotor and trochlear nerves and cerebellar plate, suggests that both mesencephalon and rhombomere 1 (r1) are delected, with the remaining neural tube fused to form a new border between the caudalmost portion of the prosencephalon (prosomere 1, or p1) and r2. Central axons accurately traverse this novel border by forming normal longitudinal tracts into the rhombencephalon, implying that the cues that direct these axons are aligned across neuromeres and are not affected by the delection. The presence of intact p1 and r2 is further supported by the retention of markers for these two neuromers, including a marker of p1, the Sim-2 gene, and an r2-specific lacZ transgene in mutant embryos. In addition, alterations in the Sim-2 expression domain in ventral prosencephalon, rostral to p1, provide novel evidence for Wnt-1 function in this region.

Animals↗

PubMed1996

Developmental and dysmorphogenic effects of glufosinate ammonium on mouse embryos in culture.

The effects of glufosinate ammonium on embryonic development in mice were examined using whole embryo and micromass cultures of midbrain and limb bud cells. In day 8 embryos cultured for 48 hr, glufosinate caused significant overall embryonic growth retardation and increased embryolethality to 37.5% at 10 micrograms/ml (5.0 x 10(-5) M). All embryos in the treated groups exhibited specific morphological defects including hypoplasia of the prosencephalon (forebrain) (100%) and visceral arches (100%). In day 10 embryos cultured for 24 hr, glufosinate significantly reduced the crown-rump length and the number of somite pairs, and produced a high incidence of morphological defects (84.6%) at 10 micrograms/ml. These embryos were characterized by blister in the lateral head (100%), hypoplasia of prosencephalon (57.1%), and cleft lips (42.9%) at 20 micrograms/ml (10.0 x 10(-5) M). Histological examination of the treated embryos showed numerous cell death (pyknotic debris) present throughout the neuroepithelium in the brain vesicle and neural tube, but did not involve the underlying mesenchyme. In micromass culture, glufosinate inhibited the differentiation of midbrain cells in day 12 embryos with 50% inhibition occurring at 0.55 microgram/ml (2.8 x 10(-6) M). The ratios of 50% inhibition concentration for cell proliferation to cell differentiation in limb bud cells were 0.76 and 1.52 in day 11 and 12 embryos, respectively. These findings indicate that glufosinate ammonium is embryotoxic in vitro. In addition to causing growth retardation, glufosinate specifically affected the neuroepithelium of the brain vesicle and neural tube, leading to neuroepithelial cell death.

Abnormalities, Drug-Induced↗

PubMed1983

A kinetic analysis of rat embryo response to cyclophosphamide exposure in vitro.

Day 10 rat embryos were exposed in vitro to a teratogenic dose of cyclophosphamide (25 micrograms/ml) in the presence of a metabolic system (activated CP) for varying lengths of time and then were recultured in drug-free medium. Development was assessed after a total of 24-26 hours of culture. Exposure periods of 2.5 hours or less had no significant effects on growth, incidence of malformed embryos, mitotic index, or necrotic index when compared to control cultures from which cofactors for metabolic activation were omitted. Embryos exposed to activated CP for 5 hours and then recultured in drug-free medium for 19-21 hours were indistinguishable from embryos exposed to activated CP continuously over a 24-26-hour period. These embryos are characterized by retarded growth as well as abnormalities of the prosencephalon, mandibular arches, limbs, and tail. Histological examination of embryos exposed to activated CP for 5 hours and immediately fixed revealed a decrease in the mitotic index and an increase in the necrotic index of the neuroepithelium and the surrounding mesenchyme of the prosencephalon. Our findings indicate that a 5-hour exposure to activated CP during day 10 of rat gestation is sufficient to produce the molecular lesions necessary to elicit the teratogenic effects of cyclophosphamide.

Abnormalities, Drug-Induced↗

PubMed1988

A SEM study on the development of the ventricular surface morphology in the diencephalon of the rat.

The morphogenesis of the ventricular surface of the diencephalon of the rat was studied using scanning electron microscopy, cryostat serial sections and direct observations under a dissection microscope. Based on these observations a description is given of the neuromeres present within the prosencephalon and of the termination of the sulcus limitans. Two conclusions are reached. First, three neuromeres are present in the prosencephalon. Neuromere I consists of the telencephalon, the hypothalamic regions and the parencephalon anterius. Neuromere II is the parencephalon posterius, neuromere III the synencephalon. Second, the sulcus limitans terminates ventrally in the parencephalon posterius and does not continue towards the preoptic recess. No exact termination point of the sulcus limitans could be delineated.

Animals↗

PubMed1990

Aprosencephaly: review of the literature and report of a case with cerebellar hypoplasia, pigmented epithelial cyst and Rathke's cleft cyst.

Aprosencephaly is a very rare brain malformation that occurs in isolated and sydromatic forms. The syndromatic form has been named "XK-aprosencephaly", and is characterized by near total absence of prosencephalon with a midline oculofacial defect similar to the most severe forms of holoprosencephaly, in association with limb and genital anomalies. We present a case of syndromatic aprosencephaly with absence of thumb and abnormal external genitalia. A previously undescribed finding was a Rathke's cleft cyst. Two other cystic structure were also identified--an ependymal cyst, which may represent a dorsal cyst as in holoprosencephaly, and a pigmented epithelial cyst, which may represent a rudimentary eye. Additional findings were extensive calcific vasculopathy in the rudimentary prosencephalon, absence of pituitary gland, forking of the aqueduct of Sylvius and marked cerebellar hypoplasia. Since calcific vasculopathy is a common accompaniment of other inflammatory diseases of the central nervous system, its presence in this case suggests that destructive processes may be involved in the genesis of some cases of aprosencephaly.

Abnormalities, Multiple↗

PubMed1987

Effect of glutathione depletion by buthionine sulfoximine on rat embryonic development in vitro.

The intracellular thiol glutathione has many functions within cells including protection against xenobiotic and oxidative damage, and a role in protein and DNA synthesis and amino acid transport. Consequently, glutathione might be an important substance for normal growth and development. In this study the extent of glutathione depletion by buthionine sulfoximine, an agent which depletes glutathione by inhibiting its synthesis, and the subsequent effects of the depletion on rat embryonic growth and development were assessed. Day 10.5 rat embryos were cultured in rat serum medium in the presence of L-buthionine-S,R-sulfoximine (0.01 to 2.0 mM) and examined for viability, malformations, growth and development 45 hr later. The glutathione concentrations of the cultured embryos and their yolk sacs were also determined. Exposure to buthionine sulfoximine produced marked and significant (P less than or equal to 0.05) depletion of glutathione at a buthionine sulfoximine concentration of 0.10 mM in the embryos and 0.05 mM in the yolk sacs. Exposure to 1 mM buthionine sulfoximine depleted glutathione to less than 7% of control in both of these tissues. None of the concentrations of buthionine sulfoximine tested had a significant effect on embryo viability; however, buthionine sulfoximine caused a significant (P less than or equal to 0.05) incidence of malformed embryos at concentrations of 0.25, 0.5, 1.0 and 2.0 mM. The types of defects induced by buthionine sulfoximine were blebs of the maxillary or nasal processes, prosencephalon or forelimb buds, small or misshapen heads, small prosencephalons and swollen hind brains, and tail defects. Embryonic growth was the most sensitive, of the variables assessed, to the effects of buthionine sulfoximine. Significant (P less than or equal to 0.05) growth retardation was observed at buthionine sulfoximine concentrations as low as 0.01 mM. At 2.0 mM buthionine sulfoximine, the yolk sac diameter, embryo crown-rump length, head length, number of somites and morphological score were reduced to 65, 72, 77, 90 and 80% of control levels respectively. We propose that the embryotoxic effects of buthionine sulfoximine are due to glutathione depletion and, consequently, that a certain basal level of endogenous glutathione is essential to allow for normal development.

Abnormalities, Drug-Induced↗