1983
DOI: 10.1016/0006-8993(83)90372-4
|View full text |Cite
|
Sign up to set email alerts
|

Time of neuron origin in the amygdaloid complex of the mouse

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

3
24
0
6

Year Published

1991
1991
2020
2020

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 42 publications
(33 citation statements)
references
References 14 publications
3
24
0
6
Order By: Relevance
“…However, it is difficult to determine whether a portion of the lateral pallium is also affected in these mutants because of a lack of specific markers for this pallial region. These amygdalar nuclei are largely generated between E11 and E14 in the mouse (McConnell and Angevine, 1983), which correlates well with the timing of the observed patterning defects in Tlx mutants. Moreover, our fate-mapping studies, using the subpallial Dlx5/6 expression domain, demonstrate a largely pallial origin for the basolateral and lateral amygdala because only a few cells are labeled in these nuclei.…”
Section: Tlx Is Required For Patterning Of the Lateral Telencephalonsupporting
confidence: 72%
“…However, it is difficult to determine whether a portion of the lateral pallium is also affected in these mutants because of a lack of specific markers for this pallial region. These amygdalar nuclei are largely generated between E11 and E14 in the mouse (McConnell and Angevine, 1983), which correlates well with the timing of the observed patterning defects in Tlx mutants. Moreover, our fate-mapping studies, using the subpallial Dlx5/6 expression domain, demonstrate a largely pallial origin for the basolateral and lateral amygdala because only a few cells are labeled in these nuclei.…”
Section: Tlx Is Required For Patterning Of the Lateral Telencephalonsupporting
confidence: 72%
“…Interestingly, although proper CSB border positioning is reestablished by midneurogenesis in Gsh2 Ϫ/Ϫ mutants (Corbin et al, 2000;Toresson et al, 2000;Toresson and Campbell, 2001;Yun et al, 2001), the loss of Dlx2 ϩ cells along the LCS, unlike the olfactory bulb interneuron defect in these mice, does not partially recover. This may reflect that fact that cells of the basal telencephalic limbic system appear to be specified during a fixed window of development (McConnell and Angevine, 1983;Bayer and Altman, 1991; present study), whereas olfactory bulb neurogenesis continues through adulthood (for review, see Alvarez-Buylla and GarciaVerdugo, 2002).…”
Section: Gsh2 Is Required For the Generation Of The Lateral Cortical mentioning
confidence: 71%
“…In the beginning, we applied DiI to the caudal ganglionic eminence of E11.5, since the initial neurogenesis of amygdalar neurons was reported at this stage (McConnell and Angevine 1983). Only small numbers of growth cones were observed to extend medially from the injection site ( Fig.…”
Section: Development Of Amygdalohypothalamic Projections As Revealed mentioning
confidence: 98%
“…The mammalian ST is considered to be involved in transfer of the emotion-related information integrated in the amygdaloid complex to the hypothalamus, interacting with each part of the BNST along the trajectory (Alheid et al 1998;Shammah-Lagnado et al 2000). Thus, ST is involved in the output of the evaluation of external sensory stimuli to the autonomic and endocrine center, the hypothalamus, and in the control of adaptive responses as revealed by anatomical, physiological and behavioral findings (Heimer et al 1991) Though the functional aspects of the amygdaloid complex have been extensively investigated, only a few studies have focused on the developmental mechanisms of the amygdala and related structures, namely birth date studies of the amygdaloid neurons (Bayer 1980;McConnell and Angevine 1983;Bayer 1987), the immunohistochemical examination of developing amygdala and BNST in the rodent and chick (Song and Harlan 1994;Al-Shamma and De Vries 1996;Han and De Vries 1999;Jurkevich et al 1999), and morphological analysis of the human fetal amygdala (Johnston 1923;Ulfig et al 1998;Ulfig 2002). Few studies carried out to date have examined the axonal development of embryonic amygdalofugal pathways.…”
Section: Introductionmentioning
confidence: 99%