Postnatal development of glycinergic neurons in the rabbit retina.

Postnatal development of glycinergic neurons in the rabbit retina.
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兔视网膜中甘氨酸能神经元的出生后发育。

DOI:
10.1002/cne.901930420
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发表时间:
1980
期刊:
The Journal of comparative neurology
影响因子:
--
通讯作者:
Lam,DM
Lam,DM
中科院分区:
--
文献类型:
--
作者:
Kong,YC;Fung,SC;Lam,DM

文献摘要

相似文献

成年兔视网膜中的某些神经元具有对甘氨酸的高亲和力摄取机制,并响应培养基中升高的K+浓度而释放甘氨酸。虽然证据还不完整,但这些特性以及药理学研究表明,甘氨酸蓄积神经元可能是无长突细胞的一个亚群,并可能使用甘氨酸作为神经递质。在本研究中,我们使用甘氨酸的摄取和K+刺激释放作为生理探针,以跟踪兔视网膜出生后发育过程中推定的甘氨酸能神经元的出现和成熟。我们表明,新生儿视网膜中的某些神经元已经具有特定的高亲和力甘氨酸吸收机制。这些细胞在发育中的视网膜中的位置和密度表明它们将成为成年视网膜的甘氨酸积累神经元。因此,类似于我们早期对视网膜中GABA能神经元发育的研究,某些视网膜神经元对甘氨酸能的承诺,如果这些细胞确实使用甘氨酸作为递质,则是在产前进行的。然而,这些假定的甘氨酸能神经元可能在出生时是不成熟的,因为它们不释放积累的甘氨酸以响应培养基中的高K+浓度。事实上,直到出生后约7天,几乎没有K+刺激的预载甘氨酸从视网膜释放,之后释放急剧增加,在第10天达到成人水平的约65%,在第12天达到80%。假设这种释放起源于突触,我们的发现表明,推定的甘氨酸能神经元可能在出生后10-12天功能成熟。此外,我们的研究结果表明,在兔视网膜发育过程中,高亲和力甘氨酸摄取机制的出现和成熟远远早于K+刺激的甘氨酸释放机制。
Certain neurons in the adult rabbit retina posses a high‐affinity uptake mechanism for glycine and release it in response to elevated K+concentrations in the medium. Although the evidence is not yet complete, these properties, together with pharmacological studies, suggest that the glycine‐accumulating neurons may be a subpopulation of amacrine cells and may use glycine as a neurotransmitter. In the present study, we have used the uptake and K+‐stimulated release of glycine as physiological probes to follow the emergence and maturation of putative glycinergic neurons during postnatal development of the rabbit retina. We show that certain neurons in the newborn retina already possess a specific high‐affinity mechanism for glycine uptake. The positions and density of these cells in the developing retina suggest that they will become glycineaccumulating neurons of the adult retina. Thus, similar to our earlier study on the development of GABA‐ergic neurons in this retina, the commitment by certain retinal neurons to be glycinergic, if indeed these cells use glycine as the transmitter, is made prenatally. These putative glycinergic neurons are, however, probably immature at birth, because they do not release the accumulated glycine in response to high K+concentrations in the medium. In fact, there is practically no K+‐ stimulated release of preloaded glycine from the retina until about 7 days after birth, after which the release increases drastically to about 65% of the adult level on day 10 and 80% on day 12. Assuming that this release originates synaptically, our finding suggests that the putative glycinergic neurons may be functionally mature by 10–12 days after birth. Additionally, our results show that during development of the rabbit retina, the mechanism for high‐affinity glycine uptake emerges and matures much earlier than the mechanism for K+‐stimulated glycine release.