Development changes in the distribution of gamma‐aminobutyric acid‐immunoreactive neurons in the embryonic chick lumbosacral spinal cord

Abstract

The development of gamma-aminobutyric acid (GABA)-immunoreactive neurons was investigated in the embryonic and posthatch chick lumbosacral spinal cord by using pre- and postembedding immunostaining with an anti-GABA antiserum. The first GABA-immunoreactive cells were detected in the ventral one-half of the spinal cord dorsal to the lateral motor column at E4. GABAergic neurons in this location sharply increased in number and, with the exception of the lateral motor column, appeared throughout the entire extent of the ventral one-half of the spinal gray matter by E6. Thereafter, GABA-immunoreactive neurons extended from ventral to dorsal regions. Stained perikarya first appeared at E8 and then progressively accumulated in the dorsal horn, while immunoreactive neurons gradually declined in the ventral horn. The general pattern of GABA immunoreactivity characteristic of mature animals had been achieved by E12 and was only slightly altered afterwards. In the dorsal horn, most of the stained neurons were observed in laminae I-III, both at the upper (LS 1-3) and at the lower (LS 5-7) segments of the lumbosacral spinal cord. In the ventral horn, the upper and lower lumbosacral segments showed marked differences in the distribution of stained perikarya. GABAergic neurons were scattered in a relatively large region dorsomedial to the lateral motor column at the level of the upper lumbosacral segments, whereas they were confined to the dorsalmost region of lamina VII at the lower segments. The early expression of GABA immunoreactivity may indicate a trophic and synaptogenetic role for GABA in early phases of spinal cord development.(ABSTRACT TRUNCATED AT 250 WORDS)

Embryonically Expressed GABA and Glutamate Drive Electrical Activity Regulating Neurotransmitter Specification

“…The widespread embryonic expression of GABA and glutamate suggested that these neurotransmitters could have significant functions (Lauder et al, 1986;Ma et al, 1992;Antal et al, 1994;Berki et al, 1995). Our findings demonstrate that GABA and glutamate signaling drive the generation of calcium spikes that in turn specify transmitter expression.…”

“…Neurotransmitters are expressed at early stages of development, long before synapse formation (Lauder et al, 1986;Ma et al, 1992;Antal et al, 1994;Berki et al, 1995), and their release can stimulate elevations of intracellular calcium (Blanton et al, 1990;Flint et al, 1999). They regulate proliferation in rat embryonic neocortical progenitor cells and subventricular zone neuroblasts, and zebrafish spinal interneurons (LoTurco et al, 1995;Liu et al, 2005;McDearmid et al, 2006).…”

ERG Conductance Expression Modulates the Excitability of Ventral Horn GABAergic Interneurons That Control Rhythmic Oscillations in the Developing Mouse Spinal Cord

“…Despite the absence of afferent and supraspinal inputs, which are important for the development of spinal circuits (Harris-Warrick and Marder, 1991;Nusbaum et al, 2001;Branchereau et al, 2002), this preparation represents a useful model for studying the dynamics of intrasegmental maturation processes that evidently rely on propriospinal neurons and circuits (Avossa et al, 2003;Rosato-Siri et al, 2004;Furlan et al, 2005;Fabbro et al, 2006). In particular, the ontogeny and functional development of GABAergic interneurons observed in vivo (Antal et al, 1994;Barbeau et al, 1999;Gao et al, 2001;Tran et al, 2003) is maintained in cultured spinal slices (Avossa et al, 2003;Furlan et al, 2005), validating the crucial importance of GABAergic connections for circuit assembly and activity (Barbeau et al, 1999). In the cultured spinal cord, ventral interneurons strongly, yet transiently, express a typical I K(ERG) (Furlan et al, 2005) that controls membrane excitability (Chiesa et al, 1997;Sacco et al, 2003) in coincidence with the appearance of developmentally regulated GABAergic markers (Avossa et al, 2003;Furlan et al, 2005).…”

“…In the immature spinal cord, as well as in other CNS areas, the ontogeny of inhibitory transmission is intriguing because of the temporal delay before the appearance of GABAergic and glycinergic inhibition (Antal et al, 1994;Barbeau et al, 1999;Gao et al, 2001;Tran et al, 2003;Nabekura et al, 2004;Allain et al, 2006). In the embryonic spinal cord, glycine progressively becomes the dominant force in driving more mature patterns of activity, such as coordinated locomotor-like bursts (Bonnot et al, 1998;Whelan et al, 2000).…”

Development of an Inhibitory Interneuronal Circuit in the Embryonic Spinal Cord

“…Early in development (E8) many of the interneuron cell bodies in the ventral part of the cord are immunopositive for GABA but by E15-16 very few are and instead are immunopositive for glycine (Antal et al 1994). Although the Antal study does not directly assess the neurotransmitter of these cells, it has led to the suggestion that there may be a conversion from a GABAergic to a glycinergic neuron.…”