Further behavioral analysis of GABA-mediated inhibition in the early chick embryo

Maderdrut, Jerome L.; Reitzel, J.; Oppenheim, Ronald W.

doi:10.1016/0165-3806(86)90165-3

Cited by 8 publications

(5 citation statements)

References 24 publications

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“…In most vertebrates studied to date, synaptic inhibition has been implicated in the phasing of flexor and extensor discharge during motor activity (for review, see Grillner and Wallen, 1985). The results of the present work suggest that synaptic inhibition also influences the phasing of activity in chick motoneurons, confirming pharmacological experiments implicating inhibition in the regulation of embryonic chick motility (Oppenheim and Reitzel, 1975;Sedlacek, 1976Sedlacek, , 1982Maderdrut et al, 1986).…”

Section: Role Of Synaptic Inhibition In the Phasing Ofjlexor And Extesupporting

confidence: 76%

Motor activity in the isolated spinal cord of the chick embryo: synaptic drive and firing pattern of single motoneurons

O’Donovan

1989

J. Neurosci.

101

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The cellular mechanisms underlying embryonic motility were investigated using intracellular recording from motoneurons and electrotonic recording from muscle nerves during motor activity generated by an isolated spinal cord preparation of 12- to 15-d-old chick embryos. DC-coupled recordings from sartorius (a flexor) and femorotibialis (an extensor) muscle nerves revealed that both sets of motoneurons were depolarized at the same time in each cycle even when the motoneurons fired out of phase. Sartorius motoneurons fired briefly on the rising phase of the depolarization and then stopped firing before discharging a second burst of spikes as the depolarization decayed. By contrast, femorotibialis motoneurons fired at the peak of their depolarization, which was coincident with the interruption in sartorius activity. Intracellular recordings from antidromically identified motoneurons confirmed that flexor and extensor motoneurons were depolarized at the same time during each cycle of activity. The discharge of femorotibialis motoneurons, and others presumed to be extensors, followed changes in membrane potential so that maximal firing occurred during peak depolarization. The relationship between discharge and membrane potential was different in sartorius motoneurons (and in others presumed to be flexors) because they fired briefly on the rising phase of the depolarization and then stopped firing during peak depolarization. In some of these cells firing resumed as the membrane potential decayed back to rest. Intracellular injection of depolarizing current into sartorius motoneurons during motor activity reversed the direction of the membrane potential change from depolarizing to hyperpolarizing during the pause in sartorius discharge. In addition, the discharge evoked by the depolarizing current was blocked during the reversed part of the synaptic potential revealing its inhibitory nature. The occurrence of the IPSP was accompanied by a large reduction in motoneuronal input impedance. Injection of depolarizing current steps into motoneurons produced steady firing with no evidence of a pause in discharge, indicating that the depolarization accompanying synaptic activity was not responsible for the pause in firing of flexor motoneurons. These results suggest that flexor and extensor motoneurons receive a similar depolarizing drive from a common set of excitatory premotor interneurons. The alternating pattern of flexor and extensor discharge is produced, in part, by the timing of a depolarizing IPSP coincident with extensor activity that silences flexor discharge.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Role Of Synaptic Inhibition In the Phasing Ofjlexor And Extesupporting

confidence: 76%

Motor activity in the isolated spinal cord of the chick embryo: synaptic drive and firing pattern of single motoneurons

O’Donovan

1989

J. Neurosci.

101

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“…Early development of GABA-containing neurons has been found throughout the nervous system (Lauder et al, 1986), and transient expression of GABA in the spinal cord has been particularly well studied (Obata et al, 1978;Reitzel et al, 1979;Maderdrut et al, 1986;Ma et al, 1992;Mitchell and Redburn, 1996). For example, in the chick spinal cord, there is a decrease in GABA-positive neurons and a complementary increase in glycine-positive neurons during embryonic development (Berki et al, 1995), and it was suggested that neurons may change transmitter phenotype.…”

Section: Development Of Glycinergic Transmission In the Medial Limbmentioning

confidence: 99%

A Developmental Shift from GABAergic to Glycinergic Transmission in the Central Auditory System

Kotak¹,

et al. 1998

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GABAergic and glycinergic circuits are found throughout the auditory brainstem, and it is generally assumed that transmitter phenotype is established early in development. The present study documents a profound transition from GABAergic to glycinergic transmission in the gerbil lateral superior olive (LSO) during the first 2 postnatal weeks. Whole-cell voltage-clamp recordings were obtained from LSO neurons in a brain slice preparation, and IPSCs were evoked by electrical stimulation of the medial nucleus of the trapezoid body (MNTB), a known glycinergic projection in adult animals. GABAergic and glycinergic components were identified by blocking transmission with bicuculline and strychnine (SN), respectively. In the medial limb of LSO, there was a dramatic change in the GABAergic IPSC component, decreasing from 78% at postnatal day 3 (P3)-P5 to 12% at P12-P16. There was an equal and opposite increase in the glycinergic component during this same period. Direct application of GABA also elicited significantly larger amplitude and longer duration responses in P3-P5 neurons compared with glycine-evoked responses. In contrast, MNTB-evoked IPSCs in lateral limb neurons were more sensitive to SN throughout development. Consistent with the electrophysiological observations, there was a reduction in staining for the beta2,3-GABAA receptor subunit from P4 to P14, whereas staining for the glycine receptor-associated protein gephyrin increased. Brief exposure to baclofen depressed transmission at excitatory and inhibitory synapses for approximately 15 min, suggesting a GABAB-mediated metabotropic signal. Collectively, these data demonstrate a striking switch from GABAergic to glycinergic transmission during postnatal development. Although GABA and glycine elicit similar postsynaptic ionotropic responses, our results raise the possibility that GABAergic transmission in neonates may play a developmental role distinct from that of glycine.

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“…It is now well established in various animals that neural circuits underlying spontaneous rhythmic motor activity are localized within the spinal cord. The alternating pattern of flexor and extensor discharge is produced by a delicate spatiotemporal activation of spinal motoneurons that is controlled by a rhythm-generating neural network comprising both excitatory and inhibitory spinal interneurons (Reitzel et al, 1979;Grillner et al, 1986;Maderdrut et al, 1986;Roberts et al, 1986;O'Donovan, 1989;Ho and O'Donovan, 1993). In addition, a recent ablation experiment performed by Ho and O'Donovan (1993) shows that the critical neural components for motoneuron alternation in the chick embryo are located immediately dorsomedial to the LMC.…”

Section: Gabaergic Neurons In Neural Circuits Underlying Spontaneous mentioning

confidence: 99%

“…The inhibitory neurotransmitter y-aminobutyric acid (GABA) is considered to play important roles in early processes of neural development. GABA is one of the earliest neurotransmitters detected in the developing central nervous system of various animals (Obata et al, 1978;Reitzel et al, 1979;Lauder et al, 1986;Maderdrut et al, 1986;Roberts et al, 1987;Chun and Shatz, 1989;Van Eden et al, 1989;Blanton and Kriegstein, 1991;Del Rio et al, 1992;Ma et al, 1992a,b;Meinecke and Rakic, 1992;Wu et al, 1992). Studies on rat superior cervical ganglia and cerebral cortex have demonstrated that, in addition to its well established neurotransmitter function, GABA also promotes neural development as a trophic and synaptoge-netic factor (Wolff et al, 1978(Wolff et al, , 1979Wolff, 1981).…”

mentioning

confidence: 99%

“…Because of its amenability to embryonic microsurgery and electrophysiological and neuropharmacological experiments, the chick embryo is a particularly useful subject for studies concerning embryogenesis. Many of the aforementioned experiments attesting to the fundamental role of GABA in early neurogenesis, especially those that focused on embryonic motility, have also been performed on chick embryos (Renaud et al, 1978;Pittman and Oppenheim, 1979;Reitzel et al, 1979;Toutant et al, 1979;Reitzel and Oppenheim, 1980;McLennan, 1983;Maderdrut et al, 1986;O'Donovan and Landmesser, 1987;O'Donovan, 1987O'Donovan, , 1989O'Donovan et al, 1992;Ho and O'Donovan, 1993). Despite many physiological, pharmacological, and behavioral experiments concerning GABA-mediated events in neural development, the neurochemical localization of GABA in the central nervous system of chick embryos has received little attention.…”

mentioning

confidence: 99%

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

Antal

Berki

Horváth

et al. 1994

J of Comparative Neurology

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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)

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Further behavioral analysis of GABA-mediated inhibition in the early chick embryo

Cited by 8 publications

References 24 publications

Motor activity in the isolated spinal cord of the chick embryo: synaptic drive and firing pattern of single motoneurons

Motor activity in the isolated spinal cord of the chick embryo: synaptic drive and firing pattern of single motoneurons

A Developmental Shift from GABAergic to Glycinergic Transmission in the Central Auditory System

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

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