Dopamine-mediated calcium channel regulation in synaptic suppression in L. stagnalis interneurons

D2 dopamine receptor-mediated suppression of synaptic transmission from interneurons plays a key role in neurobiological functions across species, ranging from respiration to memory formation. In this study, we investigated the mechanisms of D2 receptor-dependent suppression using soma-soma synapse between respiratory interneuron VD4 and LPeD1 in the mollusk Lymnaea stagnalis (L. stagnalis). We studied the effects of dopamine on voltage-dependent Ca²⁺ current and synaptic vesicle release from the VD4. We report that dopamine inhibits voltage-dependent Ca²⁺ current in the VD4 by both voltage-dependent and -independent mechanisms. Dopamine also suppresses synaptic vesicle release downstream of activity-dependent Ca²⁺ influx. Our study demonstrated that dopamine acts through D2 receptors to inhibit interneuron synaptic transmission through both voltage-dependent Ca²⁺ channel-dependent and -independent pathways. Taken together, these findings expand our understanding of dopamine function and fundamental mechanisms that shape the dynamics of neural circuit.     

A novel conserved evx1 enhancer links spinal interneuron morphology and cis-regulation from fish to mammals

Cerebellar GABAergic interneurons and glia originate from progenitors that delaminate from the ventricular neuroepithelium and proliferate in the prospective white matter. Even though this population of progenitor cells is multipotent as a whole, clonal analysis indicates that different lineages are already separated during postnatal development and little is known about the mechanisms that regulate the specification and differentiation of these cerebellar types at earlier stages. Here, we investigate the role of Ascl1 in the development of inhibitory interneurons and glial cells in the cerebellum. This gene is expressed by maturing oligodendrocytes and GABAergic interneurons and is required for the production of appropriate quantities of these cells, which are severely reduced in Ascl1^−/− mouse cerebella. Nevertheless, the two lineages are not related and the majority of oligodendrocytes populating the developing cerebellum actually derive from extracerebellar sources. Targeted electroporation of Ascl1-expression vectors to ventricular neuroepithelium progenitors enhances the production of interneurons and completely suppresses astrocytic differentiation, whereas loss of Ascl1 function has opposite effects on both cell types. Our results indicate that Ascl1 directs ventricular neuroepithelium progenitors towards inhibitory interneuron fate and restricts their ability to differentiate along the astroglial lineage.     

Regulation of the phonotactic threshold of the female cricket, Acheta domesticus : juvenile hormone III, allatectomy, L1 auditory neuron thresholds and environmental factors

Juvenile hormone III (JHIII), when applied to the abdomen of 1-day-old female Acheta domesticus (in quantities that would create JHIII titers in the hemolymph that were within the range measured in females of this species) caused a significant decrease in phonotactic thresholds (Fig. 1). Removal of the corpora allata from 5-day-old females with low phonotactic thresholds caused significantly increased phonotactic thresholds 2–5 days later. After a temporary increase (24 h) of, on average, about 25 dB, the phonotactic thresholds drop to about 10 dB above preallatectomy levels (Fig. 2), but remain significantly higher than controls. Application of JHIII to allatectomized females, with a mean increase in thresholds of 20 dB, results in significantly decreased thresholds (mean of about 20 dB) over the next 6 h (Fig. 3). Exposure to males 1 week before the imaginal molt causes the phonotactic thresholds of postimaginal females to drop 1–2 days significantly earlier than controls (Fig. 4). One- and 3-day-old females, phonotactically tested only once, exhibit lower thresholds in the early morning than they do in the late afternoon (Fig. 5). Five-day-old females do not exhibit such a diurnal rhythm. Phonotactically testing females more than once a day significantly influences their phonotactic thresholds (Figs. 6, 7). In 1-day-old females, with high (above 70 dB) phonotactic thresholds, the threshold of their L1 auditory interneurons can be 30 dB or more below their phonotactic threshold (Fig. 8). In females with phonotactic thresholds of 70 dB or lower, the L1 threshold is within 10 dB of their phonotactic threshold. Both JHIII and allatectomy influence phonotactic and L1 thresholds in a similar manner. Accepted: 29 September 1997     

Regeneration and asexual reproduction share common molecular changes: upregulation of a neural glycoepitope during morphallaxis in Lumbriculus

Neural morphallaxis is a regenerative process characterized by wide-spread anatomical and physiological changes in an adult nervous system. During segmental regeneration of the annelid worm, Lumbriculus variegatus, neural morphallaxis involved a reorganization of sensory, interneuronal, and motor systems as posterior fragments gained a more anterior body position. A monoclonal antibody, Lan 3-2, which labels a neural glyco-domain in the leech, was reactive in Lumbriculus. In the worm, this antibody labeled neural structures, particularly axonal tracts and giant fiber pathways of the central nervous system. A 60kDa protein, possessing a lumbriculid mannose-rich glycoepitope, was upregulated during neural morphallaxis, peaking in its expression at 3 weeks post-amputation. Peak upregulation of the Lan 3-2 epitope, or the protein possessing it, corresponded to the time of major neurobehavioral plasticity during regeneration. Analyses of asexually reproducing animals also revealed induction of the Lan 3-2 epitope. In this developmental context, Lan 3-2 epitope upregulation was also confined to segments expressing both changes in positional identity and neurobehavioral plasticity, but these molecular and behavioral changes occurred prior to body fragmentation. These results suggest that the lumbriculid Lan 3-2 glycoepitope and proteins that bear them have been co-opted for neural morphallactic programs, induced both in anticipation of reproductive fragmentation and in compensation for injury-induced fragmentation.     

Genetically identified neurons in avian auditory pallium mirror core principles of their mammalian counterparts

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A Population of Interneurons Signals Changes in the Basal Concentration of Serotonin and Mediates Gain Control in the Drosophila Antennal Lobe

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Probing diversity within subpopulations of locomotor‐related V0 interneurons

The V0 interneuronal population is derived from Dbx1 expressing progenitors. Initial studies on these interneurons in the mouse spinal cord demonstrated that they project commissural axons and are involved in coordinating left‐right alternation during locomotion. Subsequent work has indicated that the V0 population can be divided into genetically distinct ventral (V0_V) and dorsal (V0_D) subpopulations, and experimental evidence suggests that each is responsible for left‐right alternation at different locomotor speeds. In this study, we perform a series of experiments to probe the location and connectivity of these subpopulations in neonatal mice and demonstrate that they are more diverse than previously predicted. While the distribution of either subpopulation remains consistent along the extent of the lumbar spinal cord, a cluster of V0_D cells lateral to the central canal receive substantial input from primary afferents. Retrograde tracing and activity dependent labeling experiments demonstrate that a group of V0 interneurons located in this same region preferentially project axons towards contralateral motoneurons via an oligosynaptic pathway, and are active during fictive locomotion. Our results suggest that this subset of V0 interneurons may be primarily responsible for coordination of left‐right alternation during locomotion. Furthermore these experiments indicate that while genetic identity is one determinant of the function of a neuron during locomotion, the specific position in which the cell is located may also play a key role. © 2015 Wiley Periodicals, Inc. Develop Neurobiol 75: 1189–1203, 2015     

The ascl1a and dlx genes have a regulatory role in the development of GABAergic interneurons in the zebrafish diencephalon

During development of the mouse forebrain interneurons, the Dlx genes play a key role in a gene regulatory network (GRN) that leads to the GABAergic phenotype. Here, we have examined the regulatory relationships between the ascl1a, dlx, and gad1b genes in the zebrafish forebrain. Expression of ascl1a overlaps with dlx1a in the telencephalon and diencephalon during early forebrain development. The loss of Ascl1a function results in a loss of dlx expression, and subsequent losses of dlx5a and gad1b expression in the diencephalic prethalamus and hypothalamus. Loss of Dlx1a and Dlx2a function, and, to a lesser extent, of Dlx5a and Dlx6a, impairs gad1b expression in the prethalamus and hypothalamus. We conclude that dlx1a/2a act downstream of ascl1a but upstream of dlx5a/dlx6a and gad1b to activate GABAergic specification. This pathway is conserved in the diencephalon, but has diverged between mammals and teleosts in the telencephalon.