Wang, Quanxin; Henry, Alex M.; Harris, Julie A.; Oh, Seung Wook; Joines, Kevin M.; Nyhus, Julie; Hirokawa, Karla E.; Dee, Nick; Mortrud, Marty; Parry, Sheana; Ouellette, Benjamin; Caldejon, Shiella; Bernard, Amy; Jones, Allan R.; Zeng, Hongkui; Hohmann, John G.
doi: 10.1002/cne.23587pmid: N/A
As an anterograde neuronal tracer, recombinant adeno‐associated virus (AAV) has distinct advantages over the widely used biotinylated dextran amine (BDA). However, the sensitivity and selectivity of AAV remain uncharacterized for many brain regions and species. To validate this tracing method further, AAV (serotype 1) was systematically compared with BDA as an anterograde tracer by injecting both tracers into three cortical and 15 subcortical regions in C57BL/6J mice. Identical parameters were used for our sequential iontophoretic injections, producing injections of AAV that were more robust in size and in density of neurons infected compared with those of BDA. However, these differences did not preclude further comparison between the tracers, because the pairs of injections were suitably colocalized and contained some percentage of double‐labeled neurons. A qualitative analysis of projection patterns showed that the two tracers behave very similarly when injection sites are well matched. Additionally, a quantitative analysis of relative projection intensity for cases targeting primary motor cortex (MOp), primary somatosensory cortex (SSp), and caudoputamen (CP) showed strong agreement in the ranked order of projection intensities between the two tracers. A detailed analysis of the projections of two brain regions (SSp and MOp) revealed many targets that have not previously been described in the mouse or rat. Minor retrograde labeling of neurons was observed in all cases examined, for both AAV and BDA. Our results show that AAV has actions equivalent to those of BDA as an anterograde tracer and is suitable for analysis of neural circuitry throughout the mouse brain. J. Comp. Neurol. 522:1989–2012, 2014. © 2014 Wiley Periodicals, Inc.
Wang, Quanxin; Henry, Alex M.; Harris, Julie A.; Oh, Seung Wook; Joines, Kevin M.; Nyhus, Julie; Hirokawa, Karla E.; Dee, Nick; Mortrud, Marty; Parry, Sheana; Ouellette, Benjamin; Caldejon, Shiella; Bernard, Amy; Jones, Allan R.; Zeng, Hongkui;
Filippi, Alida; Mueller, Thomas; Driever, Wolfgang
doi: 10.1002/cne.23524pmid: 24374659
Throughout the vertebrate lineage, dopaminergic neurons form important neuromodulatory systems that influence motor behavior, mood, cognition, and physiology. Studies in mammals have established that dopaminergic neurons often use γ‐aminobutyric acid (GABA) or glutamatergic cotransmission during development and physiological function. Here, we analyze vglut2, gad1b and gad2 expression in combination with tyrosine hydroxylase immunoreactivity in 4‐day‐old larval and 30‐day‐old juvenile zebrafish brains to determine which dopaminergic and noradrenergic groups may use GABA or glutamate as a second transmitter. Our results show that most dopaminergic neurons also express GABAergic markers, including the dopaminergic groups of the olfactory bulb (homologous to mammalian A16) and the subpallium, the hypothalamic groups (A12, A14), the prethalamic zona incerta group (A13), the preoptic groups (A15), and the pretectal group. Thus, the majority of catecholaminergic neurons are gad1b/2‐positive and coexpress GABA. A very few gad1/2‐negative dopaminergic groups, however, express vglut2 instead and use glutamate as a second transmitter. These glutamatergic dual transmitter phenotypes are the Orthopedia transcription factor–dependent, A11‐type dopaminergic neurons of the posterior tuberculum. All together, our results demonstrate that all catecholaminergic groups in zebrafish are either GABAergic or glutamatergic. Thus, cotransmission of dopamine and noradrenaline with either GABA or glutamate appears to be a regular feature of zebrafish catecholaminergic systems. We compare our results with those that have been described for mammalian systems, discuss the phenomenon of transmitter dualism in the context of developmental specification of GABAergic and glutamatergic regions in the brain, and put this phenomenon in an evolutionary perspective. J. Comp. Neurol. 522:2019–2037, 2014. © 2013 Wiley Periodicals, Inc.
Šimo, Ladislav; Koči, Juraj; Kim, Donghun; Park, Yoonseong
doi: 10.1002/cne.23515pmid: 24307522
The control of tick salivary secretion, which plays a crucial role in compromising the host immune system, involves complex neural mechanisms. Dopamine is known to be the most potent activator of salivary secretion, as a paracrine/autocrine factor. We describe the invertebrate‐specific D1‐like dopamine receptor (InvD1L), which is highly expressed in tick salivary glands. The InvD1L phylogenic clade was found only in invertebrates, suggesting that this receptor was lost in vertebrates during evolution. InvD1L expressed in Chinese hamster ovary (CHO)‐K1 cells was activated by dopamine with a median effective dose (EC50) of 1.34 μM. Immunohistochemistry using the antibody raised against InvD1L revealed two different types of immunoreactivities: basally located axon terminals that are colocalized with myoinhibitory peptide (MIP) and SIFamide neuropeptides, and longer axon‐like processes that are positive only for the InvD1L antibody and extended to the apical parts of the acini. Both structures were closely associated with the myoepithelial cell, as visualized by beta‐tubulin antibody, lining the acinar lumen in a web‐like fashion. Subcellular localizations of InvD1L in the salivary gland suggest that InvD1L modulates the neuronal activities including MIP/SIFamide varicosities, and leads the contraction of myoepithelial cells and/or of the acinar valve to control the efflux of the luminal content. Combining the previously described D1 receptor with its putative function for activating an influx of fluid through the epithelial cells of acini, we propose that complex control of the tick salivary glands is mediated through two different dopamine receptors, D1 and InvD1L, for different downstream responses of the acinar cells. J. Comp. Neurol. 522:2038–2052, 2014. © 2013 Wiley Periodicals, Inc.
Holstein, Gay R.; Friedrich, Victor L.; Martinelli, Giorgio P.
doi: 10.1002/cne.23517pmid: 24323841
Changes in head position and posture are detected by the vestibular system and are normally followed by rapid modifications in blood pressure. These compensatory adjustments, which allow humans to stand up without fainting, are mediated by integration of vestibular system pathways with blood pressure control centers in the ventrolateral medulla. Orthostatic hypotension can reflect altered activity of this neural circuitry. Vestibular sensory input to the vestibulo‐sympathetic pathway terminates on cells in the vestibular nuclear complex, which in turn project to brainstem sites involved in the regulation of cardiovascular activity, including the rostral and caudal ventrolateral medullary regions (RVLM and CVLM, respectively). In the present study, sinusoidal galvanic vestibular stimulation was used to activate this pathway, and activated neurons were identified through detection of c‐Fos protein. The retrograde tracer Fluoro‐Gold was injected into the RVLM or CVLM of these animals, and immunofluorescence studies of vestibular neurons were conducted to visualize c‐Fos protein and Fluoro‐Gold concomitantly. We observed activated projection neurons of the vestibulo‐sympathetic reflex pathway in the caudal half of the spinal, medial, and parvocellular medial vestibular nuclei. Approximately two‐thirds of the cells were ipsilateral to Fluoro‐Gold injection sites in both the RVLM and CVLM, and the remainder were contralateral. As a group, cells projecting to the RVLM were located slightly rostral to those with terminals in the CVLM. Individual activated projection neurons were multipolar, globular, or fusiform in shape. This study provides the first direct demonstration of the central vestibular neurons that mediate the vestibulo‐sympathetic reflex. J. Comp. Neurol. 522:2053–2074, 2014. © 2013 Wiley Periodicals, Inc.
Showing 1 to 10 of 19 Articles
doi: 10.1002/cne.23567pmid: 24639291
As an anterograde neuronal tracer, recombinant adeno‐associated virus (AAV) has distinct advantages over the widely used biotinylated dextran amine (BDA). However, the sensitivity and selectivity of AAV remain uncharacterized for many brain regions and species. To validate this tracing method further, AAV (serotype 1) was systematically compared with BDA as an anterograde tracer by injecting both tracers into three cortical and 15 subcortical regions in C57BL/6J mice. Identical parameters were used for our sequential iontophoretic injections, producing injections of AAV that were more robust in size and in density of neurons infected compared with those of BDA. However, these differences did not preclude further comparison between the tracers, because the pairs of injections were suitably colocalized and contained some percentage of double‐labeled neurons. A qualitative analysis of projection patterns showed that the two tracers behave very similarly when injection sites are well matched. Additionally, a quantitative analysis of relative projection intensity for cases targeting primary motor cortex (MOp), primary somatosensory cortex (SSp), and caudoputamen (CP) showed strong agreement in the ranked order of projection intensities between the two tracers. A detailed analysis of the projections of two brain regions (SSp and MOp) revealed many targets that have not previously been described in the mouse or rat. Minor retrograde labeling of neurons was observed in all cases examined, for both AAV and BDA. Our results show that AAV has actions equivalent to those of BDA as an anterograde tracer and is suitable for analysis of neural circuitry throughout the mouse brain. J. Comp. Neurol. 522:1989–2012, 2014. © 2014 Wiley Periodicals, Inc.