Evidence for Somatostatin‐Containing Fibers Projecting from the Pallidal Complex to the Striatum of the Rat

Widmann, Rudolf; Mensdorff-Pouilly, N.; Pfaller, Kristian; Sperk, Günther

doi:10.1111/j.1471-4159.1987.tb05748.x

Cited by 12 publications

(3 citation statements)

References 15 publications

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“…Since these neurotoxins are known to elicit neuronal destruction sparing axons and nerve terminals, it was suggested that NPY immunoreactivity in the striatum is entirely derived from the population of interneurons. In contrast, striatal somatostatin immunoreactivity is related partly to striatal projection fibres of which the origin is still under discussion (Beal and Martin, 1983;Salin et al, submitted;Widmann et al, 1987). Several lines of evidence indicate that the nigrostriatal dopaminergic pathway influences striatal NPY metabolism.…”

Section: Fig 5 Schematic Diagram Illustrating the Topographical Chamentioning

confidence: 89%

Cortical Regulation of Striatal Neuropeptide Y (NPY)‐Containing Neurons in the Rat

Kerkerian

Salin

Nieoullon

1990

Eur J of Neuroscience

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This study examined the functional relationships established by nigral, cortical, and thalamic striatal afferent pathways with neuropeptide Y (NPY)-containing neurons in the rat rostral striatum by coupling selective deafferentation procedures and NPY immunohistochemistry. Previous experiments have shown that after unilateral 6-hydroxydopamine (6-OHDA)-induced degeneration of nigrostriatal dopaminergic neurons, the mean number of NPY-immunoreactive (Ir) neurons per frontal section was increased in the striatum ipsilateral to the lesion side and unaltered in the contralateral striatum. The present topographical analysis of the 6-OHDA lesion effects led us to state that the increase in NPY-Ir neuron density occurs in restricted ventral and medial zones of the ipsilateral striatum. Unilateral ablation of the frontoparietal cerebral cortex by thermocoagulation was moreover shown to elicit, 20 - 30 days later, a significant bilateral increase in the number of striatal NPY-Ir cells. The increase was more marked in the striatum ipsilateral to the hemidecortication where it was similar in amplitude to that induced by the 6-OHDA lesion. The topographical analysis of the cortical lesion effects also revealed an uneven striatal response, but, in contrast to that observed for the 6-OHDA lesion, changes were restricted to dorsolateral areas of the striatum in both brain sides, revealing an apparent complementarity of nigral dopaminergic and cortical influences over striatal NPY neuronal system. Combined unilateral nigral and cortical lesions surprisingly counteracted in a survival time dependent manner the effects of each lesion considered separately. In that condition topographical changes related to the 6-OHDA lesion totally disappeared and those related to the cortical lesion were attenuated but still present. These results suggest that expression of striatal dopamine - NPY interaction is dependent on corticostriatal transmission. Interestingly lesion of thalamic areas projecting to the striatum did not significantly modify the mean number of NPY-Ir neurons determined per section from the whole striatal surface, but selectively increased the NPY neuron density in the mediodorsal region of the striatum, suggesting that the striatal NPY-containing neuronal system is also influenced by thalamostriatal projections.

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Section: Fig 5 Schematic Diagram Illustrating the Topographical Chamentioning

confidence: 89%

Cortical Regulation of Striatal Neuropeptide Y (NPY)‐Containing Neurons in the Rat

Kerkerian

Salin

Nieoullon

1990

Eur J of Neuroscience

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“…The second place in which numerous perikarya were seen was just above the bed nucleus of the stria terminalis, near the globus pallidus. In the rat, the striatal afferent neurons that contain SOM may originate in the area of the globus pallidus [37]. The medium-sized, spiny interneurons that contain SOM/NPY contact the medium-sized spiny neurons through symmetrical synapses and non-synaptic junctions [38].…”

Section: Discussionmentioning

confidence: 99%

Distribution and chemical coding pattern of somatostatin immunoreactivity in the dorsal striatum of the guinea pig

Wasilewska¹,

Robak²,

Równiak³

et al. 2012

Folia Histochem Cytobiol.

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Abstract:The present study provides a detailed description of somatostatin (SOM) distribution and the colocalization pattern of SOM, neuropeptide Y (NPY) and nitric oxide synthase (NOS) in the dorsal striatum (caudate-putamen complex) of the guinea pig. Within the dorsal striatum, SOM is found in a population of medium-sized aspiny interneurons. We found that 97% of all SOM-IR neurons expressed NPY simultaneously, while 98% of all NPY-ergic perikarya was simultaneously SOM-IR. On the other hand, while 98% of all SOM-IR cells were simultaneously NOS-IR, only 91% of all NOS-containing neurons exhibited SOM-immunoreactivity. Irrespective of their chemical coding, both types of SOM-IR neurons were scattered throughout the dorsal striatum, sometimes in the form of small, loosely arranged clusters of 2-4 cells. While SOM-IR and NPY-IR nerve fibers were present in all of the studied regions, they were more numerous in the ventro-medial part of the studied structure, with the exception of its caudal portion, where SOM-IR and NPY-IR fibers additionally formed a dense network in the part corresponding to the caudate nucleus. A low expression of staining for NOS-IR fibers was seen throughout the entire dorsal striatum. In some fibers, SOM and NPY were co-expressed. Fibers expressing both SOM and NOS were not found.

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“…Subsequent studies in mammals have revealed that somatostatin is produced in several tissues and play important roles in coordinating growth, development and metabolism [8][9][10] . Somatostatin is widely expressed in the CNS where it is mainly found in the hypothalamus [11][12][13] , amygdala 14,15 , preoptic area 16 , hippocampus [17][18][19] , striatum 20 , deeper layers of the cerebral cortex [21][22][23] , brainstem 24,25 and the spinal cord [26][27][28][29] . Somatostatin has been shown to act as a neuromodulator involved in sleep 30 , learning 31,32 , food intake 33 , reproduction 34 , neuropathology 35 and locomotor activity 36,37 .…”

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confidence: 99%

Somatostatin 1.1 contributes to the innate exploration of zebrafish larva

Quan

Desban

Mirat

et al. 2020

Sci Rep

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Pharmacological experiments indicate that neuropeptides can effectively tune neuronal activity and modulate locomotor output patterns. However, their functions in shaping innate locomotion often remain elusive. For example, somatostatin has been previously shown to induce locomotion when injected in the brain ventricles but to inhibit fictive locomotion when bath-applied in the spinal cord in vitro. Here, we investigated the role of somatostatin in innate locomotion through a genetic approach by knocking out somatostatin 1.1 (sst1.1) in zebrafish. We automated and carefully analyzed the kinematics of locomotion over a hundred of thousand bouts from hundreds of mutant and control sibling larvae. We found that the deletion of sst1.1 did not impact acousto-vestibular escape responses but led to abnormal exploration. sst1.1 mutant larvae swam over larger distance, at higher speed and performed larger tail bends, indicating that Somatostatin 1.1 inhibits spontaneous locomotion. Altogether our study demonstrates that Somatostatin 1.1 innately contributes to slowing down spontaneous locomotion.

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Evidence for Somatostatin‐Containing Fibers Projecting from the Pallidal Complex to the Striatum of the Rat

Cited by 12 publications

References 15 publications

Cortical Regulation of Striatal Neuropeptide Y (NPY)‐Containing Neurons in the Rat

Cortical Regulation of Striatal Neuropeptide Y (NPY)‐Containing Neurons in the Rat

Distribution and chemical coding pattern of somatostatin immunoreactivity in the dorsal striatum of the guinea pig

Somatostatin 1.1 contributes to the innate exploration of zebrafish larva

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