特別說(shuō)明：由于文章內(nèi)容粘貼緣故，最終結(jié)果導(dǎo)致文中一些格式會(huì)消失，請(qǐng)不要在意，專注于文字內(nèi)容即可。文中文字大小為“特大”方式突出的部分是我的筆記標(biāo)識(shí)內(nèi)容，是我格外喜歡，用于推理的基礎(chǔ)，括號(hào)內(nèi)的有色文字內(nèi)容是當(dāng)時(shí)我思考的紀(jì)錄，這樣方便自己和他人直接找到那些曾經(jīng)標(biāo)記的內(nèi)容。當(dāng)然也不全限于此，靈感所致，所加內(nèi)容無(wú)所不及，唯獨(dú)不會(huì)更改原文內(nèi)容。

Pars reticulata

From Wikipedia, the free encyclopedia

Jump to navigationJump to search

Pars reticulata

Details

Identifiers

Latin

"Edible Container - Solid Mold_Ver.2" by?Mariana Boubet

?

Pars reticulata substantiae nigrae

MeSH

D065841

NeuroNames

538

NeuroLex?ID

birnlex_968

TA

A14.1.06.114

FMA

62908

Anatomical terms of neuroanatomy

[edit on Wikidata]

The?pars reticulata?is a portion of the?substantia nigra. Most of the neurons that project out of the pars reticulata are inhibitory GABAergic neurons (i.e., these neurons release?GABA, which is an inhibitory?neurotransmitter).

Contents

·?1Anatomy

·?2Function

·?3Pathology

·?4References

Anatomy[edit]

Neurons?in the pars reticulata are much less densely packed than those in the?pars compacta?(they were sometimes named pars diffusa). They are smaller and thinner than the?dopaminergic?neurons and conversely identical and morphologically similar to the?pallidal?neurons (see?primate basal ganglia). Their dendrites as well as the pallidal are preferentially perpendicular to the?striatal?afferents.[1]?The massive striatal afferents correspond to the medial end of the?nigrostriatal bundle. Nigral neurons have the same peculiar synaptology with the striatal axonal endings. They make connections with the dopamine neurons of the pars compacta?whose long dendrites plunge deeply in the pars reticulata. The neurons of the pars reticulata produce the neurotransmitter?gamma-aminobutyric acid?(GABA). The neurons of the pars reticulata through the?nigrothalamic bundle?send axons to a particular part of the motor?thalamus. The nigral territory corresponds to the?nucleus ventralis anterior?(VA) (see also?List of thalamic nuclei) (different from the pallidal VO). VA is the origin of one output of the basal ganglia system. It sends axons to the frontal and oculomotor cortex. In addition the pars reticulata sends neurons to?the pars parafascicularis of the central region of the thalamus and to the?pedunculopontine complex). The particularity of the pars lateralis is to send its axons to the superior colliculus,[2]?which is a too minimized output of the basal ganglia system.

Function[edit]

The neurons of the pars reticulata are fast-spiking pacemakers, generating?action potentials?in the absence of synaptic input.[3]?In primates they discharge at a mean rate of 68?Hz in contrast to dopaminergic neurons (below 8?Hz).(when you feel sad, you can be easily turned on by male,maybe it’s due to the activity of subthalamic nucleus which reversely inhibits SNpr)[4]?They receive abundant afferrences from the?striatum?(mainly from the associative striatum) with the same very peculiar synaptology as the?pallidum. It receives axons from the?subthalamic nucleus?and a dopaminergic innervation from the dopaminergic ensemble.

The pars reticulata is one of the two primary output?nuclei?of the?basal ganglia?system to the motor thalamus (the other output is the internal segment of the?globus pallidus). The nigral neurons have their own territory distinct from the cerebellar and the pallidal in the nucleus ventralis anterior VA. This sends axons to the frontal and oculomotor cortex. Hikosaka and Wurtz[5][6][7][8]?devoted four papers to "the visual and oculomotor functions of the monkey substantia nigra pars reticulata". This is largely involved in orientation and the control of?eyemovements in stabilisation of gaze and in?saccades.?Pars reticulata sends inhibitory projections to the?superior colliculus, inhibiting eye movement, and this inhibition is 'lifted', i.e. the projecting neurons cease firing, during saccades.[9]

Pathology[edit]

The function of the neurons of the pars compacta (not reticulata) is profoundly changed (60% of Dopamine secreting neurons, 80% decrease in dopamine in striatum) in?parkinsonism?and?epilepsy. These changes are thought to be mostly secondary to pathology elsewhere in the brain, but may be crucial to understanding the generation of the symptoms of these disorders.