Experimental reorganization of the cerebellar cortex. IV. Parallel fiber reorientation following regeneration of the external germinal layer

1973 ◽  
Vol 149 (2) ◽  
pp. 181-191 ◽  
Author(s):  
Joseph Altman
Keyword(s):  
Cerebellar Cortex ◽  
Parallel Fiber ◽  
Germinal Layer ◽  
Fiber Reorientation

scholarly journals Immunocytochemical demonstration of alpha-tubulin modification during axonal maturation in the cerebellar cortex.

1984 ◽  
Vol 98 (1) ◽  
pp. 347-351 ◽  
Author(s):  
R Cumming ◽  
R D Burgoyne ◽  
N A Lytton
Keyword(s):  
Cerebellar Cortex ◽  
Time Course ◽  
Staining Pattern ◽  
Molecular Layer ◽  
Parallel Fiber ◽  
Differential Staining ◽  
Germinal Layer ◽  
Progressive Change ◽  
Parallel Fibers ◽  
Alpha Tubulin

Previous light microscopic immunocytochemical studies using two monoclonal antibodies that recognise alpha-tubulin (YOL/34 and YL1/2) but differ in their isotypic specificity have shown that the unmyelinated parallel fiber axons in the cerebellar cortex are labeled with only one of the antibodies (YOL/34). We now show that at 10 d postnatally the parallel fibers are labeled with both antibodies, and that during development YL1/2 (but not YOL/34) immunoreactivity disappears progressively from parallel fibers in the lower regions of the molecular layer upwards towards the external germinal layer. By approximately 28 d postnatally, the differential staining pattern of parallel fibers by the antibodies is established throughout the molecular layer. The time course, light microscopic, and ultrastructural staining distribution corresponds to a progressive change in alpha-tubulin immunoreactivity as the parallel fibers form synaptic contacts. This modification of alpha-tubulin (which was not observed in Purkinje cell dendrites or Bergmann glia) may be related to the formation of a basic isotype of alpha-tubulin within parallel fiber axons at maturation.

Glutamate microinjections in cerebellar cortex reproduce cerebrovascular effects of parallel fiber stimulation

1996 ◽  
Vol 271 (6) ◽  
pp. R1568-R1575 ◽  
Author(s):  
G. Yang ◽  
C. Iadecola
Keyword(s):  
Glutamate Receptors ◽  
Cerebellar Cortex ◽  
Glutamate Release ◽  
Molecular Layer ◽  
Parallel Fiber ◽  
Synaptic Activity ◽  
No Production ◽  
Doppler Flowmetry ◽  
Cranial Window ◽  
Fiber Stimulation

Electrical stimulation of cerebellar parallel fibers releases glutamate and increases local blood flow (BFcrb), an effect in part mediated by glutamate-induced nitric oxide (NO) production. We studied whether local microinjection of glutamate into the cerebellar cortex would produce increases in BFcrb comparable to those elicited by parallel fiber stimulation. In halothane-anesthetized rats equipped with a cranial window, glutamate was microinjected into the cerebellar molecular layer, and BFcrb was monitored by laser-Doppler flowmetry. Glutamate microinjections increased BFcrb dose dependently (2-200 pmol in 200 nl) (n = 9) and by 55 +/- 6% at 200 pmol (mean +/- SE). The magnitude and temporal profile of the increases in BFcrb compared favorably with the increase in flow produced by parallel fiber stimulation. The glutamate-induced BFcrb increase was attenuated by superfusion with the Na2+ channel blocker tetrodotoxin (10 microM; -50 +/- 10%; n = 5; P < 0.05; t-test) or by blocking synaptic activity by treatment of the cerebellar cortex with Ringer containing 20 mM Mg2+ and 0 mM Ca2+ (-80 +/- 4%; n = 6; P < 0.05). The glutamate-receptor antagonist kynurenate (10 mM) attenuated the increase in BFcrb by 59 +/- 6% (P < 0.05; n = 5). The relatively selective inhibitor of neuronal NO synthase 7-nitroindazole (100 mg/kg ip) reduced the flow response evoked by microinjection of glutamate (-46 +/- 7%; n = 5; P < 0.05) but not acetylcholine (10 microM; P > 0.05; n = 6). We conclude that glutamate microinjections increase local BFcrb via activation of glutamate receptors. The glutamate-induced vasodilation is mediated, in part, by neurally derived NO. The striking similarities between the vascular responses evoked by parallel fiber stimulation and that produced by microinjection of glutamate support the hypothesis that the increase in BFcrb produced by parallel fiber stimulation is mediated by glutamate release and activation of glutamate receptors. The data also strengthen the hypothesis that glutamate and NO are important mediators in the mechanisms linking synaptic activity to BFcrb in cerebellar cortex.

Therapeutic Motor Training Increases Parallel Fiber Synapse Number Per Purkinje Neuron in Cerebellar Cortex of Rats Given Postnatal Binge Alcohol Exposure

1997 ◽  
Vol 21 (7) ◽  
pp. 1257 ◽  
Author(s):  
Anna Y. Klintsova ◽  
Jessica T. Matthews ◽  
Charles R. Goodlett ◽  
Ruth M. A. Napper ◽  
William T. Greenough
Keyword(s):  
Cerebellar Cortex ◽  
Alcohol Exposure ◽  
Purkinje Neuron ◽  
Parallel Fiber ◽  
Motor Training

scholarly journals Low-Frequency Oscillations in the Cerebellar Cortex of the Tottering Mouse

2009 ◽  
Vol 101 (1) ◽  
pp. 234-245 ◽  
Author(s):  
Gang Chen ◽  
Laurentiu S. Popa ◽  
Xinming Wang ◽  
Wangcai Gao ◽  
Justin Barnes ◽  
...  
Keyword(s):  
Cerebellar Cortex ◽  
Ampa Receptors ◽  
Cortical Neurons ◽  
Low Frequency ◽  
Autosomal Recessive Disorder ◽  
Parallel Fiber ◽  
Emg Activity ◽  
Gene Encoding ◽  
Low Frequencies ◽  
Low Frequency Oscillations

The tottering mouse is an autosomal recessive disorder involving a missense mutation in the gene encoding P/Q-type voltage-gated Ca2+channels. The tottering mouse has a characteristic phenotype consisting of transient attacks of dystonia triggered by stress, caffeine, or ethanol. The neural events underlying these episodes of dystonia are unknown. Flavoprotein autofluorescence optical imaging revealed transient, low-frequency oscillations in the cerebellar cortex of anesthetized and awake tottering mice but not in wild-type mice. Analysis of the frequencies, spatial extent, and power were used to characterize the oscillations. In anesthetized mice, the dominant frequencies of the oscillations are between 0.039 and 0.078 Hz. The spontaneous oscillations in the tottering mouse organize into high power domains that propagate to neighboring cerebellar cortical regions. In the tottering mouse, the spontaneous firing of 83% (73/88) of cerebellar cortical neurons exhibit oscillations at the same low frequencies. The oscillations are reduced by removing extracellular Ca2+and blocking L-type Ca2+channels. The oscillations are likely generated intrinsically in the cerebellar cortex because they are not affected by blocking AMPA receptors or by electrical stimulation of the parallel fiber–Purkinje cell circuit. Furthermore, local application of an L-type Ca2+agonist in the tottering mouse generates oscillations with similar properties. The beam-like response evoked by parallel fiber stimulation is reduced in the tottering mouse. In the awake tottering mouse, transcranial flavoprotein imaging revealed low-frequency oscillations that are accentuated during caffeine-induced attacks of dystonia. During dystonia, oscillations are also present in the face and hindlimb electromyographic (EMG) activity that become significantly coherent with the oscillations in the cerebellar cortex. These low-frequency oscillations and associated cerebellar cortical dysfunction demonstrate a novel abnormality in the tottering mouse. These oscillations are hypothesized to be involved in the episodic movement disorder in this mouse model of episodic ataxia type 2.

scholarly journals Local Estrogen Synthesis Regulates Parallel Fiber–Purkinje Cell Neurotransmission Within the Cerebellar Cortex

Endocrinology ◽  
2018 ◽  
Vol 159 (3) ◽  
pp. 1328-1338 ◽  
Author(s):  
Valerie L Hedges ◽  
Gang Chen ◽  
Lei Yu ◽  
Amanda A Krentzel ◽  
Joseph R Starrett ◽  
...  
Keyword(s):  
Purkinje Cell ◽  
Cerebellar Cortex ◽  
Metabotropic Glutamate Receptor ◽  
Receptor Activation ◽  
Parallel Fiber ◽  
Aromatase Activity ◽  
Glutamatergic Neurotransmission ◽  
Metabotropic Glutamate ◽  
Estrogen Synthesis ◽  
Glutamatergic Signaling

Abstract Estrogens affect cerebellar activity and cerebellum-based behaviors. Within the adult rodent cerebellum, the best-characterized action of estradiol is to enhance glutamatergic signaling. However, the mechanisms by which estradiol promotes glutamatergic neurotransmission remain unknown. Within the mouse cerebellum, we found that estrogen receptor activation of metabotropic glutamate receptor type 1a strongly enhances neurotransmission at the parallel fiber–Purkinje cell synapse. The blockade of local estrogen synthesis within the cerebellum results in a diminution of glutamatergic neurotransmission. Correspondingly, decreased estrogen availability via gonadectomy or blockade of aromatase activity negatively affects locomotor performance. These data indicate that locally derived, and not just gonad-derived, estrogens affect cerebellar physiology and function. In addition, estrogens were found to facilitate parallel fiber–Purkinje cell synaptic transmission in both sexes. As such, the actions of estradiol to support cerebellar neurotransmission and cerebellum-based behaviors might be fundamental to understanding the normal processing of activity within the cerebellar cortex.

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