scholarly journals Semi-quantitative distribution of excitatory amino acid (glutamate) transporters 1–3 (EAAT1-3) and the cystine-glutamate exchanger (xCT) in the adult murine spinal cord

2020 ◽  
Vol 140 ◽  
pp. 104811
Author(s):  
Qiu-Xiang Hu ◽  
Gesa M. Klatt ◽  
Ruben Gudmundsrud ◽  
Sigrid Ottestad-Hansen ◽  
Lise Verbruggen ◽  
...  
1999 ◽  
Vol 81 (5) ◽  
pp. 2037-2045 ◽  
Author(s):  
James T. Buchanan

Commissural interneurons in rhythm generation and intersegmental coupling in the lamprey spinal cord. To test the necessity of spinal commissural interneurons in the generation of the swim rhythm in lamprey, longitudinal midline cuts of the isolated spinal cord preparation were made. Fictive swimming was then induced by bath perfusion with an excitatory amino acid while recording ventral root activity. When the spinal cord preparation was cut completely along the midline into two lateral hemicords, the rhythmic activity of fictive swimming was lost, usually replaced with continuous ventral root spiking. The loss of the fictive swim rhythm was not due to nonspecific damage produced by the cut because rhythmic activity was present in split regions of spinal cord when the split region was still attached to intact cord. The quality of this persistent rhythmic activity, quantified with an autocorrelation method, declined with the distance of the split spinal segment from the remaining intact spinal cord. The deterioration of the rhythm was characterized by a lengthening of burst durations and a shortening of the interburst silent phases. This pattern of deterioration suggests a loss of rhythmic inhibitory inputs. The same pattern of rhythm deterioration was seen in preparations with the rostral end of the spinal cord cut compared with those with the caudal end cut. The results of this study indicate that commissural interneurons are necessary for the generation of the swimming rhythm in the lamprey spinal cord, and the characteristic loss of the silent interburst phases of the swimming rhythm is consistent with a loss of inhibitory commissural interneurons. The results also suggest that both descending and ascending commissural interneurons are important in the generation of the swimming rhythm. The swim rhythm that persists in the split cord while still attached to an intact portion of spinal cord is thus imposed by interneurons projecting from the intact region of cord into the split region. These projections are functionally short because rhythmic activity was lost within approximately five spinal segments from the intact region of spinal cord.


1991 ◽  
Vol 69 (7) ◽  
pp. 1048-1048
Author(s):  
J. R. Ledsome

A meeting was held at the University of British Columbia on May 28–29, 1990 to honour the many important scientific contributions made by Dr. Hugh McLennan to our understanding of chemical neurotransmission in the brain and spinal cord. The invited speakers were those with whom Dr. McLennan has at one time or another collaborated, and their presentations reflected Hugh's early interest in GÀBA (factor I) as an inhibitory transmitter and his research over the last two decades into the physiology and pharmacology of acidic amino acid receptors.The session on GABA opened with an intriguing discussion by Professor Florey of the history of the isolation and identification of GABA as a neurotransmitter and was followed by papers dealing with the electrophysiological actions of GABA. Professor Curtis discussed its pre- and post-synaptic actions in the spinal cord, while Dr. Mathers presented data derived from GABA-gated chloride channels isolated from cultured neurones. Professor Krnjević was unfortunately unable to attend the symposium.Work presented by Professors Watkins and Lodge and Dr. Curry provided an excellent historical perspective on the birth and rapid development of excitatory amino acid pharmacology, a field to which Dr. McLennan has contributed enormously.Among the topics pertaining to the electrophysiological actions of acidic amino acids was the role of the NMDA receptor both in long-term potentiation (Dr. Collingridge) and in synaptic transmission in the kainic acid-lesioned hippocampus (Dr. Wheal), the effects of antagonists on synaptic transmission in the thalamus (Dr. Hicks), and the modulation by catecholamines of glutamate-induced neuronal excitations (Dr. Marshall).In his closing address Dr. McLennan, with characteristic grace and style, acknowledged the efforts of his co-workers in his many achievements. Those of us who have had the great pleasure of collaborating with Hugh here at UBC or within the scientific community wish him all the best in his retirement.


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