Glutamate and kainate effects on the noradrenergic neurons innervating the rat vas deferens

Lara, Hernán E.; Bastos-Ramos, W. P.

doi:10.1002/jnr.490190209

Cited by 16 publications

(8 citation statements)

References 18 publications

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“…In fact, application of kainate to peripheral noradrenergic ganglia innervating the rat vas deferens was earlier shown to induce a time-dependent decrease of noradrenaline in this organ (Lara and Bastos-Ramos 1988). Moreover, NMDA receptor activation in isolated segments of the guinea pig colon potentiates the electrically stimulated noradrenaline overflow, a presynaptic effect probably exerted at sympathetic nerve terminals (Cosentino et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Some lumbar sympathetic neurons develop a glutamatergic phenotype after peripheral axotomy with a note on VGLUT2-positive perineuronal baskets

Brumovsky

Seroogy

Lundgren

et al. 2011

Experimental Neurology

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Glutamate is the main excitatory neurotransmitter in the nervous system, including in primary afferent neurons. However, to date a glutamatergic phenotype of autonomic neurons has not been described. Therefore, we explored the expression of vesicular glutamate transporters (VGLUTs) type 1, 2 and 3 in lumbar sympathetic chain (LSC) and major pelvic ganglion (MPG) of naïve BALB/C mice, as well as after pelvic nerve axotomy (PNA), using immunohistochemistry and in situ hybridization. Colocalization with activating transcription factor-3 (ATF-3), tyrosine hydroxylase (TH), vesicular acetylcholine transporter (VAChT) and calcitonin generelated peptide was also examined. Sham-PNA, sciatic nerve axotomy (SNA) or naïve mice were included. In naïve mice, VGLUT2-like immunoreactivity (LI) was only detected in fibers and varicosities in LSC and MPG; no ATF-3-immunoreactive (IR) neurons were visible. In contrast, PNA induced upregulation of VGLUT2 protein and transcript, as well as of ATF-3-LI in subpopulations of LSC neurons. Interestingly, VGLUT2-IR LSC neurons coexpressed ATF-3, and often lacked the noradrenergic marker TH. SNA only increased VGLUT2 protein and transcript in scattered LSC neurons. Neither PNA nor SNA upregulated VGLUT2 in MPG neurons. We also found perineuronal baskets immunoreactive either for VGLUT2 or the acetylcholinergic marker VAChT in non-PNA MPGs, usually around TH-IR neurons. VGLUT1-LI was restricted to some varicosities in MPGs, was absent in LSCs, and remained largely unaffected by PNA or SNA. This was confirmed by the lack of expression of VGLUT1 or VGLUT3 mRNAs in LSCs, even after PNA or SNA. Taken together, axotomy of visceral and non-visceral nerves results in a glutamatergic phenotype of some LSC neurons. In addition, we show previously non-described MPG perineuronal glutamatergic baskets.

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Section: Discussionmentioning

confidence: 99%

Some lumbar sympathetic neurons develop a glutamatergic phenotype after peripheral axotomy with a note on VGLUT2-positive perineuronal baskets

Brumovsky

Seroogy

Lundgren

et al. 2011

Experimental Neurology

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“…High-affinity glutamate binding was demonstrated also in membranes obtained from sym pathetic ganglia. This binding was however displaced by kainate and quisqualate, though not by NMDA [45], Hoffmann et al [46] reported that the dissociative anesthetic ketamine, which besides other effects antago nizes the NMDA receptor complex, improved the neuro logical outcome of incomplete cerebral ischemia in rats by a mechanism related to a decrease in plasma catechol amine activity. These authors suggested that ketamine might produce sympatholytic effects in association with anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Excitatory Amino Acids Are Involved in Stress-Induced Adrenocorticotropin and Catecholamine Release

Jezová

Tokarev

Rusnak³

1995

Neuroendocrinology

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The effect of N-methyl-D-aspartic acid (NMDA) receptor blockade on adrenocorticotropin (ACTH) and catecholamine activation during stress was investigated in conscious rats with indwelling catheters for both blood sampling and drug treatment. Secretion of ACTH in response to immobilization stress (20 min) was inhibited by pretreatment (20 min before stress exposure) with the centrally acting noncompetitive antagonist of NMDA receptors MK-801 (dizocilpine, the racemic form, 1 mg/kg i.p.) but not by 3-[( ± )-2-carboxypiperazin-4-yl]propyl-1-phosphonic acid (CPP; 10 mg/kg i.p.), a competitive NMDA receptor antagonist. Administration of MK-801 (1 mg/kg i.p.) inhibited norepinephrine and totally prevented epinephrine response during acute immobilization stress. Pretreatment with a low dose of MK-801 (0.1 mg/kg i.p.) failed to modify basal or stress-induced ACTH and catecholamine release. The stress-induced rise in plasma epinephrine was found to be attenuated by the peripherally injected competitive antagonist CPP (10 mg/kg i.p.) suggesting that modulation not only of central but also of peripheral NMDA receptors may come into play. Our results indicate the involvement of endogenous excitatory amino acids in the control of ACTH and particularly of epinephrine secretion during stress.

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“…In the testis, these receptors have a specific affinity for different structures. There is intense anti-mGluR 2/3 immunolabeling of the head of the mature spermatids, spermatozoa, interstitial cells, myoid cells 102 , seminal vesicles 37 , and vas deferens 625 . This distribution suggests that GluRs may be involved in spermatogenesis, spermatozoa motility, testicular development, and vas deferens control.…”

Section: Reproductive Organsmentioning

confidence: 99%

“…This distribution suggests that GluRs may be involved in spermatogenesis, spermatozoa motility, testicular development, and vas deferens control. In fact, GluRs might be important for the contractile activity of the vas deferens and hence in the control of seminal fluid 625 . In the rat female reproductive system, GluRs also have a unique distribution within areas of the reproductive tract 102 .…”

Section: Reproductive Organsmentioning

confidence: 99%

A Review of Glutamate Receptors II: Pathophysiology and Pathology

Rousseaux

2008

J Toxicol Pathol

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Seventy years ago it was discovered that glutamate plays a central role in brain metabolism and is abundant in the brain. Glutamate was then found to be the principal excitatory neurotransmitter in the brain. As stated in the first article of this series, there are three families of ionotropic receptors with intrinsic cation permeable channels: Nmethyl-D-aspartate [NMDA], α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [AMPA] and kainate [Ka].Among these there are three groups of metabotropic, G protein-coupled glutamate receptors [mGluR] that modify neuronal and glial excitability through G protein subunits acting on membrane ion channels and second messengers such as diacylglycerol and cAMP. There are also two glial glutamate transporters and three neuronal transporters in the brain. Although glutamate is the most abundant amino acid in the diet, there is no evidence for brain damage in humans resulting from dietary glutamate. However, a Ka analog, domoate, is sometimes ingested accidentally in blue mussels; this potent toxin causes limbic seizures, which can lead to hippocampal and related pathology and amnesia. Endogenous glutamate may contribute to the brain damage occurring acutely after status epilepticus, cerebral ischemia or traumatic brain injury by activating NMDA, AMPA or mGluR 1 receptors. Glutamate may also contribute to chronic neurodegeneration in such disorders as amyotrophic lateral sclerosis and Huntington's disease. In animal models of cerebral ischemia and traumatic brain injury, NMDA and AMPA receptor antagonists protect against acute brain damage and delayed behavioral deficits. Other clinical conditions that may respond to drugs acting on glutamatergic transmission include epilepsy, amnesia, anxiety, hyperalgesia and psychosis. In this second part of this review, we will explore those diseases in which the pathophysiology and pathology are associated, in part, with the glutamate system. (J Toxicol Pathol 2008; 21: 133-173)

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Glutamate and kainate effects on the noradrenergic neurons innervating the rat vas deferens

Cited by 16 publications

References 18 publications

Some lumbar sympathetic neurons develop a glutamatergic phenotype after peripheral axotomy with a note on VGLUT2-positive perineuronal baskets

Some lumbar sympathetic neurons develop a glutamatergic phenotype after peripheral axotomy with a note on VGLUT2-positive perineuronal baskets

Endogenous Excitatory Amino Acids Are Involved in Stress-Induced Adrenocorticotropin and Catecholamine Release

A Review of Glutamate Receptors II: Pathophysiology and Pathology

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