Vasopressin-induced neurotrophism in cultured neurons of the cerebral cortex: dependency on calcium signaling and protein kinase C activity

Chen, Q.; Patel, Rekha; Sales, A.D.; Oji, George S; Kim, J.; Monreal, Alex W.; Brinton, Roberta Dı́az

doi:10.1016/s0306-4522(00)00323-7

Cited by 24 publications

(12 citation statements)

References 52 publications

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“…Of note are reports of impaired neural functions in the vasopressin-deficient Brattleboro rat (reviewed in Bohus and de Weid 1998). AVP does influence neuronal growth and development in various preparations (reviewed in Carter et al 1993), including hippocampal and cortical neuronal cultures (Brinton et al 1994;Chen et al 2000;Tarumi et al 2000), and accelerates neurite outgrowth from cultured embryonic neurons (Brinton and Gruener 1987). Interestingly, AVP, but not oxytocin, is reported to have a neurotrophic action in cultured explants of spinal cord (Iwasaki et al 1991).…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological Evidence for Vasopressin V₁Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

Öz

Kolaj

Renaud

2001

Journal of Neurophysiology

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Prominent arginine-vasopressin (AVP) binding and AVP V(1) type receptors are expressed early in the developing rat spinal cord. We sought to characterize their influence on neural excitability by using patch-clamp techniques to record AVP-induced responses from a population of motoneurons and interneurons in neonatal (5-18 days) rat spinal cord slices. Data were obtained from 58 thoracolumbar (T(7)-L(5)) motoneurons and 166 local interneurons. A majority (>90%) of neurons responded to bath applied AVP (10 nM to 3 microM) and (Phe(2), Orn(8))-vasotocin, a V(1) receptor agonist, but not V(2) or oxytocin receptor agonists. In voltage-clamp, postsynaptic responses in motoneurons were characterized by slowly rising, prolonged (7-10 min) and tetrodotoxin-resistant inward currents associated with a 25% reduction in a membrane potassium conductance that reversed near -100 mV. In interneurons, net AVP-induced inward currents displayed three patterns: decreasing membrane conductance with reversal near -100 mV, i.e., similar to that in motoneurons (24 cells); increasing conductance with reversal near -40 mV (21 cells); small reduction in conductance with no reversal within the current range tested (41 cells). A presynaptic component recorded in most neurons was evident as an increase in the frequency but not amplitude (in motoneurons) of inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs), in large part due to AVP-induced firing in inhibitory (mainly glycinergic) and excitatory (glutamatergic) neurons synapsing on the recorded cells. An increase in frequency but not amplitude of miniature IPSCs and EPSCs also indicated an AVP enhancement of neurotransmitter release from axon terminals of inhibitory and excitatory interneurons. These observations provide support for a broad presynaptic and postsynaptic distribution of AVP V(1) type receptors and indicate that their activation can enhance the excitability of a majority of neurons in neonatal ventral spinal cord.

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Section: Discussionmentioning

confidence: 99%

Electrophysiological Evidence for Vasopressin V₁Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

Öz

Kolaj

Renaud

2001

Journal of Neurophysiology

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“…It remains unclear however as to whether there is a linear correlation between peripheral and central levels of AVP. Nevertheless, the identification of vasopressin-induced neurotrophism warrants further research into the effect of hormones on cognitive function in dehydrated persons (Chen et al, 2000).…”

Section: Hormonal Theoriesmentioning

confidence: 99%

Impaired cognitive function and mental performance in mild dehydration

2003

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Dehydration is a reliable predictor of impaired cognitive status. Objective data, using tests of cortical function, support the deterioration of mental performance in mildly dehydrated younger adults. Dehydration frequently results in delirium as a manifestation of cognitive dysfunction. Although, the occurrence of delirium suggests transient acute global cerebral dysfunction, cognitive impairment may not be completely reversible. Animal studies have identified neuronal mitochondrial damage and glutamate hypertransmission in dehydrated rats. Additional studies have identified an increase in cerebral nicotinamide adenine dinucleotide phosphate-diaphorase activity (nitric oxide synthase, NOS) with dehydration. Available evidence also implicates NOS as a neurotransmitter in long-term potentiation, rendering this a critical enzyme in facilitating learning and memory. With ageing, a reduction of NOS activity has been identified in the cortex and striatum of rats. The reduction of NOs synthase activity that occurs with ageing may blunt the rise that occurs with dehydration, and possibly interfere with memory processing and cognitive function. Dehydration has been shown to be a reliable predictor of increasing frailty, deteriorating mental performance and poor quality of life. Intervention models directed toward improving outcomes in dehydration must incorporate strategies to enhance prompt recognition of cognitive dysfunction.

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“…В ходе онтогенеза этот гормон способен стимулиро-вать рост отростков нейронов (нейротрофизм) (Chen et al, 2000), а также дифференцировку клеток печени (Serriere et al, 2008). AVP также способен ингибировать пролиферацию злокачественных клеток (Forti, Armelin, 2011).…”

Section: роль вазопрессина в организмеunclassified

Comparison of natural and artificial vasopressin deficiency: why the latter is lethal?

Зелена¹

2016

Vestn. VOGiS

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The transgenic mouse technology is widespread, however, untill now 22.0 % of tested null mutations was found to be lethal. The complete lack of vasopressin (AVP) resulted also in preweaning lethality. It is surprising take into consideration the viability of the AVP mutant Brattleboro rats. Thus, AVP is essential for survival, but which of its ubiquiter role is the most important. AVP exerts its effect through specific plasma memb ane receptors. V1a receptors can induce vasoconstriction maintaining blood pressure during hypovolemia. The V1b receptor on the anterior pituitary has a role in stress adaptation. The V2 subtype is located in the kidney and contributes to the antidiuresis. The avp gene consists of a signal peptide, AVP, neurophysin 2 and a C-terminal glycopeptide. The naturally occuring AVP-deficie t Brattleboro rat has a framshift mutation in the neurophysin portion resulting in cental diabetes insipidus. In its hypothalamus AVP is not produced, while in certain peripheral tissues it may be expressed, suggesting the existence of a different synthetic pathway. The avp knockout mice can also be produced, they will be born, but without peripheral AVP administration they will not survive. Comparing available knockout models we can conclude that the combined V1a and V2 receptor mediated effects, namely hypotension and water lost together may led to lethality. As in Brattleboro and targetted knockout mice the local synthesis of AVP in the heart can be maintained and AVP can be released into the general circulation. Thus, in these animals vasoconstriction can compensate the hypovolemia.Key words: Brattleboro rat, vasopressin knockout mice, vasopressin gene, vasopressin receptors, hypovolaemia.Технологии получения трансгенных мышей широко используются при анализе физиологических функций, однако к настоящему времени установлено, что 22,0 % исследованных нуль-мутаций являются летальными. Полное отсутствие вазопрессина (AVP) у трансгенных мышей приводит к их гибели к возрасту отъема от матери. Вместе с тем природные мутантные крысы Brattleboro, лишенные AVP, вполне жизнеспособны. Безусловно, AVP имеет существенное значение для выживания, однако какая из его разнообразных функций является наиболее важной для этого -остается неясным. AVP оказывает свое действие через специфи-ческие рецепторы плазматической мембраны. Рецепторы V1a типа могут вызывать сужение кровеносных сосудов для поддержания артериального давления в течение гиповолемии. Рецептор V1B в передней доле гипофиза играет важную роль в адаптации к стрессу. Рецепторы V2 подтипа, экспрессируемые в почках, способствуют задержке воды в организме. Ген avp содержит последовательности нуклеотидов, кодирующие сигнальный пептид, собственно AVP, нейрофизин 2 и С-терминальный гликопептид. Возникшая естественным путем мутация в районе, кодирующем нейрофизин, вызывает сдвиг рамки считывания и тем самым приводит к появлению AVP-дефицитных крыс Браттлборо (Brattleboro) с центральным несахарным диабетом. В гипоталамусе этих животных AVP не синтезируется, однако в некото...

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Vasopressin-induced neurotrophism in cultured neurons of the cerebral cortex: dependency on calcium signaling and protein kinase C activity

Cited by 24 publications

References 52 publications

Electrophysiological Evidence for Vasopressin V₁Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

Electrophysiological Evidence for Vasopressin V₁Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

Impaired cognitive function and mental performance in mild dehydration

Comparison of natural and artificial vasopressin deficiency: why the latter is lethal?

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Vasopressin-induced neurotrophism in cultured neurons of the cerebral cortex: dependency on calcium signaling and protein kinase C activity

Cited by 24 publications

References 52 publications

Electrophysiological Evidence for Vasopressin V1Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

Electrophysiological Evidence for Vasopressin V1Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

Impaired cognitive function and mental performance in mild dehydration

Comparison of natural and artificial vasopressin deficiency: why the latter is lethal?

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Product

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Electrophysiological Evidence for Vasopressin V₁Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

Electrophysiological Evidence for Vasopressin V₁Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons