Regional differences in the effect of pargyline on dopamine concentrations in the rat hypophysis

Self Cite

The effect of dehydration on dopamine (DA) release from the neural and intermediate lobes of the rat pituitary gland after electrical stimulation of the pituitary stalk was studied in vitro. The amount of DA released from pituitary lobes of dehydrated rats (no water for 72 h), in which the hormone secretion from the hypophysis, especially the neural lobe, is known to be greatly enhanced, was significantly higher when compared with that from control tissues. In control and dehydrated rats the evoked DA release from the intermediate lobe was higher than that from the neural lobe. After dehydration, the stimulus-evoked DA release from the neural lobe increased by more than 200%, whereas that from the intermediate lobe increased by only 60%, indicating a preferential activation of the DA system of the neural lobe. There was a decrease in DA released per pulse from the combined neuro-intermediate lobe of control rats with increasing number of stimulation pulses. In contrast, DA release per pulse from the neuro-intermediate lobe of dehydrated rats showed a tendency to increase with increasing number of pulses. As the availability of newly synthesized DA is believed to be the limiting factor for transmitter release, the present observations suggested a higher in vitro DA synthesis rate in the tissues from dehydrated rats. This agrees with in vivo results of Alperand his colleagues who found an increased accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in neuro-intermediate lobes of dehydrated rats after inhibition of DOPA-decarboxylase.

Section: Discussionmentioning

confidence: 92%

Section: Da Releasementioning

confidence: 99%

Dehydration Increases the Electrically Evoked Dopamine Release from the Neural and Intermediate Lobes of the Rat Hypophysis

Racké¹,

Holzbauer²,

Cooper³

et al. 1986

Self Cite

“…In accord with these and other earlier studies, electrically evoked release of [3H]-NA from the neurohypophysis was effectively abolished by inclusion of 10"6 M tetrodotoxin during S; (S::S|, 0.023 ±0.006: n = 4) and is thus due to propagation of ac tion potentials into terminals. Dopamine is the major cat echolamine in the neurohypophysis, the dopamine content of the isolated neural lobe being some 3^4 times that of N A [27]. Uptake of ['F1]-NA.…”

Section: Na Releasementioning

confidence: 99%

“…However, our experiments suggest that the opioid peptides acting to modulate neurohormone secretion are derived from the neurohypophysis itself [I I]. We have thus perfor med the present studies on the neurohypophysis dissected free of intermediate lobe tissue, a procedure which also al lowed us to study output from NA terminals located exclu sively in the neurohypophysis [14,27], Here we investigated the action of endogenous opioids on electrically evoked re lease of OXT, AVP, and NA and the opioid receptor subtypes mediating these actions. In the accompanying paper [64] we have investigated the possible neuromodulatory actions of released NA on secretion from neurohor mone terminals.…”

mentioning

confidence: 99%

Opioid-Noradrenergic Interactions in the Neurohypophysis

Chapman²,

Rj³

1988

The actions of opioids on electrically evoked release of oxytocin, vasopressin, and noradrenaline – using the [³H]-noradrenaline technique – from the rat neurohypophysis were examined in vitro. Antagonism of the action of endogenous neurohypophysial opioids with naloxone enhanced release of peptides and [³H]-noradrenaline differentially. Naloxone enhanced oxytocin release by 100 and 173% in two series of experiments (ED50 7× 10^–7M), whilst vasopressin release was enhanced by only 30 and 20%, respectively. [³H]-noradrenaline release was maximally enhanced by 41% (ED50 2× 10^–7M). We examined the opioid receptor subtypes mediating these effects using selective receptor agonists. The ĸ-agonist U-50,488H inhibited oxytocin and vasopressin release to a similar extent, but did not modify [³H]-noradrenaline release. The effects of U-50,488H were completely prevented by a tenfold molar excess of naloxone. The µ-agonist (Z)-Ala², MePhe⁵ Gly-ol)-enkephalin also failed to inhibit [³H]-noradrenaline release and caused only a minor inhibition of oxytocin and vasopressin secretion. The δ-agonist (D-Pen², D-Pen⁵)-enkephalin was without effect. We conclude that (1) ĸ-re-ceptors sensitive to U-50,488H mediate opioid inhibition of secretion from oxytocin and vasopressin nerve terminals; (2) when opioid actions are blocked by naloxone, opioid peptides within the neurohypophysis are shown to exert a much greater influence over oxytocin compared to vasopressin terminals; (3) neurohypophysial opioids also regulate release from noradrenergic terminals, although the nature of the receptors involved remains unclear, and (4) ĸ-receptors can mediate inhibition of neurohormone secretion by an action independent of the neurohypophysial noradrenergic innervation.

“…The neurohypophysis contains 1-2 pmol of NA (14], and NA is released upon depolarization of the nerve terminals in vitro [24]. We have used [3H]-NA prelabelling of NA stores to demonstrate release from NA terminals by electri cal stimulation [28].…”

Section: Opioid-na Interactions and Oxt Releasementioning

confidence: 99%

Opioid-Noradrenergic Interactions in the Neurohypophysis

Bg¹,

Chapman²,

Brown

et al. 1988

The function of noradrenaline in the rat neurohypophysis was investigated by examining the effects of selective adrenergic receptor agents on electrically evoked release of oxytocin, arginine vasopressin, and noradrenaline using the [³H]-noradrenaline technique. Since endogenous opioids in the neurohypophysis suppress release of both neurohormones and of noradrenaline, we assessed the role of noradrenaline in mediating opioid actions on neurohormone secretion by examining modification of the action of the opioid antagonist naloxone by adrenergic receptor agents. The data suggest (1) that in addition to opioid receptors, ‘presynaptic’ α₂receptors regulate release from neurohypophysial noradrenaline terminals; (2) noradrenaline released from neurohypophysial terminals acts on β- and α₁-receptors to facilitate both oxytocin and arginine vasopressin release: this action only becoming evident at elevated levels of endogenous noradrenaline release attained following removal of presynaptic opioid or α₂regulation, and (3) opioid peptides within the neurohypophysis act to inhibit oxytocin and, to a lesser extent, arginine vasopressin secretion, partly through inhibiting release of facilitatory noradrenaline. We propose a model in which opioids act in the neurohypophysis both independently of noradrenaline via ĸ-receptors on neurosecretory terminals or pituicytes and also via interaction with the noradrenaline system.