Morphological plasticity of the tuberoinfundibular dopaminergic neurones in the rat during the oestrous cycle and lactation

Abstract

The hypothalamic tuberoinfundibular dopaminergic (TIDA) neurones are critical with respect to regulating prolactin secretion from the anterior pituitary. Under most physiological conditions, they are stimulated by prolactin to release dopamine into the median eminence which subsequently suppresses further prolactin secretion from the lactotrophs. During lactation, the TIDA neurones are known to undergo both electrophysiological and neurochemical changes that alleviate this negativefeedback, thus allowing circulating prolactin levels to rise. The present study aimed to determine whether TIDA neurone morphology, most notably spine density, is also modified during lactation. This was achieved by stereotaxically injecting the arcuate nucleus of female, tyrosine hydroxylase-promoter driven Cre-recombinase transgenic rats with Cre-dependent adeno-associated virus-expressing Brainbow. This resulted in the highly specifici transfection of between 10% and 30% of the TIDA neurones, thus allowing the morphologies on multiple individual neurones to be examined in a single hypothalamic slice. The transfected neurones exhibited a range of complex forms, including a diversity of soma and location of axonal origin. Neuronal spine counting showed that the density of somatic, but not dendritic, spines was significantly higher during lactation than at any other reproductive stage. There was also a significant fall in somatic spine density across the oestrous cycle from dioestrus to oestrus. Although the functional characteristics of the additional somatic spines have not been determined, if, as might be expected, they represent an increased excitatory input to the TIDA neurones, this could have important physiological implications by perhaps supporting altered neurotransmitter release at their neuroendocrine terminals. Enhanced excitatory input may, for example, favour the release of the opioid peptide enkephalin rather than dopamine, which is potentially significant because the expression of the peptide is known to increase in the TIDA neurones during lactation and, in contrast to dopamine, it stimulates rather than inhibits prolactin secretion from the pituitary.

Norepinephrine modulation of heat dissipation in female rats lacking estrogen

“…Z‐stack images were taken at 1‐μm steps through the ARC (1 AU pinhole). Close apposition of DBH‐ir fiber on kisspeptin soma or proximal dendrites was defined by the absence of black pixels between the two stained structures in at least two consecutive Z‐planes 32 . The proportion of kisspeptin‐ir neurons with at least one apposition was calculated for the ARC of OVX rats (3 fields/rat; n = 3).…”

“…Close apposition of DBH-ir fiber on kisspeptin soma or proximal dendrites was defined by the absence of black pixels between the two stained structures in at least two consecutive Z-planes. 32 The proportion of kisspeptin-ir neurons with at least one apposition was calculated for the ARC of OVX rats (3 fields/ rat; n = 3). To maximize the number of neurons evaluated, the fields analyzed were selected based on the highest density of kisspeptin-ir neurons.…”

Alterations in Hypothalamic Mechanisms Associated with Reduced Suckling-Induced Prolactin Secretion in the Lactation-Deficient OFA hr/hr Rat

“…Previous and most current reports suggested that neurochemical [8, 15], electrophysiological [16], and morphological [17] changes are present in TIDA neurons which allow the maintenance of elevated PRL levels during lactation. These effects seem to be downstream of the PRL-R, because its expression in dopamine neurons was demonstrated in lactating rats [18].…”

Growth hormone and prolactin: So much still to learn

“…Two studies reported here provide insights into the plasticity of TIDA neurones that may underlie their altered function during lactation. Yip et al 6 elegantly demonstrate a change in somatic spine density that would be expected to result in increased TIDA neurone excitatory output; it is possible that this supports the release of a TIDA neurone neuropeptide, such as met‐enkephalin that has been shown to be produced in these neurones in lactation, 7 which would stimulate prolactin release in a feed‐forward loop. This possibility is supported in the study by Silva et al 8 in this special issue, who show that reduced dopamine alone does not account for suckling induced rises in prolactin, indicative of a role for a prolactin‐releasing factor, such as met‐enkephalin.…”

“…5 Two studies reported here provide insights into the plasticity of TIDA neurones that may underlie their altered function during lactation. Yip et al 6 elegantly demonstrate a change in somatic spine density that would be expected to result in increased TIDA neurone excitatory output; it is possible that this supports the release of a TIDA neurone neuropeptide, such as met-enkephalin that has been shown to be produced in these neurones in lactation, 7 The diversity of papers presented in this special issue and the novelty of many findings illustrate that investigation of the prolactin 2 of 2 | EDITORIAL and GH systems is not merely a matter of refining the understanding of a well-described system. Exciting advances in all aspects of both hormones are currently being made and will continue for the foreseeable future, from regulation by the brain and periphery, to temporal and differential effects on tissues that are only beginning to be understood.…”