Inhibition of Prolactin Release in Conscious Sheep Following Stimulation of Nucleus accumbens and Caudate Nucleus

1979 ◽  
Vol 28 (3) ◽  
pp. 160-168 ◽  
Author(s):  
P.V. Malven
Keyword(s):  
Nucleus Accumbens ◽  
Caudate Nucleus ◽  
Prolactin Release ◽  
Conscious Sheep ◽  
Stimulation Of

Behavioural effects of 7-OH-DPAT are solely due to stimulation of dopamine D2 receptors in the shell of the nucleus accumbens; jaw movements

1996 ◽  
Vol 308 (3) ◽  
pp. 227-234 ◽  
Author(s):  
Noriaki Koshikawa ◽  
Yasuhiro Miwa ◽  
Kazunori Adachi ◽  
Masafumi Kobayashi ◽  
Alexander R. Cools
Keyword(s):  
Nucleus Accumbens ◽  
D2 Receptors ◽  
Dopamine D2 Receptors ◽  
Jaw Movements ◽  
Dopamine D2 ◽  
Behavioural Effects ◽  
Stimulation Of

Delusions following deep brain stimulation of the nucleus accumbens

2019 ◽  
Vol 12 (3) ◽  
pp. 770-771
Author(s):  
Ilse Graat ◽  
Isidoor O. Bergfeld ◽  
Pelle de Koning ◽  
Nienke Vulink ◽  
P. Richard Schuurman ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Nucleus Accumbens ◽  
Brain Stimulation ◽  
Deep Brain ◽  
Stimulation Of

PLASMA CONCENTRATIONS OF PROLACTIN AND THYROTROPHIN DURING SUCKLING: EFFECTS OF STIMULATION OF THE MEDIAN EMINENCE

1978 ◽  
Vol 76 (3) ◽  
pp. 557-558 ◽  
Author(s):  
J. B. WAKERLEY ◽  
M. B. TER HAAR
Keyword(s):  
Direct Effect ◽  
Median Eminence ◽  
Plasma Concentrations ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Animal Physiology ◽  
Inhibiting Factor ◽  
Hypothalamic Level ◽  
Stimulation Of

A.R.C. Institute of Animal Physiology, Babraham, Cambridge, CB2 4AT (Received 1 November 1977) Thyrotrophin releasing hormone (TRH) can have a stimulatory effect on the release of both prolactin and thyrotrophin (TSH; Deis & Alonso, 1973), although in the rat, supraphysiological doses of TRH are required to affect the secretion of prolactin (Burnet & Wakerley, 1976). A more important factor in the control of the release of prolactin is considered to be prolactin release inhibiting factor (PIF), which is thought to act through the catecholamine, dopamine (MacLeod, 1976). Stimuli which cause the concomitant release of TSH and prolactin are thought to have a direct effect at the hypothalamic level such that neurones releasing TRH are excited, whereas those releasing PIF are inhibited. In the present work, we have tested this hypothesis using the suckling stimulus to elicit the simultaneous release of prolactin and TSH (Blake, 1974; Burnet & Wakerley, 1976). If

scholarly journals Dopamine neurons projecting to medial shell of the nucleus accumbens drive heroin reinforcement

2018 ◽  
Author(s):  
Julie Corre ◽  
Ruud van Zessen ◽  
Michaël Loureiro ◽  
Tommaso Patriarchi ◽  
Lin Tian ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Causal Link ◽  
The Self ◽  
Dopamine Neurons ◽  
Self Administration ◽  
Gaba Neurons ◽  
Calcium Indicators ◽  
Compulsive Consumption ◽  
Self Stimulation ◽  
Stimulation Of

AbstractThe dopamine (DA) hypothesis posits the increase of mesolimbic dopamine levels as a defining commonality of addictive drugs, initially causing reinforcement, eventually leading to compulsive consumption. While much experimental evidence from psychostimulants supports this hypothesis, it has been challenged for opioid reinforcement. Here, we use genetically encoded DA and calcium indicators as well as cFos to reveal that heroin activates DA neurons located in the medial part of the VTA, preferentially projecting to the medial shell of the nucleus accumbens (NAc). Chemogenetic and optogenetic manipulations of VTA DA or GABA neurons establish a causal link to heroin reinforcement. Inhibition of DA neurons blocked heroin self-administration, while heroin inhibited optogenetic self-stimulation of DA neurons. Likewise, heroin occluded the self-inhibition of VTA GABA neurons. Together, these experiments support a model of disinhibition of a subset of VTA DA neurons in opioid reinforcement.

scholarly journals Stress decreases serotonin tone in the nucleus accumbens to promote aversion and potentiate cocaine preference via decreased stimulation of 5-HT1B receptors

2021 ◽  
Author(s):  
Harrison M Fontaine ◽  
Phillip R Silva ◽  
Carlie Neiswanger ◽  
Rachelle Tran ◽  
Antony D Abraham ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Indirect Pathway ◽  
Lateral Aspect ◽  
Drug Reward ◽  
Cholinergic Interneurons ◽  
Medial Nucleus ◽  
Conditional Deletion ◽  
Pharmacological Blockade ◽  
Monoaminergic Neurons ◽  
Stimulation Of

Stress-induced release of dynorphins (Dyn) activates kappa opioid receptors (KOR) in monoaminergic neurons to produce dysphoria and potentiate drug reward; however, the circuit mechanisms responsible for this effect are not known. We found that conditional deletion of KOR from Slc6a4 (SERT)-expressing neurons blocked stress-induced potentiation of cocaine conditioned place preference (CPP). Within the dorsal raphe nucleus (DRN), two overlapping populations of KOR-expressing neurons: Slc17a8 (VGluT3) and SERT, were distinguished functionally and anatomically. Optogenetic inhibition of these SERT+ neurons potentiated subsequent cocaine CPP, whereas optical inhibition of the VGluT3+ neurons blocked subsequent cocaine CPP. SERT+/VGluT3- expressing neurons were concentrated in the lateral aspect of the DRN. SERT projections from the DRN were observed in the medial nucleus accumbens (mNAc), but VGluT3 projections were not. Optical inhibition of SERT+ neurons produced place aversion, whereas optical stimulation of SERT+ terminals in the mNAc attenuated stress-induced increases in forced swim immobility and subsequent cocaine CPP. KOR neurons projecting to mNAc were confined to the lateral aspect of the DRN, and the principal source of dynorphinergic (Pdyn) afferents in the mNAc was from local neurons. Excision of Pdyn from the mNAc blocked stress-potentiation of cocaine CPP. Prior studies suggested that stress-induced dynorphin release within the mNAc activates KOR to potentiate cocaine preference by a reduction in 5-HT tone. Consistent with this hypothesis, a transient pharmacological blockade of mNAc 5-HT1B receptors potentiated subsequent cocaine CPP. 5-HT1B is known to be expressed on 5-HT terminals in NAc, and 5-HT1B transcript was also detected in Pdyn+, Adora2a+ and ChAT+ (markers for direct pathway, indirect pathway, and cholinergic interneurons, respectively). Following stress exposure, 5-HT1B transcript was selectively elevated in Pdyn+ cells of the mNAc. These findings suggest that Dyn/KOR regulates serotonin activation of 5HT1B receptors within the mNAc and dynamically controls stress response, affect, and drug reward.

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