Responsiveness of mesolimbic, mesocortical, septal and hippocampal cholecystokinin and substance P neuronal systems to stress, in the male rat

Siegel, Richard A.; Düker, E.; Fuchs, Eberhard; Pahnke, Ulrich; Wuttke, W.

doi:10.1016/0197-0186(84)90011-1

Cited by 61 publications

(22 citation statements)

References 34 publications

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“…We have previously reported that certain extrahypotha lamic limbic CCK and SP neuronal systems (mesolimbic, mesocortical, septal and hippocampal) are responsive to stress [27], The present study extends these findings to the hypothalamus. Thus, both CCK and SP may play major roles as neurotransmitters and/or neuromodulators in the integrated function of the limbic system, in the rat.…”

Section: Discussionsupporting

confidence: 75%

Stress-Induced Changes in Cholecystokinin and Substance P Concentrations in Discrete Regions of the Rat Hypothalamus

Siegel¹,

Düker²,

Pahnke³

et al. 1987

Neuroendocrinology

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The effects of acute stress exposure upon cholecystokinin (CCK) and substance P (SP) concentrations in discrete hypothalamic regions of the adult male rat brain were studied. Animals were exposed to foot shock stress for periods of 2, 4, 10, 30 or 60 min duration; immediately afterwards they were decapitated; brains were frozen and subsequently microdissected. CCK and SP concentrations were assayed by a specific RIA, as were serum levels of ACTH, corticosterone, PRL, GH, LH and testosterone. Stress had no effect upon SP concentrations in the anterior or posterior parts of the arcuate nucleus (ARC), but led to elevated CCK levels in the posterior ARC following 60 min of exposure. In both the ventromedial and dorsomedial hypothalamic areas, stress induced depletions of both neuropeptides. In the anterior (but not the posterior) portions of the lateral hypothalamic area, CCK and SP concentrations were reduced by stress exposure. These studies demonstrate that discrete hypothalamic CCK and SP neuronal systems are responsive to stress. This suggests that endogenous hypothalamic CCK and SP participate, along with other neurotransmitters/neuromodulators, in the integrated hypothalamic stress response, and mediate stress-neuroendocrine interactions.

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Section: Discussionsupporting

confidence: 75%

Stress-Induced Changes in Cholecystokinin and Substance P Concentrations in Discrete Regions of the Rat Hypothalamus

Siegel¹,

Düker²,

Pahnke³

et al. 1987

Neuroendocrinology

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“…CCK interneurons are the major cell type expressing endocannabinoid CB1 receptors in the rodent forebrain [50] . There is also evidence that CCK in the medial PFC plays a role in stress and anxiety-related behaviors and that CB1 modulation of CCK transmission can alter social interaction and withdrawal behavior [51][52][53] . Therefore one can speculate that alteration in CCK neuron function caused by prenatal immune activation could potentially alter the reactivity to stress and cannabinoid use, which are risk factors for the development of overt psychosis in adolescence [54,55] , as well as impact social interaction.…”

Section: Discussionmentioning

confidence: 99%

Early Development of Parvalbumin-, Somatostatin-, and Cholecystokinin-Expressing Neurons in Rat Brain following Prenatal Immune Activation and Maternal Iron Deficiency

Boksa

Zhang²,

Nouel³

et al. 2016

Dev Neurosci

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Prenatal maternal infection and maternal iron deficiency during pregnancy are 2 early environmental insults associated with increased risk for schizophrenia in offspring. Substantial evidence suggests that abnormalities in inhibitory γ-aminobutyric acid (GABA) interneuron function, especially in the parvalbumin subtype of GABA interneuron, both developmentally and in adulthood, may contribute mechanistically to cognitive deficits and psychotic symptoms in schizophrenia. This study used a rat model to test whether prenatal immune activation with lipopolysaccharide (LPS; at gestation days, GD, 15 and 16) or maternal iron deficiency (from GD2 to postnatal day P7) or the combination of both insults alters major subtypes of GABAergic interneurons (parvalbumin, somatostatin, cholecystokinin) in brain regions relevant to schizophrenia (medial and dorsolateral prefrontal cortex [PFC], hippocampal CA1 and dentate gyrus, ventral subiculum) in offspring at P14 or P28. Prenatal LPS treatment significantly increased the density of parvalbumin-immunoreactive neurons at P14 in the medial PFC, dorsolateral PFC, and ventral subiculum of offspring born from iron-sufficient but not iron-deficient dams. Prenatal LPS also increased cholecystokinin neuron density in the medial PFC at P28, under both iron-sufficient and iron-deficient conditions. We observed a large increase in parvalbumin neuron density from P14 to P28 in the medial PFC and subiculum across all birth groups, that was not observed in other brain regions, and significant decreases in somatostatin neuron density from P14 to P28 in all brain regions examined across all birth groups, indicating differential developmental trajectories for parvalbumin and somatostatin neurons in various brain regions during this early postnatal period. Thus, it appears that the medial PFC and ventral subiculum, brain regions involved in circuitry modulating ventral tegmental dopamine and nucleus accumbens activities, may be regions vulnerable to effects of prenatal LPS on specific subpopulations of interneurons. It is known that the timing of maturation and expansion of parvalbumin neurons in early development provides threshold levels of inhibition that trigger critical periods for cortical plasticity, leading to long-term circuit consolidation. Thus, our finding of increased parvalbumin neuron density at early developmental times might suggest a mechanism by which an acute prenatal insult like LPS exposure could produce long-term changes in prefrontal cortical or subicular function.

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“…1,2 In rats, neurochemical studies have demonstrated an increase in septal and hippocampal substance P content following inescapable footshock. 3 Other studies reported a decrease in substance P content after immobilization stress. 4 Because these and other studies suggest that the activity of substance P-containing pathways is moduCorrespondence: E Fuchs, Division of Neurobiology, German Primate Center, Kellnerweg 4, 37077 Gö ttingen, Germany.…”

Section: Introductionmentioning

confidence: 99%

Substance P receptor antagonist and clomipramine prevent stress-induced alterations in cerebral metabolites, cytogenesis in the dentate gyrus and hippocampal volume

et al. 2002

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The neuropeptide substance P and its receptor, the neurokinin 1 receptor (NK 1 R) have been proposed as possible targets for new antidepressant therapies. The present study investigated the effect of the NK 1 R antagonist L-760,735 and the tricyclic antidepressant clomipramine in the chronic psychosocial stress paradigm of adult male tree shrews. Animals were subjected to a 7-day period of psychosocial stress before the onset of daily oral administration of L-760,735 (10 mg kg −1 day −1 ) or clomipramine (50 mg kg −1 day −1 ). The psychosocial stress continued throughout the treatment period of 28 days. Brain metabolite concentrations were determined in vivo by proton magnetic resonance spectroscopy. Cell proliferation in the dentate gyrus and hippocampal volume were measured post mortem. Stress significantly decreased in vivo concentrations of N-acetyl-aspartate (−14%), creatine and phosphocreatine (−15%) and choline-containing compounds (−15%). The proliferation rate of the granule precursor cells in the dentate gyrus was reduced (−45%), and hippocampal volume was decreased (−14%). The stress-induced changes of brain metabolites, hippocampal volume and dentate cytogenesis rate were prevented by concomitant drug administration. Elevated myoinositol concentrations after both treatments hint to an astrocytic enhancement. These results suggest that-despite a different pharmacological profile-the NK 1 R antagonist L-760,735, a member of a novel class of antidepressant drugs, has comparable neurobiological efficacy to tricyclic antidepressants such as clomipramine. Molecular Psychiatry (2002) 7, 933-941.

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Responsiveness of mesolimbic, mesocortical, septal and hippocampal cholecystokinin and substance P neuronal systems to stress, in the male rat

Cited by 61 publications

References 34 publications

Stress-Induced Changes in Cholecystokinin and Substance P Concentrations in Discrete Regions of the Rat Hypothalamus

Stress-Induced Changes in Cholecystokinin and Substance P Concentrations in Discrete Regions of the Rat Hypothalamus

Early Development of Parvalbumin-, Somatostatin-, and Cholecystokinin-Expressing Neurons in Rat Brain following Prenatal Immune Activation and Maternal Iron Deficiency

Substance P receptor antagonist and clomipramine prevent stress-induced alterations in cerebral metabolites, cytogenesis in the dentate gyrus and hippocampal volume

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