Centrum medianum—parafascicularis lesions and reactivity to noxious and non-noxious stimuli

Kaelber, William W.; Mitchell, Clifford L.; Yarmat, A.J.; Afifi, Adel K.; Lorens, Stanley A.

doi:10.1016/0014-4886(75)90135-1

Cited by 51 publications

(9 citation statements)

References 9 publications

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“…A body of literature suggests that CRH neurons in the CM-Sf complex may participate in processing somatosensory and visceral information related to stress. (Kaelber and Mitchell, 1975; Kaelber et al , 1975; Fuchs and Siegel, 1984; Hsu et al , 2001; Parent and Parent, 2005). …”

Section: Discussionmentioning

confidence: 99%

Neurobiology of Stress-Induced Reproductive Dysfunction in Female Macaques

2008

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It is now well accepted that stress can precipitate mental and physical illness. However, it is becoming clear that given the same stress, some individuals are very vulnerable and will succumb to illness while others are more resilient and cope effectively, rather than becoming ill. This difference between individuals is called stress sensitivity. Stress-sensitivity of an individual appears to be influenced by genetically inherited factors, early life (even prenatal) stress, and by the presence or absence of factors that provide protection from stress. In comparison to other stress-related diseases, the concept of sensitivity versus resilience to stress-induced reproductive dysfunction has received relatively little attention. The studies presented herein were undertaken to begin to identify stable characteristics and the neural underpinnings of individuals with sensitivity to stress-induced reproductive dysfunction. Female cynomolgus macaques with normal menstrual cycles either stop ovulating (Stress Sensitive) or to continue to ovulate (Stress Resilient) upon exposure to a combined metabolic and psychosocial stress. However, even in the absence of stress, the stress sensitive animals have lower secretion of the ovarian steroids, estrogen and progesterone, have higher heart rates, have lower serotonin function, have fewer serotonin neurons and lower expression of pivotal serotonin-related genes, have lower expression of 5HT2A and 2C genes in the hypothalamus, have higher gene expression of GAD67 and CRH in the hypothalamus and have reduced GnRH transport to the anterior pituitary. Altogether, the results suggest that the neurobiology of reproductive circuits in stress sensitive individuals is compromised. We speculate that with the application of stress, the dysfunction of these neural systems becomes exacerbated and reproductive function ceases.

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Section: Discussionmentioning

confidence: 99%

Neurobiology of Stress-Induced Reproductive Dysfunction in Female Macaques

2008

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“…It receives nociceptive afferents(22, 33) and noxious peripheral stimulation evokes neural activity in nPf(17, 60). Ablation of nPf relieves the emotional suffering associated with chronic pain in humans(40, 61) and reduces affective responses of animals to noxious stimulation(18, 30, 53). Reduced pain reports of Alzheimer’s patients are correlated with neuronal degeneration in nPf(52, 55).…”

Section: Introductionmentioning

confidence: 99%

Contribution of the Periaqueductal Gray to the Suppression of Pain Affect Produced by Administration of Morphine Into the Intralaminar Thalamus of Rat

Munn

Harte

Lagman

et al. 2009

The Journal of Pain

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The parafascicular nucleus of the intralaminar thalamus is implicated in the processing of pain affect in both animals and humans. Administration of morphine into nPf results in preferential suppression of the affective reaction to noxious tailshock in rats. The involvement of the ventrolateral periaqueductal gray in mediating the antinociceptive action of morphine injected into nPf was evaluated. Vocalizations that occur after tailshock offset (vocalization afterdischarges) are a validated rodent model of pain affect, and were preferentially suppressed by injection of morphine into nPf. Vocalizations that occur during tailshock were suppressed to a lesser degree, whereas, spinal motor reflexes (tail flick and hindlimb movements) were unaffected by injection of morphine into nPf. Inactivation of the vPAG via the microinjection of muscimol (GABAA agonist) produced dose-dependent antagonism of morphine-induced increases in vocalization thresholds. The results demonstrate that a functional link between the nPf and vPAG in generating the antinociceptive action of morphine injected into nPf. Perspective: Microinjection of morphine into nucleus parafascicular preferentially suppressed rats’ affective reaction to noxious stimulation. This affective analgesia was reversed by inactivation of the ventrolateral periaqueductal gray. Understanding the neurobiology underlying the suppression of pain affect will provide insights into new treatments for pain and its associated affective disorders.

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“…The PFN receives inputs from the spinal cord, the superior colliculus, the pedunculopontine tegmental nucleus, various vestibular nuclei, and the substantia nigra pars reticulata (Royce et al, 1991;Shiroyama et al, 1995;Kobayashi and Nakamura, 2003;Nakamura et al, 2006). The functions of the PFN are still only partially understood: it has been implicated in the response to pain (Kaelber et al, 1975;Harte et al, 2000Harte et al, , 2004Harte et al, , 2005Weigel and Krauss, 2004;Saade et al, 2007), in attentiondependent orientation (Minamimoto and Kimura, 2002), and in memory in the context of an odor discrimination task (QuirozPadilla et al, 2007). Interestingly, the PFN and the centromedian nucleus show substantial degeneration in postmortem brains from Parkinson's disease patients, whereas adjacent thalamic nuclei are unaffected (Xuereb et al, 1991;Henderson et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

An Essential Role for Frizzled5 in Neuronal Survival in the Parafascicular Nucleus of the Thalamus

Liu¹,

Wang²,

Smallwood³

et al. 2008

J. Neurosci.

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Frizzled5 (Fz5), a putative Wnt receptor, is expressed in the retina, hypothalamus, and the parafascicular nucleus (PFN) of the thalamus. By constructing Fz5 alleles in which ␤-galactosidase replaces Fz5 or in which Cre-mediated recombination replaces Fz5 with alkaline phosphatase, we observe that Fz5 is required continuously and in a cell autonomous manner for the survival of adult PFN neurons, but is not required for proliferation, migration, or axonal growth and targeting of developing PFN neurons. A motor phenotype associated with loss of Fz5 establishes a role for the PFN in sensorimotor coordination. Transcripts coding for Wnt9b, the likely Fz5 ligand in vivo, and ␤-catenin, a mediator of canonical Wnt signaling, are both downregulated in the Fz5 Ϫ/Ϫ PFN, implying a positive feedback mechanism in which Wnt signaling is required to maintain the expression of Wnt signaling components. These data suggest that defects in WntFrizzled signaling could be the cause of neuronal loss in degenerative CNS diseases.

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Centrum medianum—parafascicularis lesions and reactivity to noxious and non-noxious stimuli

Cited by 51 publications

References 9 publications

Neurobiology of Stress-Induced Reproductive Dysfunction in Female Macaques

Neurobiology of Stress-Induced Reproductive Dysfunction in Female Macaques

Contribution of the Periaqueductal Gray to the Suppression of Pain Affect Produced by Administration of Morphine Into the Intralaminar Thalamus of Rat

An Essential Role for Frizzled5 in Neuronal Survival in the Parafascicular Nucleus of the Thalamus

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