Localization and quantification of beta‐adrenergic receptors in human brain

Reznikoff, G.; Manaker, Scott; Rhodes, C. H.; Winokur, Andrew; Rainbow, T. C.

doi:10.1212/wnl.36.8.1067

Cited by 73 publications

(33 citation statements)

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“…3). This agrees with ␤-adrenergic autoradiographic distributions reported previously in human brain (Reznikoff et al, 1986). There were no significant differences in receptor densities in the cerebellar cortices of all AD patients taken together versus controls (data not shown).…”

Section: Cerebellumsupporting

confidence: 92%

Adrenergic Receptors in Alzheimer’s Disease Brain: Selective Increases in the Cerebella of Aggressive Patients

Russo-Neustadt

Cotman

1997

J. Neurosci.

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In this study, the distribution and concentration of ␤ 1 , ␤ 2 , and ␣ 2 adrenergic receptors were examined in the frontal cortex, hypothalamus, and cerebellum of Alzheimer's disease (AD) and age-matched control human brains by receptor autoradiography. The purpose of this study was to detect changes in adrenergic receptor concentrations in key areas of the brain known to affect behavior. For these studies, 3 H]UK-14,304 was used to localize the ␣ 2 sites. Essentially no significant difference in adrenergic receptor concentration was found between total AD cases taken together and control patients. It was found, however, that there were important distinctions within the AD group when cases were subdivided according to the presence or absence of aggression, agitation, and disruptive behavior. Aggressive AD patients had markedly increased (by ϳ70%) concentrations of ␣ 2 receptors in the cerebellar cortex compared with nonaggressive patients with similar levels of cognitive deficit. The levels of cerebellar ␣ 2 receptors in aggressive AD patients were slightly above the healthy elderly controls, suggesting that these receptors are preserved and perhaps increased in this subgroup of AD. ␤ 1 And ␤ 2 adrenergic receptors of the cerebellar cortex showed smaller but significant (ϳ25%) increases in concentration in aggressive AD subjects versus both nonaggressive AD patients and controls. No significant differences were found in adrenergic receptor concentrations within the frontal cortex or hypothalamus. These results point out the importance of distinguishing behavioral subgroups of AD when looking for specific neurochemical changes. These autoradiographic results may reflect the importance of the cerebellum in behavioral control.

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Section: Cerebellumsupporting

confidence: 92%

Adrenergic Receptors in Alzheimer’s Disease Brain: Selective Increases in the Cerebella of Aggressive Patients

Russo-Neustadt

Cotman

1997

J. Neurosci.

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“…This deficiency may lead to the stimulation of compensatory mechanisms and result in hyperactivation of the misery-fleeing system. β-Adrenoceptors are predominantly located in the cerebral cortex, nucleus accumbens, and striatum (Pazos et al, 1985; Reznikoff et al, 1986; Arango et al, 1990; Joyce et al, 1992). By downregulating β-adrenoceptors in the NAcbS, antidepressants would dampen the misery-fleeing response by reducing its activity (Loonen and Ivanova, 2015, 2016a).…”

Section: The Monoamine Hypothesismentioning

confidence: 99%

Circuits Regulating Pleasure and Happiness—Mechanisms of Depression

Loonen

Ivanova

2016

Front. Hum. Neurosci.

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According to our model of the regulation of appetitive-searching vs. distress-avoiding behaviors, the motivation to display these essential conducts is regulated by two parallel cortico-striato-thalamo-cortical, re-entry circuits, including the core and the shell parts of the nucleus accumbens, respectively. An entire series of basal ganglia, running from the caudate nucleus on one side, to the centromedial amygdala on the other side, controls the intensity of these reward-seeking and misery-fleeing behaviors by stimulating the activity of the (pre)frontal and limbic cortices. Hyperactive motivation to display behavior that potentially results in reward induces feelings of hankering (relief leads to pleasure). Hyperactive motivation to exhibit behavior related to avoidance of misery results in dysphoria (relief leads to happiness). These two systems collaborate in a reciprocal fashion. In clinical depression, a mismatch exists between the activities of these two circuits: the balance is shifted to the misery-avoiding side. Five theories have been developed to explain the mechanism of depressive mood disorders, including the monoamine, biorhythm, neuro-endocrine, neuro-immune, and kindling/neuroplasticity theories. This paper describes these theories in relationship to the model (described above) of the regulation of reward-seeking vs. misery-avoiding behaviors. Chronic stress that leads to structural changes may induce the mismatch between the two systems. This mismatch leads to lack of pleasure, low energy, and indecisiveness, on one hand, and dysphoria, continuous worrying, and negative expectations on the other hand. The neuroplastic effects of monoamines, cortisol, and cytokines may mediate the induction of these structural alterations. Long-term exposure to stressful situations (particularly experienced during childhood) may lead to increased susceptibility for developing this condition. This hypothesis opens up the possibility of treating depression with psychotherapy. Genetic and other biological factors (toxic, infectious, or traumatic) may increase sensitivity to the induction of relevant neuroplastic changes. Reversal or compensation of these neuroplastic adjustments may explain the effects of biological therapies in treating depression.

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“…Attempts to discriminate ␤-AR subtypes using immunohistochemistry techniques have been compounded by the cross-reactivity of available ␤-AR antibodies (Milner et al, 2000). Furthermore, marked differences in neuronal AR distribution exist between species, making it difficult to draw comparisons between animal studies (Reznikoff et al, 1986;Booze et al, 1993).…”

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confidence: 99%

Functional Characterization of the β-Adrenergic Receptor Subtypes Expressed by CA1 Pyramidal Cells in the Rat Hippocampus

Hillman¹,

Doze²,

Porter³

2005

J Pharmacol Exp Ther

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Recent studies have demonstrated that activation of the ␤-adrenergic receptor (AR) using the selective ␤-AR agonist isoproterenol (ISO) facilitates pyramidal cell long-term potentiation in the cornu ammonis 1 (CA1) region of the rat hippocampus. We have previously analyzed ␤-AR genomic expression patterns of 17 CA1 pyramidal cells using single cell reverse transcriptionpolymerase chain reaction, demonstrating that all samples expressed the ␤2-AR transcript, with four of the 17 cells additionally expressing mRNA for the ␤1-AR subtype. However, it has not been determined which ␤-AR subtypes are functionally expressed in CA1 for these same pyramidal neurons. Using cell-attached recordings, we tested the ability of ISO to increase pyramidal cell action potential (AP) frequency in the presence of subtype-selective ␤-AR antagonists. ICI-118,551 did not significantly affect the pyramidal cell response to ISO. However, at higher concentrations, atenolol significantly decreased the potency for ISO-mediated AP frequencies. From these curves, an apparent atenolol K b value of 3162 nM was calculated. This pharmacological profile for subtype-selective ␤-AR antagonists indicates that ␤2-AR activation is mediating the increased AP frequency. Knowledge of functional AR expression in CA1 pyramidal neurons will aid future long-term potentiation studies by allowing selective manipulation of specific ␤-AR subtypes.

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Localization and quantification of beta‐adrenergic receptors in human brain

Cited by 73 publications

References 0 publications

Adrenergic Receptors in Alzheimer’s Disease Brain: Selective Increases in the Cerebella of Aggressive Patients

Adrenergic Receptors in Alzheimer’s Disease Brain: Selective Increases in the Cerebella of Aggressive Patients

Circuits Regulating Pleasure and Happiness—Mechanisms of Depression

Functional Characterization of the β-Adrenergic Receptor Subtypes Expressed by CA1 Pyramidal Cells in the Rat Hippocampus

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