Autoradiographic localization of (125I-Tyr4)bombesin-binding sites in rat brain

Zarbin, M. A.; Kuhar, MJ; Tl, O'Donohue; Ss, Wolf; Moody, T.W.

doi:10.1523/jneurosci.05-02-00429.1985

Cited by 110 publications

(29 citation statements)

References 23 publications

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“…Apparent dissociation constants (KD) ranging from 3 x 10-10 to 7 x 10-9 M were obtained for radiolabelled substance P or physalaemin bound to brain slices (Rothman et al 1984b;Mantyh et al 1984a;Schults et al 1984;Wolf et al 1985;Mohini, Bahouth, Brundish & Musacchio, 1985), whereas radiolabelled bombesin binding had an apparent KD of 4-6 x 10-9 M (Zarbin et al 1985). The relatively high apparent KD values for the electrophysiological effects may be due to several factors.…”

Section: Effects Of Bombesitnmentioning

confidence: 97%

“…Moreover, the distribution of substance P binding sites present in this as well as in other brain regions has been shown to correlate with the amount of substance P-induced hydrolysis of inositol phospholipids in the same areas (Mantyh, Pinnock, Downes, Goedert & Hunt, 1984c). The rat hippocampus also contains numerous bombesin binding sites (Zarbin, Kuhar, O'Donohue, Wolf & Moody, 1985) and, in its ventral part, densely staining ranatensin immunoreactive fibres (Chronwall, Pisano, Bishop, Moody & O'Donohue, 1985) probably originating from the dorsal tegmental pons (Chronwall, Skirboll & O'Donohue, 1985).…”

Section: Introductionmentioning

confidence: 95%

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Tachykinins and bombesin excite non‐pyramidal neurones in rat hippocampus.

Dreifuss¹,

Raggenbass²

1986

The Journal of Physiology

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SUMMARY1. The effects of substance P, eledoisin and physalaemin -which are structurally similar and all belong to the tachykinin family -and of bombesin, a gastrin-releasing peptide, on non-pyramidal neurones were studied using unitary extracellular recordings from rat hippocampal slices. The peptides were added to the perifusion solution, or locally applied by pressure ejection from a micropipette, at concentrations ranging from 10-8 to 10-6 M.2. 104 out of 115 non-pyramidal neurones responded to tachykinins, and 26 out of 27 responded to bombesin, by a reversible, concentration-dependent increase in firing.3. The responsive neurones retained their sensitivity to the tachykinins and to bombesin under the condition of synaptic blockade. 4. A synthetic peptide known to antagonize the effects of oxytocin on hippocampal non-pyramidal neurones did not affect the excitations induced by the tachykinins or bombesin. The action of the tachykinins was not blocked by the muscarinic antagonist, atropine.5. These results indicate that hippocampal non-pyramidal neurones -which were previously shown to possess oxytocin receptors and #u-type opiate receptors -bear receptors for peptides of the tachykinin and of the gastrin-releasing families.6. The hippocampal effects of tachykinins and of bombesin, however, were not blocked by synthetic structural analogues of substance P, known to antagonize the action of these peptides on some non-nervous tissues. The possibility must be considered that brain receptors for tachykinins and for gastrin-releasing peptides may be distinct from the peripheral receptors for these peptides.

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Section: Effects Of Bombesitnmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 95%

Tachykinins and bombesin excite non‐pyramidal neurones in rat hippocampus.

Dreifuss¹,

Raggenbass²

1986

The Journal of Physiology

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“…One is gastrin-releasing peptide (GRP) 1-27 (a 27-amino acid peptide sometimes referred to as mammalian BN), and the second is its decapeptide form, GRP [18][19][20][21][22][23][24][25][26][27] [often referred to as neuromedin C (NMC)] [12]. Neuromedin B (NMB) (in both its molecular forms, NMB 1-32 , and NMB [23][24][25][26][27][28][29][30][31][32] ) belongs to the second or Ranatensin subfamily [13]. Receptors for BN-LPs have also been isolated and were subsequently localized in mammalian tissue.…”

Section: Bn-lpsmentioning

confidence: 99%

Role of bombesin-related peptides in the mediation or integration of the stress response

Merali¹,

Kent²,

Anisman

2002

CMLS, Cell. Mol. Life Sci.

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In addition to the relatively well established role of corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP) in the mediation of the stress response, there is reason to believe that bombesin-like peptides (BN-LPs) may also contribute to the mediation or integration of these responses and thus might be considered as putative 'stress peptides'. This review provides evidence supporting this contention by showing that (i) BN-LPs are present at brain sites known to be activated by stressors, (ii) stressor exposure alters utilization of BN-related peptides, (iii) exogenous BN administration mimics the endocrine, autonomic and/or behavioral effects elicited by stressors, and (iv) antagonism of BN action attenuates the behavioral and/or neurochemical effects of stressors or of exogenously administered peptide. The evidence presented also suggests that BN-LPs mediate their stress-relevant effects through activation of CRH and/or AVP neurons. Several hypothetical mechanisms for such peptidergic interactions are discussed as to the implications of considering BN-LPs as 'stress peptides'.

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“…1992 veal high density of BB-binding sites in the hypothalamus and hippocampus, and autoradiographic studies using a radiolabeled BB ligand in rat brain slices [10] further show high grain densities in the suprachiasmatic, periven tricular, and paraventricular nuclei of rat hypothalamus. All these findings indicate that BB may play a significant role in the hypothalamus.…”

Section: Introductionmentioning

confidence: 95%

Central Administration of Bombesin Blocks the Estrogen-Induced Afternoon Prolactin Surge

Mai¹,

Pan²

1993

Neuroendocrinology

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The effect of central administration of bombesin (BB), a neuropeptide originally isolated from the skin of frogs, on the estrogen-induced afternoon prolactin (PRL) surge was studied. Two doses of BB, 0.15 and 0.75 µg/rat, were injected into the lateral cerebroventricle of estrogen-primed ovariectomized rats at 12.00 h through preimplanted cannulae. Serial blood samples were obtained through preimplanted intra-atrial catheters during the whole afternoon hours. The small dose of BB delayed the afternoon PRL surge for an hour, but did not prevent it from occurring. The large dose of BB, however, blocked the surge completely. When the same effective dose of BB was co-administered with a BB antagonist, [Leu¹³-ψ(CH₂NH) Leu¹⁴]-BB (LψL-BB), it no longer inhibited the PRL surge. The afternoon PRL surge was also reinstated in BB-treated rats by giving a single injection of sulpiride (1 µg/rat, i.v.), a dopamine antagonist, at 14.00 h in the same afternoon. These results suggest that BB, by acting through specific BB receptors, can inhibit the PRL surge possibly through activating the dopaminergic systems.

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Autoradiographic localization of (125I-Tyr4)bombesin-binding sites in rat brain

Cited by 110 publications

References 23 publications

Tachykinins and bombesin excite non‐pyramidal neurones in rat hippocampus.

Tachykinins and bombesin excite non‐pyramidal neurones in rat hippocampus.

Role of bombesin-related peptides in the mediation or integration of the stress response

Central Administration of Bombesin Blocks the Estrogen-Induced Afternoon Prolactin Surge

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