Opioid modulation of cell proliferation in the ventricular zone of adult zebra finches (Taenopygia guttata)

Abstract

Besides modulating pain, stress, physiological functions, motivation, and reward, the opioid system has been implicated in developmental and adult mammalian neurogenesis and gliogenesis. In adult male songbirds including zebra finches, neurons generated from the ventricular zone (VZ) of the lateral ventricles are incorporated throughout the telencephalon, including the song control nuclei, HVC, and area X. Although the endogenous opioid met-enkephalin is present in neurons adjacent to the VZ and is upregulated in song control regions during singing, it is not known whether the opioid system can modulate adult neurogenesis/gliogenesis in zebra finches. We used quantitative RT-PCR and in situ hybridization to demonstrate that μ- and δ-opioid receptors are expressed by the VZ of adult male zebra finches. Treating cultured VZ cells from male birds with the opioid antagonist naloxone led to an increase in cell proliferation measured by 5-bromo-2-deoxyuridine incorporation, whereas administering met-enkephalin had the opposite effect, compared with saline-treated cultures. Systemically administering naloxone (2.5 mg/kg body wt) to adult male zebra finches for 4 d also led to a significant increase in cell proliferation in the ventral VZ of these birds, compared with saline-treated controls. Our results show that cell proliferation is augmented by naloxone in the VZ adjacent to the anterior commissure, suggesting that the endogenous opioids modulate adult neurogenesis/gliogenesis by inhibiting cell proliferation in songbirds.

Hemispheric Asymmetry in New Neurons in Adulthood Is Associated with Vocal Learning and Auditory Memory

“…Thus, the evaluation of the developing (and mature) song in comparison with the tutor song memory may be left-side lateralized, and perhaps mediated via neurotrophins such as BDNF [55], local synthesis of estradiol in NCM in response to hearing song [56], [57], or by neuromodulators involved in reward and reinforcement, such as dopamine and opioid peptides [58], [59], [60], [61]. These transmitter types have been associated with regulating neurogenesis and new neuron survival [60], [62], [63], [64] and have been shown to function in a hemisphere-specific manner [65], [66], [67] although their role in NCM has not been determined [68]. Regardless of the specific trophic mechanism regulating new neuron survival, it must be turned on in an asymmetric way, either because producing a good imitation engages the hemispheres differentially (perhaps through a matching mechanism), or because the trophic process induced by a good imitation is itself asymmetrical.…”

Opioid receptor mu 1 gene, fat intake and obesity in adolescence

“…Alternatively, OPRM1 may influence embryonic development of the amygdala and, subsequently, its function. It has been shown that Oprm1 is expressed very early on in the embryonic rat brain, including the amygdaloid complex, 52 and that opioids may inhibit neurogenesis 53 (Figure 3, right pathway).…”

Neurogenesis in the olfactory bulb induced by paced mating in the female rat is opioid dependent

“…Not only the administration of compounds that interact with the opioid system modulate neurogenesis (see introduction ), it has been shown that μ and k opioid receptors play a modulatory role in the differentiation of stem-cell-derived neuronal progenitors [ 45 ] and that μ opioid receptor proteins are expressed in neuroepithelia of the lateral ventricles and radial glia in the embryonic mouse brain [ 46 ]. Mu and delta opioid receptors are expressed in the ventricular zone of adult zebra finches [ 47 ] as well, and opioid receptors and mRNA of different opioids are expressed in the proliferative zones in the fetal rat brain [ 48 ]. Based on the evidence described above, it is possible that opioids released during paced mating could directly influence proliferative zones and induce neurogenesis.…”