Through their displayed interaction with ERBB receptors, NRG1 isoforms induce the growth and differentiation of epithelial, neuronal, glial, and other types of cells.

It has been shown that a loss of Neuregulin 1 within cortical projection neurons results in increased inhibitory connections and reduced synaptic plasticity.

[8] Similarly, overexpression of Neuregulin 1 results in disrupted excitatory-inhibitory connections, reduced synaptic plasticity, and abnormal dendritic spine growth.

In addition, recent research in Drosophila model has also shown Nrg's involvement in regulating dendritic pruning in ddaC neurons in a Rab5/ESCRT-mediated endocytic pathway.

[9] Thus, careful regulation of the amount of Neuregulin 1 must be maintained in order to preserve an intricate balance between excitatory and inhibitory connections within the central nervous system (CNS).

Administration of exogenous Neuregulin 1 to the basolateral amygdala of anxious mice produced an anxiolytic effect, which has been attributed to the enhancement of GABAergic neurotransmission.

[21] Since Neuregulin 1 promotes myelination and is decreased in schizophrenic patients, along with the finding that schizophrenic patients experience white matter deficits, mutations within Neuregulin 1 may underlie cognitive deficits associated with lower white matter integrity, especially within frontotemporal connections.

[24] There is also strong evidence that NRG1 plays a critical role in Schwann cell maturation, survival, and motility,[25] important in research related to neurofibromatosis type two (NF2).

[citation needed] Neuregulin-1 (NRG-1), a cardioactive growth factor released from endothelial cells, is necessary for cardiac development, structural maintenance, and functional integrity of the heart.

NRG-1 and its receptor family ErbB can play a beneficial role in the treatment of chronic heart failure (CHF) by promoting survival of cardiac myocytes, improving sarcomeric structure, balancing Ca2+ homeostasis, and enhancing pumping function.

[27] In contrast to embryonic and neonatal cardiomyocytes, adult myocardial cells are terminally differentiated and have lost the ability to proliferate.

[31] The cMLCK protein is an important regulator of sarcomere assembly through activation of the myosin regulatory light chain, as well as playing a role in heart contractility.

[37] Preliminary studies have revealed that rhNRG-normalizes SERCA function and enhances myocardial contractility through the inhibition of increasedPP1 expression, which leads to increased PLB phosphorylation and activation of SERCA2.

[41] A schizophrenia associated- missense mutation in Neuregulin 1 has been shown to be associated with changes in cytokine expression using lymphoblastoid cells of heterozygous carriers vs homozygous wild type individuals [42] Specifically, the missense mutation involves a single nucleotide change of a valine to a leucine within the transmembrane domain of Type 3 Neuregulin 1.

It is thought that this single nucleotide change affects the ability of γ-secretase to cleave the intracellular domain (ICD) of the Type 3 isoform of Neureglin 1.

Mice were experimented on to find out more about the NRG1 gene and its link to schizophrenia and mood disorders along with physical impairments and locomotor function.

Past research had shown that in human studies using post mortem brain tissue of schizophrenic patients had evidence of increased NRG1 and ErbB4 gene expression and hyperactivation.

Results of this experiment were slowed weight gain, ventricular enlargement, neuroinflammation, hyperactive locomotive activity, and reduced inhibitory neurotransmission in the NRG1 mice.

This was uncovered by the authors via machine learning techniques to create transcriptomic datasets of patients with MDD and healthy controls (HC).