[2] Throughout Fischbach's career, much of his research has focused on the formation and function of the neuromuscular junction, which stemmed from his innovative use of cell culture to study synaptic mechanisms.

[1][5] Much of Fischbach's research concentrated on the mechanisms controlling action potentials and synapses, from which he pioneered the use of neuron and muscle cell culture to study neuromuscular junctions.

[3] Fischbach used this technique to reconstruct neuromuscular junctions from dissociated spinal cord and muscle cells from chick embryos to show that functional synaptic connections reformed and were capable of sending spontaneous or induced action potentials.

[6] This technique proved to be an important model for further studies to determine the essential mechanisms controlling neuromuscular junction development and maintenance.

[1][5] Towards the end of his tenure at the National Institutes of Health, Fischbach began to search for motor neuron molecules responsible for regulating the number of acetylcholine receptors on postsynaptic cells.

[1][7] After his time at the National Institutes of Health, Fischbach obtained a position as an associate professor at Harvard Medical School's Department of Pharmacology in 1973.

[8] Later on he continued his research on ARIA that he started at the National Institutes of Health, specifically focusing on the expression of the protein's isoforms and their effects on tyrosine kinases.

[10] In addition to his ARIA work, Fischbach also researched rapid desensitization of glutamate receptors in chicken spinal cord and rat hippocampal neurons.

[5] Fischbach accomplished many things while director of NINDS, one of which being helping to shape national policy on important neurological research issues.

The Audubon Center is the only research park that is affiliated with a university in New York City and holds the only incubator for business related to biotechnology.

After his arrival to Columbia, Fischbach was focused on the expression of neuregulin in regards to neuromuscular synapses, signaling pathways in the brain, transcription factors, as well as work on autism.

[2][18] Additionally, Fischbach and his colleagues are working on the Simons Simplex Collection (SSC), which is designed to identify genetic factors that increase the risk of autism.

Ultimately, the goal of the SSC is to expand the number of individuals enrolled in the program in hope of identifying penetrant CNVs, small de novo mutations, and single nucleotide polymorphisms that are linked to a higher risk of autism.

The hope is that a better understanding of the central role of the synapse in autistic symptoms can be discovered as well as which specific regions of the brain are responsible for these behaviors.

Within the next decade, the ultimate goal of this research is to determine the precise neural circuitry involved in autism and how it translates to the autistic behaviors displayed.