Examining the nature of the generation of action potentials in single cells to better understand behavior implies that abnormal behavior should be associated with abnormalities in the behavior of neurons. In a sense, this approach to studying behavioral neurophysiology views the nervous system as an information superhighway for our bodies. In addition, all behavior, both internal (unobservable) and external can be conceptualized as forms of communication both within our bodies from one structure to the next and between ourselves and our external environment. At the basis of these communications is the neuron. The observable/measurable behavior of the neuron takes the form of the action potential. Disruptions in the behavior of neurons can take a number of forms, but essentially in each case, there is a disruption in the communication of one neuron to the approximately 1000 neurons onto which it projects. The ultimate expression of that neuron/the end product of its action potential is the release of neurochemicals into the synaptic cleft. Therefore, a disruption in the generation of potentials should be expressed in altered levels of neurotransmitters being released. This disruption in communication amongst neurons should correlate with disruptions in a person's overt behaviors.

One example of a breakdown in affective and cognitive behavior that is associated with altered levels of neurochemicals is schizophrenia. Studies of schizophrenics have found a correlation between the negative symptoms of schizophrenia and a decrease in metabolic activity and a decrease > in dopaminergic activity in the prefrontal cortex, a condition referred to as > hypofrontality. Axons from cell bodies in the VTA comprise the MFB, and their terminal endings project onto the prefrontal cortex. One of the structures with which these dopaminergic endings synapse is the nucleus acumbens, a mediator of attention and reward mechanisms. In people not suffering from schizophrenia, the EPSPs from glutaminergic neurons, which synapse with the the dopaminergic neurons at the nucleus acumbens, ensure what is referred to as a tonic release of dopamine. However, in schizophrenics there is a decrease in activity of glutaminergic excitatory input to the dopaminergic neurons resulting (characterized as phasic rather than as tonic) in an subsequent decrease in the release of dopamine to the synaptic gap at the NA. This decrease in mesolimbic dopaminergic activity is associated with the negative symptoms of schizophrenia. Conversely, one hypothesis to explain the positive symptoms of schizophrenia is that due to the decreased dopaminergic activity at the synapse, the DA receptors in the nucleus acumbens actually become more sensitive.

Numerous other examples of how behavioral dysfunction correlates with neural communication gone awry -- Parkinson's disease, the frozen addicts, and even sociopathology to name a few -- exist. What these examples imply is that by examining abnormalities in the outputs of individual neurons, the biological source of the disruption in behavior can be found. In other words, altered single unit activity can communicate to a doctor the possible disruption of specific structures, > regulatory mechanisms, or even the generation of potentials themselves.

Nice and important examples of the material basis of behavior. Interestingly, it comes from a tradition, neuropharmacology, which doesn't strictly depend on knowing how action potentials work ... and in fact didn't pay much attention to that for a long period of time (perhaps appropriately). We'll talk a little about the relation between the two traditions in the next lecture, as it happens. PG