Conditioning is a learning mechanism that is best understood with a study on synaptic plasticity that is induced with the training of behavior. There have been demonstrations that synaptic changes in the frontal cortex of the brain can be attained through fear conditioning. Fear is an evolutionary emotion critical for the survival of human beings. Fear helps in triggering defense reactions which help in countering events that are a threat to human beings. Usually, the frontal cortex has part of the brain that takes part in motor learning, fear memory, and emotional behavior. Fear learning can be observed from changes in the somatic and autonomic responses such as freezing and the rate of heart beat. The responses are produced from a neutral stimulus conditioned with fear. The involvement of the cerebellar in fear condition is made possible by the long-term synaptic changes between the Purkinje cell and parallel fibers. The alterations in the neural activities and the emotional experiences resulting from fear conditioning also leads to changes in the amygdala and hippocampus.
Synaptic plasticity in the frontal cortex has been demonstrated in the text using rats (Watson and Breedlove). The mice in the experimental group were subjected to tone followed by foot shock. From the case, a microscope that could observe the neurons beneath the surface of a living brain was used. The technique used low energy light. Two-photon excitation microscopy that uses lasers was used to shine a light on tissues on the frontal cortex of the mouse. Changes associated with fear conditioning were then observed. Additionally, scientists used the special microscope to observe the dendritic spines of the neurons in the frontal cortex of mice. Repeated observations showed that the dendritic spines wax and wane with time. According to the study findings, the pairing of tone and foot shock increased the elimination of dendritic spines from the mice. Therefore, fear conditioning alters the synapses in the frontal cortex.
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The stimulation of the frontal cortex induces complex behavioral patterns that result from the arousal of emotions in animals and psychotic symptoms in human beings (Rao‐Ruiz et al., 2015). Pathologies in the cerebellar are also associated with the many emotional disorders such as autism and depression in human beings. Behavioral and autonomic responses from fear conditioning result from the dysfunction of frontal cortex. According to a report done by Rao‐Ruiz et al. (2015), the retention of fear conditioning can be abolished by inactivating frontal cortex. The effect can be obtained with the injection of tetrodotoxin after a conditioning session that involves acquisition of behavior. Importantly, the procedure did not allow for the interference of motor or sensory responses. However, the study does not show changes in the synapse in the frontal cortex after the conditioning.
In a study by Sacchetti et al. (2004), fear conditioning was observed to elicit long-term potentiation (LTP) of parallel fiber (PF) to Purkinje cell (PC) synapses. The research examined three groups of rats; naïve that were not trained, conditioned that received paired tone and electric shock, and control group that received unpaired tone and electric shock treatment. Expression of fear and freezing were used to analyze fear retention. The study concluded that the behavior from conditioned rats was related to the underlying emotional memories. The study showed that fear conditioning causes a long-term change in the PF-PC synapse and as a result the cerebellar dysfunctions (Sacchetti et al., 2004). The alteration of the synapse impairs both the long and short-term retention of the learning paradigm.
According to Monday & Castillo (2017), long-term potentiation and long-term depression in the PF-PC synapses from electrical stimulation in vitro in the cerebellar cortex. The parallel fiber facilitates motor learning. Additionally, another study on rats where conditioning was done by paring sound with a foot shock showed that fear conditioning alters synapses (Sacchetti, Scelfo, & Strata, 2005). The study measures the excitatory postsynaptic PC that is induced using current by the stimulation of the PF with a patch-clamp recording from both the experimental and the control groups. Fear stimulation displayed by the current showed higher levels in the control group compared to the experimental group. The results show that the extended changes in the synapses were induced in the cerebellum.
Synaptic changes affect different parts of the brain, and the plasticity usually implies higher memory storage. According to Monday & Castillo (2017), the synaptic changes are highly likely part of the substrates in the neural of fear memory. Further, the PF-PC are essential points for fear learning. The synaptic changes usually persist with fear conditioning which explains phenomena such as long-term potentiality. Additionally, the dysfunctional of the PF-PC affects fear memory. Fear conditioning affects the synapse of animals. The changes in synaptic plasticity are long term as the impacts can be experienced long after behaviors have been acquired. The changes in the strength of the synapse are the reason for the learned behavior.
Fear conditioning is associated with prolonged changes in the PF-PC synapses. Usually, cerebella participate in the neural circuitry. Additionally, the frontal cortex is also linked to the amygdala, neocortical, Paralympic, and limbic system. Usually, dysfunction of the cerebellar causes the emotional abnormalities. Moreover, stimulation of vernal affects the functioning of the hippocampus, the amygdala, and the septum, while the lesion of the vermin affects the behavioral and autonomic fear conditioning responses (Ostroff et al., 2010). In a study by Ostroff et al. (2010), the interference of anxiety state is not linked to amnestic effect in mice. Also, there was no control of emotions and motor responses by the cerebellum. The study thus implied that there was a link between the cerebellum and the sensory stimulus, emotions and associated behaviors. With the view, it can be concluded that fear conditioning leads to persistent modification of the PF-PC synapses which happen in the lobule.
The different studies that have examined fear conditioning on mice show that the conditioning alters the synapse. Usually, the PF-PC synapses are involved in fear memory. Conditioning alters patterns of the PF-PC. Importantly, the effects are usually long lasting with persistent conditioning. As such, the behavior that results from the fear conditioning can be explained by the changes in the synapse. Importantly, the stronger the synapse change resulting from prolonged conditioning, the persistent the learned behavior. In as much as the amygdala mediates different emotional aspects such as fear in the caudate nucleus, neocortex, and hippocampus, the cerebellar also contributes to the integrated networks.
References
Monday, H. R., & Castillo, P. E. (2017). Closing the gap: long-term presynaptic plasticity in brain function and disease. Current opinion in neurobiology , 45 , 106-112.
Ostroff, L. E., Cain, C. K., Bedont, J., Monfils, M. H., & LeDoux, J. E. (2010). Fear and safety learning differentially affect synapse size and dendritic translation in the lateral amygdala. Proceedings of the National Academy of Sciences , 107 (20), 9418-9423.
Rao‐Ruiz, P., Carney, K. E., Pandya, N., van der Loo, R. J., Verheijen, M. H., van Nierop, P., ... & Spijker, S. (2015). Time‐dependent changes in the mouse hippocampal synaptic membrane proteome after contextual fear conditioning. Hippocampus , 25 (11), 1250-1261.
Sacchetti, B., Scelfo, B., & Strata, P. (2005). The cerebellum: synaptic changes and fear conditioning. The Neuroscientist , 11 (3), 217-227.
Sacchetti, B., Scelfo, B., Tempia, F., & Strata, P. (2004). Long-term synaptic changes induced in the cerebellar cortex by fear conditioning. Neuron , 42 (6), 973-982.
Watson, N. V. and Breedlove, S. M. Biological psychology: An introduction to behavioral, cognitive, and clinical neuroscience .
