Sensory cortex lesion triggers compensatory neuronal plasticity

Abstract

BackgroundLesions to the human brain often cause dramatic impairments in the life of patients because of the very limited capacity of the mammalian nervous system to regenerate. On the other hand, neuronal tissue has a high capacity to reorganize itself so that loss of function due to brain damage may be compensated through neuroplastic reorganization of undamaged tissue in brain regions adjacent or contralateral to the lesion site. In this study we investigated the effect of serial lesions of the auditory cortices (AC) in both hemispheres of Mongolian gerbils on discrimination performance for fast amplitude modulated tones (AM). Healthy animals were trained to discriminate two fast AM, an ability that has previously been shown to critically depend on cortical processing. Their ability to maintain significant discrimination performance was retested after unilateral AC lesion, and again after lesion of the contralateral AC, with 15 days of continuing training in between the two lesions.ResultsAfter bilateral cortical ablation of both AC and 45 days of training the animals show no change in pure tone detection threshold as measured with modulation of the acoustic startle reflex which has been shown to rely on subcortical structures. In contrast to simultaneous bilateral ablation of AC that results in complete loss of AM discrimination ability in this paradigm we found compensatory plasticity that seems to be triggered by unilateral cortical ablation with subsequent training and that is able to almost fully compensate for the lost cortical functions.ConclusionsOur results demonstrate that AM discrimination ability that normally depends on AC may be transferred to other brain regions when the brain has time to activate compensatory plasticity between the lesions of the two AC hemispheres. For this process to take place obviously one intact AC hemisphere is needed. This finding may open perspectives for new therapeutic strategies that may alleviate the impairments after multiple ischemic strokes.

What can we learn from inactivation studies? Lessons from auditory cortex

“…Permanent lesions are likely to have profound effects on areas upstream and downstream of the lesioned site; indeed, retrograde degeneration of the ventral division of the medial geniculate body (MBGv) is a hallmark of a successful A1 lesion [16]. Thus, the behavioural effects of lesioning may High Dependent on how completely the target brain area is removed [88] Compensatory plasticity [88,89] Damage to fibres of passage a [90] Degeneration of upstream areas (e.g., thalamus) [88] Pharmacological Activation of inhibitory neurons via reagents [82] Moderate Dependent on ligand diffusion [82] Area of effect relies on diffusion of reagent which may vary between reagents (e.g., muscimol spreads maximally and γ-aminobutyric acid [GABA] minimally) [82] Difficult to apply to certain brain areas Cooling Reduction of cortical temperature to reduce spiking [21] Moderate Dependent on temperature conduction through tissue [7,8] Slow but sustained control of inactivation [88] Area of effect is dependent on the size of the cooling loop/probe [21] Can cool nontarget areas via cooled blood vessels [21]…”

The Organization of Somatostatin-Immunoreactive Cells in the Visual Cortex of the Gerbil

“…Gerbils are widely used as research models in areas such as aging [ 48 ], metabolism [ 49 , 50 , 51 , 52 , 53 , 54 ], anatomy [ 55 , 56 ], and parasitic diseases [ 57 , 58 ]. In neuroscience research, gerbils have been widely used to study sensory systems [ 59 , 60 , 61 , 62 , 63 ], neural diseases [ 61 , 64 , 65 , 66 ], and brain structure [ 67 , 68 , 69 ]. Mice and rats are common in biomedical and neuroscience research due to their genetic manipulability and well-published data.…”

“…Furthermore, gerbils have a specialized retinal region, which is similar to the human fovea [ 72 , 74 ]. Accordingly, gerbils have been used widely in studies of the central visual system, such as the retina [ 71 , 72 , 75 , 76 ] and sensory cortex, including the VC [ 61 , 62 , 63 , 77 ].…”

Neuronal plasticity mechanisms induced by brain-machine interfaces: connecting brain to artificial neural network

“…Brain-computer interface (BCI) is the device that connect the brain to machines in order to restore sensorimotor functions in compromised patients [1,2] . Neuronal plasticity is related to the capacity of reorganization of neuronal circuits, by processes ranging from learning to repair of neuronal damage [3,4] .…”

“…There is evidence suggesting that neuronal plasticity is one of the mechanisms present in the functional repair of neuronal injuries and which can be induced by the use of a BCI in the rehabilitation of sensorimotor function for patients with stroke and trauma brain injury with brain damage [3,4] . In order to control or induce neuronal plasticity to restore sensorimotor functionality, we first need to understand how neurons respond to stimuli and encode/decode the signals that characterize the formation of neuronal circuits.…”