Unmasking of latent synaptic connections in the cortex of the rat, elicited by a facial nerve transection

Peripheral nerve injury elicits plastic changes in the cortex, resulting in reorganization of the somatotopic representation maps. These processes begin within minutes after nerve injury, and last for weeks. Although the mechanisms leading to these plastic changes are not known in a detail, a number of results suggest that the key element in the starting of these processes is a decrease in the function of the cortical GABAergic system, which allows the unmasking of pre-existing but normally silent synapses. The somatosensory and motor cortices of the rat brain are involved in strong and mutual interaction. This study of the early changes induced in this relationship by unilateral facial nerve transection (N7x) revealed that the disinhibition of associational and commissural connections caused by N7x allowed the appearance and enhancement of potentials in the motor cortices on both sides, evoked by right-side trigeminal stimulation, though these responses were strictly lateralized in normal animals. In response to the juxtacellular application of GABA and muscimol, reversal was observed in a small population of neurons (3 out of 84) tested with microelectrode recordings and pressure microinjections. These results suggest that a peripheral nerve injury (N7x) rapidly induces GABA(A) receptor-dependent disinhibition in the cortex

Muscarinic cholinergic effects on stimulus-evoked responses in rat primary somatosensory cortex. An electrophysiological study

Neuron terminals originating from the nucleus basalis magnocellularis (NOM) are the major source of the cortical cholinergic innervation, which is thought to play an essential role in higher brain functions. Electrophysiological studies have shown that activation of muscarinic cholinergic receptors caused a marked enhancement of sensory stimuli onto cortical neurons. Diminished cholinergic innervation of somatosensory cortical areas are manifested in decreased stimulus-evoked activity and impaired performance in a sensory discrimination task. We examined the effects of ACh and its muscarinic agonists on the response properties of layer IV-V barrel cortex neurons evoked by precisely controlled vibrissa deflections. The cholinergic pharmacons displayed their mostly facilitatory effects in latency-dependent manner: In most cases only one latency component of On and/or Off responses were changed

Weak if any effect of estrogen on spatial memory in rats

In a number of species, males appear to have spatial abilities that are superior to those of females. The favored explanation for this cognitive difference is hormonal: higher testosterone levels in males than in females. An alternative explanation focuses on the role of varying levels of estrogens in females during the estrus cycle; females perform as well as males on days of low estrogen, but more poorly on days of high estrogen. Other investigators have reported that estrogens improve both types of memory processes, which depend on the striatal (nonspatial navigation) and hippocampal (spatial) memory systems. Additionally, estrogens have been found to protect the working memory. These contradictory results initiated the present study, in which ovariectomized female rats were trained to escape in a Morris water maze. The daily trials were preceded by estradiol application in low doses (Experiment I) or in higher doses (Experiment II). In Experiment I, no differences at all were found between the latencies of the treated and control groups to reach a submerged platform in a Morris water maze. In Experiment II, however, the animals treated with the higher dose of estradiol showed a small deficit in the acquisition of the Morris water maze task. This study indicates that estradiol at around the physiological level has no effect on spatial learning and memory functions