Facial nerve axotomy induces morphological changes in hippocampal pyramidal neurons.

Facial nerve injury in rats have been widely used to study functional and structural changes that occur in the injured motoneurons and other central nervous system structures related with sensorimotor processing. A decrease in long-term potentiation of hippocampal CA3-to-CA1 commissural synapse has recently been reported related to this peripheral injury. Additionally, it has been found increased corticosterone plasmatic levels, impairment in spatial memory consolidation, and hippocampal microglial activation in animals with facial nerve axotomy.

Facial nerve injury-associated hippocampal microglial activation.

Introduction: Facial nerve injury induces changes in hippocampal long-term synaptic plasticity and affects both object recognition memory and spatial memory consolidation (i.e., hippocampus-dependent tasks).

Facial Nerve Axotomy Induces Changes on Hippocampal CA3-to-CA1 Long-term Synaptic Plasticity.

Peripheral facial axotomy induces functional and structural central nervous system changes beyond facial motoneurons, causing, among others, changes in sensorimotor cortex and impairment in hippocampal-dependent memory tasks. Here, we explored facial nerve axotomy effects on basal transmission and long-term plasticity of commissural CA3-to-CA1 synapses. Adult, male rats were submitted to unilateral axotomy of the buccal and mandibular branches of facial nerve and allowed 1, 3, 7, or 21 days of recovery before performing electrophysiological recordings of contralateral CA3 (cCA3) stimulation-evoked CA1 field postsynaptic potential in basal conditions and after high frequency stimulation (HFS) (six, one-second length, 100 Hz stimuli trains).

[Facial nerve injuries cause changes in central nervous system microglial cells].

Introduction: Our research group has described both morphological and electrophysiological changes in motor cortex pyramidal neurons associated with contralateral facial nerve injury in rats. However, little is known about those neural changes, which occur together with changes in surrounding glial cells.

Objective: To characterize the effect of the unilateral facial nerve injury on microglial proliferation and activation in the primary motor cortex.

Vibrissal paralysis produces increased corticosterone levels and impairment of spatial memory retrieval.

This research was aimed at establishing how the absence of active whisking in rats affects acquisition and recovery of spatial memory. The mystacial vibrissae were irreversibly paralyzed by cutting the facial nerve's mandibular and buccal branches bilaterally in the facial nerve lesion group (N=14); control animals were submitted to sham-surgery (N=15). Sham-operated (N=11) and facial nerve-lesioned (N=10) animals were trained (one session, eight acquisition trials) and tested 24h later in a circular Barnes maze.

Layer 5 Pyramidal Neurons' Dendritic Remodeling and Increased Microglial Density in Primary Motor Cortex in a Murine Model of Facial Paralysis.

This work was aimed at characterizing structural changes in primary motor cortex layer 5 pyramidal neurons and their relationship with microglial density induced by facial nerve lesion using a murine facial paralysis model. Adult transgenic mice, expressing green fluorescent protein in microglia and yellow fluorescent protein in projecting neurons, were submitted to either unilateral section of the facial nerve or sham surgery. Injured animals were sacrificed either 1 or 3 weeks after surgery.

[Peripheral facial nerve lesion induced long-term dendritic retraction in pyramidal cortico-facial neurons].

Introduction: Little evidence is available concerning the morphological modifications of motor cortex neurons associated with peripheral nerve injuries, and the consequences of those injuries on post lesion functional recovery.

Objective: Dendritic branching of cortico-facial neurons was characterized with respect to the effects of irreversible facial nerve injury.

Materials And Methods: Twenty-four adult male rats were distributed into four groups: sham (no lesion surgery), and dendritic assessment at 1, 3 and 5 weeks post surgery.

Vibrissal paralysis unveils a preference for textural rather than positional novelty in the one-trial object recognition task in rats.

In order to explore the role of active whisking in object novelty detection, the performance of rats having bilateral vibrissal paralysis was compared to that of non-lesioned animals in three modified versions of the one-trial object recognition task performed in the dark. Vibrissal paralysis was induced by crushing the buccal and mandibular branches of the facial nerve. Lesioned animals were not different from non-lesioned ones in terms of weight-gain, locomotive activity, motivation to explore, and ability to become habituated to a given environment.

Histone deacetylase inhibitors improve learning consolidation in young and in KA-induced-neurodegeneration and SAMP-8-mutant mice.

Histone deacetylases (HDAC) are enzymes that maintain chromatin in a condensate state, related with absence of transcription. We have studied the role of HDAC on learning and memory processes. Both eyeblink classical conditioning (EBCC) and object recognition memory (ORM) induced an increase in histone H3 acetylation (Ac-H3).

Learning-dependent potentiation in the vibrissal motor cortex is closely related to the acquisition of conditioned whisker responses in behaving mice.

The role of the primary motor cortex in the acquisition of new motor skills was evaluated during classical conditioning of vibrissal protraction responses in behaving mice, using a trace paradigm. Conditioned stimulus (CS) presentation elicited a characteristic field potential in the vibrissal motor cortex, which was dependent on the synchronized firing of layer V pyramidal cells. CS-evoked and other event-related potentials were particular cases of a motor cortex oscillatory state related to the increased firing of pyramidal neurons and to vibrissal activities.

Cholinergic septo-hippocampal innervation is required for trace eyeblink classical conditioning.

We studied the effects of a selective lesion in rats, with 192-IgG-saporin, of the cholinergic neurons located in the medial septum/diagonal band (MSDB) complex on the acquisition of classical and instrumental conditioning paradigms. The MSDB lesion induced a marked deficit in the acquisition, but not in the retrieval, of eyeblink classical conditioning using a trace paradigm. Such a deficit was task-selective, as lesioned rats were able to acquire a fixed-interval operant conditioning as controls, and was not due to nonspecific motor alterations, because spontaneous locomotion and blink reflexes were not disturbed by the MSDB lesion.

Classical conditioning of eyelid and mystacial vibrissae responses in conscious mice.

The murine vibrissae sensorimotor system has been scrutinized as a target of motor learning through trace classical conditioning. Conditioned eyelid responses were acquired by using weak electrical whisker-pad stimulation as conditioned stimulus (CS) and strong electrical periorbital stimulation as unconditioned stimulus (US). In addition, conditioned vibrissal protraction was obtained pairing either weak electrical whisker-pad stimulation or a tone as CS, with a strong electric shock delivered in the whisker-pad as US.

Two related forms of memory in the crab Chasmagnathus are differentially affected by NMDA receptor antagonists.

A visual danger stimulus (VDS) elicits an escape response in the crab Chasmagnathus that declines after a few iterative presentations. Long-lasting retention of such decrement, termed context-signal memory (CSM), is mediated by an association between danger stimulus and environmental cues, cycloheximide sensitive, correlated with PKA activity and NFkappa-B activation, positively modulated by angiotensins, and selectively regulated by a muscarinic-cholinergic mechanism. The present research was aimed at studying the possible involvement of NMDA-like receptors in CSM, given the role attributed to these receptors in vertebrate memory and their occurrence in invertebrates including crustaceans.