Geniculate Ganglion
Tongue
Facial Nerve
Taste Buds
Chorda Tympani Nerve
Herpes Zoster Oticus
Stomatognathic System
Facial Nerve Diseases
Taste
Cranial Nerve Neoplasms
Facial Paralysis
Ganglia
Retinal Ganglion Cells
Ganglia, Spinal
Role of brain-derived neurotrophic factor in target invasion in the gustatory system. (1/47)
Brain-derived neurotrophic factor (BDNF) is a survival factor for different classes of neurons, including gustatory neurons. We have studied innervation and development of the gustatory system in transgenic mice overexpressing BDNF under the control of regulatory sequences from the nestin gene, an intermediate filament gene expressed in precursor cells of the developing nervous system and muscle. In transgenic mice, the number and size of gustatory papillae were decreased, circumvallate papillae had a deranged morphology, and there was also a severe loss of lingual taste buds. Paradoxically, similar deficits have been found in BDNF knock-out mice, which lack gustatory neurons. However, the number of neurons in gustatory ganglia was increased in BDNF-overproducing mice. Although gustatory fibers reached the tongue in normal numbers, the amount and density of nerve fibers in gustatory papillae were reduced in transgenic mice compared with wild-type littermates. Gustatory fibers appeared stalled at the base of the tongue, a site of ectopic BDNF expression, where they formed abnormal branches and sprouts. Interestingly, palatal taste buds, which are innervated by gustatory neurons whose afferents do not traverse sites of ectopic BDNF expression, appeared unaffected. We suggest that lingual gustatory deficits in BDNF overexpressing mice are a consequence of the failure of their BDNF-dependent afferents to reach their targets because of the effects of ectopically expressed BDNF on fiber growth. Our findings suggest that mammalian taste buds and gustatory papillae require proper BDNF-dependent gustatory innervation for development and that the correct spatial expression of BDNF in the tongue epithelium is crucial for appropriate target invasion and innervation. (+info)Gustatory neuron types in rat geniculate ganglion. (2/47)
We used extracellular single-cell recording procedures to characterize the chemical and thermal sensitivity of the rat geniculate ganglion to lingual stimulation, and to examine the effects of specific ion transport antagonists on salt transduction mechanisms. Hierarchical cluster analysis of the responses from 73 single neurons to 3 salts (0.075 and 0.3 M NaCl, KCl, and NH(4) Cl), 0.5 M sucrose, 0.01 M HCl, and 0.02 M quinine HCl (QHCl) indicated 3 main groups that responded best to either sucrose, HCl, or NaCl. Eight narrowly tuned neurons were deemed sucrose-specialists and 33 broadly tuned neurons as HCl-generalists. The NaCl group contained three identifiable subclusters: 18 NaCl-specialists, 11 NaCl-generalists, and 3 QHCl-generalists. Sucrose- and NaCl-specialists responded specifically to sucrose and NaCl, respectively. All generalist neurons responded to salt, acid, and alkaloid stimuli to varying degree and order depending on neuron type. Response order was NaCl > HCl = QHCl > sucrose in NaCl-generalists, HCl > NaCl > QHCl > sucrose in HCl-generalists, and QHCl = NaCl = HCl > sucrose in QHCl-generalists. NaCl-specialists responded robustly to low and high NaCl concentrations, but weakly, if at all, to high KCl and NH(4) Cl concentrations after prolonged stimulation. HCl-generalist neurons responded to all three salts, but at twice the rate to NH(4) Cl than to NaCl and KCl. NaCl- and QHCl-generalists responded equally to the three salts. Amiloride and 5-(N,N-dimethyl)-amiloride (DMA), antagonists of Na(+) channels and Na(+)/H(+) exchangers, respectively, inhibited the responses to 0.075 M NaCl only in NaCl-specialist neurons. The K(+) channel antagonist, 4-aminopyridine (4-AP), was without a suppressive effect on salt responses, but, when applied alone in solution, it evoked a response in many HCl-generalists and one QHCl-generalist neuron so tested. Of the 39 neurons tested for their sensitivity to temperature, 23 responded to cooling and chemical stimulation, and 20 of these neurons were HCl-generalists. Moreover, the responses to the four standard stimuli were reduced progressively at lower temperatures in HCl- and QHCl-generalist neurons, but not in NaCl-specialists. Thus sodium channels and Na(+)/H(+) exchangers appear to be expressed exclusively on the membranes of receptor cells that synapse with NaCl-specialist neurons. In addition, cooling sensitivity and taste-temperature interactions appear to be prominent features of broadly tuned neuron groups, particularly HCl-generalists. Taken all together, it appears that lingual taste cells make specific connections with afferent fibers that allow gustatory stimuli to be parceled into different input pathways. In general, these neurons are organized physiologically into specialist and generalist types. The sucrose- and NaCl-specialists alone can provide sufficient information to distinguish sucrose and NaCl from other stimuli, respectively. (+info)Preganglionic and postganglionic neurons responsible for cerebral vasodilation mediated by nitric oxide in anesthetized dogs. (3/47)
The authors performed investigations to functionally determine the route of efferent innervation in vivo responsible for cerebral vasodilation mediated by nitric oxide (NO). In anesthetized beagles, electrical stimulation of the pterygopalatine ganglion vasodilated ipsilateral cerebral arteries such as the middle cerebral and posterior communicating arteries. Intravenous injections of NG-nitro-L-arginine (L-NA) markedly inhibited the response to nerve stimulation, and the effect was reversed by L-arginine. Stimulation of the proximal portion of the greater superficial petrosal nerve, upstream of the pterygopalatine ganglion, also produced cerebral vasodilation, which was abolished by L-NA and restored by L-arginine. Treatment with hexamethonium abolished the response to stimulation of the petrosal nerve but did not affect the response to pterygopalatine ganglion stimulation. Destruction of the pterygopalatine ganglion by cauterization constricted the cerebral arteries. Postganglionic denervation abolished the vasodilation, lacrimation, and nasal secretion induced on the ipsilateral side by stimulation of the pterygopalatine ganglion and petrosal nerve. The vasodilator response was suppressed by L-NA but unaffected by atropine, whereas lacrimation and nasal secretion were abolished solely by atropine. It is concluded that postganglionic neurons from the pterygopalatine ganglion play crucial roles in cerebral vasodilation mediated by NO from the nerve, and preganglionic neurons, possibly from the superior salivatory nucleus through the greater superficial petrosal nerve, innervate the pterygopalatine ganglion. Tonic discharges from the vasomotor center participate significantly in the maintenance of cerebral vasodilation. (+info)The effects of short-term experimental strabismus on the visual system in Macaca mulatta. (4/47)
Experimental esotropia was produced surgically in infant rhesus monkeys (Macaca mulatta) for brief periods of time. Electrophysiological studies of the visual cortex showed that esotropia of only 2 weeks duration in an infant monkey is sufficient to cause a marked shift of dominance in favor of the fixating eye and to virtually extinguish cortical neuronal responses from the esotropic eye. In the lateral geniculate nucleus cell (LGN), shrinkage of 6% to 8% occurred in the parvocellular layers connected with the esotropic eye, the magnocellular layers showing no changes. After the fixating eye had been sutured for 3 weeks, a complete reversal of the cortical physiology in favor of the esotropic eye occurred, whereas no recovery in cell size was observed in the LGN. Surgical realignment of an esotropic eye caused recovery of cortical neuronal responses from the formerly esotropic eye, but the number of binocularly responsive cells remained reduced. (+info)Biophysical properties and responses to neurotransmitters of petrosal and geniculate ganglion neurons innervating the tongue. (5/47)
The properties of afferent sensory neurons supplying taste receptors on the tongue were examined in vitro. Neurons in the geniculate (GG) and petrosal ganglia (PG) supplying the tongue were fluorescently labeled, acutely dissociated, and then analyzed using patch-clamp recording. Measurement of the dissociated neurons revealed that PG neurons were significantly larger than GG neurons. The active and passive membrane properties of these ganglion neurons were examined and compared with each other. There were significant differences between the properties of neurons in the PG and GG ganglia. The mean membrane time constant, spike threshold, action potential half-width, and action potential decay time of GG neurons was significantly less than those of PG neurons. Neurons in the PG had action potentials that had a fast rise and fall time (sharp action potentials) as well as action potentials with a deflection or hump on the falling phase (humped action potentials), whereas action potentials of GG neurons were all sharp. There were also significant differences in the response of PG and GG neurons to the application of acetylcholine (ACh), serotonin (5HT), substance P (SP), and GABA. Whereas PG neurons responded to ACh, 5HT, SP, and GABA, GG neurons only responded to SP and GABA. In addition, the properties of GG neurons were more homogeneous than those of the PG because all the GG neurons had sharp spikes and when responses to neurotransmitters occurred, either all or most of the neurons responded. These differences between neurons of the GG and PG may relate to the type of receptor innervated. PG ganglion neurons innervate a number of receptor types on the posterior tongue and have more heterogeneous properties, while GG neurons predominantly innervate taste buds and have more homogeneous properties. (+info)Evidence for nitroxidergic innervation in monkey ophthalmic arteries in vivo and in vitro. (6/47)
In anesthetized monkeys, electrical stimulation (ES) of the pterygopalatine or geniculate ganglion dilated the ipsilateral ophthalmic artery (OA). The induced vasodilatation was unaffected by phentolamine but potentiated by atropine. Intravenous N(G)-nitro-L-arginine (L-NNA) abolished the response, which was restored by L-arginine. Hexamethonium-abolished vasodilator responses induced solely by geniculate ganglionic stimulation. The L-NNA constricted OA; L-arginine reversed the effect. Destruction of the pterygopalatine ganglion constricted the ipsilateral artery. Helical strips of OA isolated under deep anesthesia from monkeys, denuded of endothelium, responded to transmural ES with relaxations, which were abolished by tetrodotoxin and L-NNA but were potentiated by atropine. It is concluded that neurogenic vasodilatation of monkey OA is mediated by nerve-derived nitric oxide (NO), and the nerve is originated from the ipsilateral pterygopalatine ganglion that is innervated by cholinergic neurons from the brain stem via the geniculate ganglion. The OA appears to be dilated by mediation of NO continuously liberated from nerves that receive tonic discharges from the vasomotor center. Acetylcholine liberated from postganglionic cholinergic nerves would impair the release of neurogenic NO. (+info)Electrophysiologic evidence for normal optic nerve fiber projections in normally pigmented squinters. (7/47)
The Siamese cat, a type of albino, has a visual pathway anomaly in which too many optic nerve fibers cross at the optic chiasm, and also frequently has strabismus. The correlation of strabismus with this defect suggests that a similar pathway defect without pigmentation anomalies, may be the cause of much human strabismus. Creel, Witkop, and King have used evoked potential methods to show that such a pathway defect likely occurs in the human albino. While unpublished control experiments verified their results on human albinos, no such defect has been found in the normally-pigmented human squinter. It is concluded that the visual pathway anomaly is limited to albinism and is not a likely cause of most human strabismus. (+info)Brn3a is a transcriptional regulator of soma size, target field innervation and axon pathfinding of inner ear sensory neurons. (8/47)
The POU domain transcription factors Brn3a, Brn3b and Brn3c are required for the proper development of sensory ganglia, retinal ganglion cells, and inner ear hair cells, respectively. We have investigated the roles of Brn3a in neuronal differentiation and target innervation in the facial-stato-acoustic ganglion. We show that absence of Brn3a results in a substantial reduction in neuronal size, abnormal neuronal migration and downregulation of gene expression, including that of the neurotrophin receptor TrkC, parvalbumin and Brn3b. Selective loss of TrkC neurons in the spiral ganglion of Brn3a(-/-) cochlea leads to an innervation defect similar to that of TrkC(-/-) mice. Most remarkably, our results uncover a novel role for Brn3a in regulating axon pathfinding and target field innervation by spiral and vestibular ganglion neurons. Loss of Brn3a results in severe retardation in development of the axon projections to the cochlea and the posterior vertical canal as early as E13.5. In addition, efferent axons that use the afferent fibers as a scaffold during pathfinding also show severe misrouting. Interestingly, despite the well-established roles of ephrins and EphB receptors in axon pathfinding, expression of these molecules does not appear to be affected in Brn3a(-/-) mice. Thus, Brn3a must control additional downstream genes that are required for axon pathfinding. (+info)The geniculate ganglion is a sensory ganglion (a cluster of nerve cell bodies) located in the facial nerve (cranial nerve VII). It is responsible for the special sense of taste for the anterior two-thirds of the tongue and the sensation of skin over the external ear and parts of the face. The term "geniculate" means "knee-shaped," which describes the appearance of this part of the facial nerve.
In medical terms, the tongue is a muscular organ in the oral cavity that plays a crucial role in various functions such as taste, swallowing, and speech. It's covered with a mucous membrane and contains papillae, which are tiny projections that contain taste buds to help us perceive different tastes - sweet, salty, sour, and bitter. The tongue also assists in the initial process of digestion by moving food around in the mouth for chewing and mixing with saliva. Additionally, it helps in forming words and speaking clearly by shaping the sounds produced in the mouth.
The facial nerve, also known as the seventh cranial nerve (CN VII), is a mixed nerve that carries both sensory and motor fibers. Its functions include controlling the muscles involved in facial expressions, taste sensation from the anterior two-thirds of the tongue, and secretomotor function to the lacrimal and salivary glands.
The facial nerve originates from the brainstem and exits the skull through the internal acoustic meatus. It then passes through the facial canal in the temporal bone before branching out to innervate various structures of the face. The main branches of the facial nerve include:
1. Temporal branch: Innervates the frontalis, corrugator supercilii, and orbicularis oculi muscles responsible for eyebrow movements and eyelid closure.
2. Zygomatic branch: Supplies the muscles that elevate the upper lip and wrinkle the nose.
3. Buccal branch: Innervates the muscles of the cheek and lips, allowing for facial expressions such as smiling and puckering.
4. Mandibular branch: Controls the muscles responsible for lower lip movement and depressing the angle of the mouth.
5. Cervical branch: Innervates the platysma muscle in the neck, which helps to depress the lower jaw and wrinkle the skin of the neck.
Damage to the facial nerve can result in various symptoms, such as facial weakness or paralysis, loss of taste sensation, and dry eyes or mouth due to impaired secretion.
A taste bud is a cluster of specialized sensory cells found primarily on the tongue, soft palate, and cheek that are responsible for the sense of taste. They contain receptor cells which detect specific tastes: sweet, salty, sour, bitter, and umami (savory). Each taste bud contains supporting cells and 50-100 taste receptor cells. These cells have hair-like projections called microvilli that come into contact with food or drink, transmitting signals to the brain to interpret the taste.
The chorda tympani nerve is a branch of the facial nerve (cranial nerve VII) that has both sensory and taste functions. It carries taste sensations from the anterior two-thirds of the tongue and sensory information from the oral cavity, including touch, temperature, and pain.
Anatomically, the chorda tympani nerve originates from the facial nerve's intermediate nerve, which is located in the temporal bone of the skull. It then travels through the middle ear, passing near the tympanic membrane (eardrum) before leaving the skull via the petrotympanic fissure. From there, it joins the lingual nerve, a branch of the mandibular division of the trigeminal nerve (cranial nerve V), which carries the taste and sensory information to the brainstem for processing.
Clinically, damage to the chorda tympani nerve can result in loss of taste sensation on the anterior two-thirds of the tongue and altered sensations in the oral cavity. This type of injury can occur during middle ear surgery or as a result of various medical conditions that affect the facial nerve or its branches.
Herpes zoster oticus, also known as Ramsay Hunt syndrome type 2, is a viral infection that affects the facial nerve (cranial nerve VII). It is caused by the reactivation of the varicella-zoster virus, which is the same virus responsible for chickenpox. After an initial chickenpox infection, the virus can remain dormant in the body and later reactivate, causing herpes zoster oticus.
In this condition, the virus affects the geniculate ganglion of the facial nerve, leading to inflammation and damage to the nerve fibers. This results in various symptoms, including:
1. Painful rash around the ear, on the face, or in the mouth
2. Facial weakness or paralysis on one side of the face
3. Hearing loss, tinnitus (ringing in the ears), or vertigo (dizziness)
4. Loss of taste sensation on the anterior two-thirds of the tongue
5. Difficulty closing one eye, leading to dryness and irritation
Immediate medical attention is necessary for proper diagnosis and treatment, which typically involves antiviral medications and corticosteroids to reduce inflammation and speed up recovery. Early treatment can help minimize the risk of complications, such as permanent facial nerve damage or hearing loss.
The stomatognathic system is a term used in medicine and dentistry to refer to the coordinated functions of the mouth, jaw, and related structures. It includes the teeth, gums, tongue, palate, lips, cheeks, salivary glands, as well as the muscles of mastication (chewing), swallowing, and speech. The stomatognathic system also involves the temporomandibular joint (TMJ) and associated structures that allow for movement of the jaw. This complex system works together to enable functions such as eating, speaking, and breathing. Dysfunction in the stomatognathic system can lead to various oral health issues, including temporomandibular disorders, occlusal problems, and orofacial pain.
Facial nerve diseases refer to a group of medical conditions that affect the function of the facial nerve, also known as the seventh cranial nerve. This nerve is responsible for controlling the muscles of facial expression, and it also carries sensory information from the taste buds in the front two-thirds of the tongue, and regulates saliva flow and tear production.
Facial nerve diseases can cause a variety of symptoms, depending on the specific location and extent of the nerve damage. Common symptoms include:
* Facial weakness or paralysis on one or both sides of the face
* Drooping of the eyelid and corner of the mouth
* Difficulty closing the eye or keeping it closed
* Changes in taste sensation or dryness of the mouth and eyes
* Abnormal sensitivity to sound (hyperacusis)
* Twitching or spasms of the facial muscles
Facial nerve diseases can be caused by a variety of factors, including:
* Infections such as Bell's palsy, Ramsay Hunt syndrome, and Lyme disease
* Trauma or injury to the face or skull
* Tumors that compress or invade the facial nerve
* Neurological conditions such as multiple sclerosis or Guillain-Barre syndrome
* Genetic disorders such as Moebius syndrome or hemifacial microsomia
Treatment for facial nerve diseases depends on the underlying cause and severity of the symptoms. In some cases, medication, physical therapy, or surgery may be necessary to restore function and relieve symptoms.
In a medical context, taste is the sensation produced when a substance in the mouth reacts with taste buds, which are specialized sensory cells found primarily on the tongue. The tongue's surface contains papillae, which house the taste buds. These taste buds can identify five basic tastes: salty, sour, bitter, sweet, and umami (savory). Different areas of the tongue are more sensitive to certain tastes, but all taste buds can detect each of the five tastes, although not necessarily equally.
Taste is a crucial part of our sensory experience, helping us identify and differentiate between various types of food and drinks, and playing an essential role in appetite regulation and enjoyment of meals. Abnormalities in taste sensation can be associated with several medical conditions or side effects of certain medications.
Cranial nerve neoplasms refer to abnormal growths or tumors that develop within or near the cranial nerves. These nerves are responsible for transmitting sensory and motor information between the brain and various parts of the head, neck, and trunk. There are 12 pairs of cranial nerves, each with a specific function and location in the skull.
Cranial nerve neoplasms can be benign or malignant and may arise from the nerve itself (schwannoma, neurofibroma) or from surrounding tissues that invade the nerve (meningioma, epidermoid cyst). The growth of these tumors can cause various symptoms depending on their size, location, and rate of growth. Common symptoms include:
* Facial weakness or numbness
* Double vision or other visual disturbances
* Hearing loss or tinnitus (ringing in the ears)
* Difficulty swallowing or speaking
* Loss of smell or taste
* Uncontrollable eye movements or drooping eyelids
Treatment for cranial nerve neoplasms depends on several factors, including the type, size, location, and extent of the tumor, as well as the patient's overall health. Treatment options may include surgery, radiation therapy, chemotherapy, or a combination of these approaches. Regular follow-up care is essential to monitor for recurrence or complications.
Facial paralysis is a loss of facial movement due to damage or dysfunction of the facial nerve (cranial nerve VII). This nerve controls the muscles involved in facial expressions, such as smiling, frowning, and closing the eyes. Damage to one side of the facial nerve can cause weakness or paralysis on that side of the face.
Facial paralysis can result from various conditions, including:
1. Bell's palsy - an idiopathic (unknown cause) inflammation of the facial nerve
2. Trauma - skull fractures, facial injuries, or surgical trauma to the facial nerve
3. Infections - Lyme disease, herpes zoster (shingles), HIV/AIDS, or bacterial infections like meningitis
4. Tumors - benign or malignant growths that compress or invade the facial nerve
5. Stroke - damage to the brainstem where the facial nerve originates
6. Congenital conditions - some people are born with facial paralysis due to genetic factors or birth trauma
Symptoms of facial paralysis may include:
* Inability to move one or more parts of the face, such as the eyebrows, eyelids, mouth, or cheeks
* Drooping of the affected side of the face
* Difficulty closing the eye on the affected side
* Changes in saliva and tear production
* Altered sense of taste
* Pain around the ear or jaw
* Speech difficulties due to weakened facial muscles
Treatment for facial paralysis depends on the underlying cause. In some cases, such as Bell's palsy, spontaneous recovery may occur within a few weeks to months. However, physical therapy, medications, and surgical interventions might be necessary in other situations to improve function and minimize complications.
A ganglion is a cluster of neuron cell bodies in the peripheral nervous system. Ganglia are typically associated with nerves and serve as sites for sensory processing, integration, and relay of information between the periphery and the central nervous system (CNS). The two main types of ganglia are sensory ganglia, which contain pseudounipolar neurons that transmit sensory information to the CNS, and autonomic ganglia, which contain multipolar neurons that control involuntary physiological functions.
Examples of sensory ganglia include dorsal root ganglia (DRG), which are associated with spinal nerves, and cranial nerve ganglia, such as the trigeminal ganglion. Autonomic ganglia can be further divided into sympathetic and parasympathetic ganglia, which regulate different aspects of the autonomic nervous system.
It's worth noting that in anatomy, "ganglion" refers to a group of nerve cell bodies, while in clinical contexts, "ganglion" is often used to describe a specific type of cystic structure that forms near joints or tendons, typically in the wrist or foot. These ganglia are not related to the peripheral nervous system's ganglia but rather are fluid-filled sacs that may cause discomfort or pain due to their size or location.
Retinal Ganglion Cells (RGCs) are a type of neuron located in the innermost layer of the retina, the light-sensitive tissue at the back of the eye. These cells receive visual information from photoreceptors (rods and cones) via intermediate cells called bipolar cells. RGCs then send this visual information through their long axons to form the optic nerve, which transmits the signals to the brain for processing and interpretation as vision.
There are several types of RGCs, each with distinct morphological and functional characteristics. Some RGCs are specialized in detecting specific features of the visual scene, such as motion, contrast, color, or brightness. The diversity of RGCs allows for a rich and complex representation of the visual world in the brain.
Damage to RGCs can lead to various visual impairments, including loss of vision, reduced visual acuity, and altered visual fields. Conditions associated with RGC damage or degeneration include glaucoma, optic neuritis, ischemic optic neuropathy, and some inherited retinal diseases.
Spinal ganglia, also known as dorsal root ganglia, are clusters of nerve cell bodies located in the peripheral nervous system. They are situated along the length of the spinal cord and are responsible for transmitting sensory information from the body to the brain. Each spinal ganglion contains numerous neurons, or nerve cells, with long processes called axons that extend into the periphery and innervate various tissues and organs. The cell bodies within the spinal ganglia receive sensory input from these axons and transmit this information to the central nervous system via the dorsal roots of the spinal nerves. This allows the brain to interpret and respond to a wide range of sensory stimuli, including touch, temperature, pain, and proprioception (the sense of the position and movement of one's body).
The basal ganglia are a group of interconnected nuclei, or clusters of neurons, located in the base of the brain. They play a crucial role in regulating motor function, cognition, and emotion. The main components of the basal ganglia include the striatum (made up of the caudate nucleus, putamen, and ventral striatum), globus pallidus (divided into external and internal segments), subthalamic nucleus, and substantia nigra (with its pars compacta and pars reticulata).
The basal ganglia receive input from various regions of the cerebral cortex and other brain areas. They process this information and send output back to the thalamus and cortex, helping to modulate and coordinate movement. The basal ganglia also contribute to higher cognitive functions such as learning, decision-making, and habit formation. Dysfunction in the basal ganglia can lead to neurological disorders like Parkinson's disease, Huntington's disease, and dystonia.