Xalatan

You may have to look at the distribution of the receptors in the body, and the route of your drug administration. TRPV1 is typically a heat/acid/capsaicin receptor, so you'd think they occur peripherally in the first order neurons rather than in the CNS. CB1 may be more CNS-distributed given its psychotropic effects. So if you injected intradermally, you may elicit a stronger TRPV1 response relative to the CB1 response. If you gave the drug systemically, if it crosses the blood brain barrier you may get more of a CB1 response.

It may be harder with the laryngeal nerves. They branch off the vagus, which is entirely visceral. The recurrently laryngeal nerves loop around the subclavian and ligamentum arteriosum; the superior laryngeal nerves branch off in the neck around where the thyroid gland is. So it may not be like the facial nerve with the chorda tympani or nerve to the stapedius are exposed in the middle ear. Perhaps try trigeminal nerve with tensor tympani? Or perhaps tympanic nerve from the inferior salivary nucleus/glossopharyngeal nerve. It may be possible to test parotid salivation with eletrode stimulation of the tympanic nerve.

Oxygen saturation is how well the haemoglobin in the RBC are holding onto the oxygen. It's dependent on the arterial oxygen tension in the blood. My understanding is the probe shines a light at your finger, and the colour (frequency of light) that your finger glows can be measured as how well your haemoglobin is holding onto the oxygen. 100% would be a shade of red that shows your haemoglobins are being 100% saturated with oxygen. Haemoglobin follows a sigmoid dissociation curve so when your sats dip below 94% or so it corresponds to a significant drop off in arterial oxygen tension.

Binary fission. Bacterial spores are only for survival not for reproduction.

Are you talking about C4b2a or C3b2a? C4b2a and C3bBb are both C3 convertases - C3 convertase is the point at which both the classic and alternative cascades converge. Once C4b2a cleaves C3, C4b2a3b is the C5 convertase, while C3a is a pyrogen.

In the first figure it looks like GNC, my understanding is typically they are Neisseria? Is this discharge or sputum? May be Morexella. I wonder if your second figure is due to changes in staining protocol, but there are other cocci in the background where the crystal violet has washed off. This suggests there is thicker cell wall in a portion of the cells. You may be able to make an educated guess by their clumping morpholgy - diplococci? Grape-like clusters? If it's sputum it could be Strept. The third cell may be a syncytial macrophage? Neutrophils typically have a single nucleus that is polymorphic, but these look multinuclear. Also I don't see any granules that are characteristic of granulocytes. If you are saying any GPC is rejected... you may wish to get a second opinion to see if those are GPC in the second and third figure.

As far as I know type 1 diabetes is more considered a genetically inherited disease, perhaps through an autoimmune process that kills off the pancreatic beta islets. Type 2 diabetes may be more considered as a polygenic disease, as such the inheritance pattern may be more difficult to predict. A major component of type 2 insulin resistance is lifestyle, so lifestyle choices such as diet and exercise also factor into developing type 2 diabetes in a big way. Metabolic syndrome, waist circumference, glucose intolerance are things we can control, so it may be worth considering that it may be it is the lifestyle behaviour that is being passed on, as well as the genes in type 2 diabetes.

Fat is in the subcutaneous tissue primarily for insulation (humans are electrically conductive, and we don't want to be hit by lightning). Also excess energy can be stored as fat, to be later broken down into acetyl-CoA and glycerol to be fed into the Kreb's cycle/gluconeogenesis when food is not available. The reason why facial fat is typically not depicted in anatomical drawinings may be because anatomical models try to demonstrate learning points of facial anatomy - usually muscles, nervous, blood supply, bones. Skin and subcutaneous fat are in more superficial layers so they may be removed in the models for better visibility of deeper structures.

The facial nerve controls the muscles of facial expression through action potential, basically electrical signal coupled to transduced chemical acetylcholine signal at the neuromuscular synapse. Different neurons in the facial motor nucleus (pons/medulla) each controls a corresponding motor unit, which consists of a neuron and the muscle fibres it synapses with. Depending on which muscle of the facial nerve is to be activated, different neurons in the facial nucleus will fire off action potentials to contract that muscle (and specify strength of contraction), for example orbicularis oculi. Nervous control doesn't work on different frequencies per se because action potential is an all-or-none response. It is either on, or off. Rather it works by specifying which motor unit is to be activated, and the number of action potential being fired off per unit time (barring refractory period, called temporal summation) determines the strength of contraction.

You're describing the blue field entoptic phenomenon.

If you vibrate the tympanic membrane through electrodes you may be able to generate audio. As long as the ossicles move and transmit the pressure impulses to the oval window it may achieve the goal. However, the adverse effects of mechanically vibrating the membrane may cause pain via the gsa as you described via trigeminal nerve. It may scar the tympanum membrane in the long term.

Why not just use foremen rotundum to access pterygopalatine ganglion?

You still need normal blood pressure to pump what's left of the rbc around to the tissues. It's one thing to lose RBC and oxygen carrying capacity, and another to lose the blood volume required for preloading the heart. Without adequate stroke volume the body will go into shock irrespective of haematocrit.

Presumably by high conductance you are referring to the process of myelination, in which case yes you could argue compared to patients with MS for example, normal myelination improves cognition and perhaps consciousness. But my understanding of consciousness - defined as wakefulness, having a normal mental state, and ability to follow instructions, is more of a function of structural and functional integrity to certain sets of neurons in the brainstem - for example the reticular formation. If you were to reduce conductance of the reticular formation neurons you may reduce consciousness, but almost all pathologies to the brain stem would lead to the same outcome of loss of consciousness, it's not solely limited to a problem with neuronal conductance. I hope this helps!

What's makes neurons special for Herpesvirus to rest latently in them? Is it because neurons don't divide?

Yes it does - when maxillary nerve enters the foramen rotundum it will enter the superior pterygopalatine fossa. Foramen rotundum connects the middle cranial fossa with the pterygopalatine fossa. So by passing through the foramen maxillary nerve by definition enters the pterygopalatine fossa. It does so briefly in transit before entering the orbit through the inferior orbital fissure but it enters the pterygopalatine fossa nonetheless.

How come the olfactory bulb projects straight to the amygdala and the olfactory cortex without going through a tertiary thalamic nuclear relay (and cross-over)?

When other brainstem cranial nerves don't?

Visual memory may be explained by the two streams hypothesis. http://en.wikipedia.org/wiki/Two-streams_hypothesis. According to this hypothesis, the primary visual cortex would relay visual stimulus via the ventral stream to the temporal lobe, stimulating new long term memory formation. This is one way to think about memory formation.

Hi how are you? I am new to the forum. My question is whether someone with only one functional eye can still have an accommodative reflex? Presumably the brain needs depth perception to tell whether an object is moving from far to near - so without stereoscopic vision provided by two eyes, can monocular vision still accommodate? I'm thinking yes because depth perception is not completely lost with monocular vision - it's just not as precise as if one had two eyes. But then this raises the question of whether accommodative reflex is partially impaired when someone closes one eye? Thank you!