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Brain and Behavior Test 2

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Hormones and sex dimorphic parts of the brain SDN of the POA
Sexual differentiation is reflected in the structure of certain neurons. The size and number of neurons in medial preoptic nucleus is greater in males than females. This is the sexually dimorphic nucleus of the preoptic area. The size difference is defined in the first 10 days postpartum. The volume and number of SDN cells declines with age. The function of this nucleus is as of yet undetermined.
The interstitial nucleus in the AHA is smaller in Homosexual men vs. heterosexual men. There is also sexual dimpophism in the corpus callosum and in the anterior commissure. Studies have also found that homosexual men have a larger anterior commissure as compared to heterosexual men or women. There may be a genetic basis for this.
The limbic system consist of
hippocampus, amygdala, septal area, and cingulated gyrus
Related structures include the prefrontal cortex, hypothalamus, and Periaquiductal gray. It also involves the “limbic-hypothalamic-midbrain axis”
Pathways in the limbic system include the
fornix goes from hippocampus, splits at the bed nucleus of the stria terminalis. The posterior commissural at the fibers terminate mammilary bodies.
stria terminalis goes from the central amygdala to the Bed Nucleus of the stria terminalis
MMT or Mammillothalamic tract goes from the mammilary bodies to the anterior thalamic nuclei
VAF bundle or Ventral-Amygdalofugal pathway goes from the central amygdala directly to the ventral medial hypothalamius
Diagonal Band of Broca goes from the septum to the anterior hypothalamus, and the MFB or Medial forebrain bundle goes from the midbrain (tagmentum) throught the lateral hypothalamus to the lateral preoptic area to the anterior hypothalamus and then to the septum. It is a lateral pathway.
fornix
goes from hippocampus, splits at the bed nucleus of the stria terminalis. The posterior commissural at the fibers terminate mammilary bodies.
stria terminalis
goes from the central amygdala to the Bed Nucleus of the stria terminalis
MMT
Mammillothalamic tract goes from the mammilary bodies to the anterior thalamic nuclei
VAF
Ventral-Amygdalofugal pathway goes from the central amygdala directly to the ventral medial hypothalamius
Diagonal Band of Broca
from the septum to the anterior hypothalamus
MFB
Medial forebrain bundle goes from the midbrain (tagmentum) throught the lateral hypothalamus to the lateral preoptic area to the anterior hypothalamus and then to the septum. It is a lateral pathway.
. Agression pathways, lat and med hypothalamus , attack and defense
Stimulation of the ventral medial hypothalamus causes affective defense (defensive rage) in cats or a Halloween cat. Through silver impregnation it is shown that the Medial Hypothalamus has projections to:
Septum, diagonal band of broca ß Medial Hypothalamus à central grey, Periaquiductal Grey matter
Affective defense is the principle ascending and descending projections of the medial hypothalamus. The ascending fibers are mainly from the ventomedial hypothalamus to the anteromedial hypothalamus and POA. Descending fibers are mianly from the anteromedial hypothalamus to the PAG.
Stimulation of the lateral hypothalamus causes quiet biting attack. Through silver impregnation it was shown that the lateral hypothalamus has fibers that progect:
Anterior hypothalamus, thalamus ß Lateral Hypothalamus à Tagmentum
The quiet biting attack involves the principle ascending ad decending projections of the perifornical lateral hypothalamus.
Medial Hypothalamus has projections to
Septum, diagonal band of broca <-- Medial Hypothalamus --> central grey, Periaquiductal Grey matter
Affective defense pathway
principle ascending and descending projections of the medial hypothalamus. The ascending fibers are mainly from the ventomedial hypothalamus to the anteromedial hypothalamus and POA. Descending fibers are mianly from the anteromedial hypothalamus to the PAG.
Stimulation of the lateral hypothalamus
causes quiet biting attack. Through silver impregnation it was shown that the lateral hypothalamus has fibers that progect:
Anterior hypothalamus, thalamus ß Lateral Hypothalamus à Tagmentum
The quiet biting attack involves the principle ascending ad decending projections of the perifornical lateral hypothalamus.
What neural steps are stimulated and inhibited by stress? Which hormones? Fast v slow response? Sympathetic v parasympathetic system?
There are two endocrince responses to different stressors. In the fast sympathetic NS response the medulla of the adrenal glands on top of the kidneys secrete adrenaline. In the other slower stress response the cortex of the adrenal glands secretes glucocorticoids such as cortisol or coticosterone.
The slow acting stress response begins when a stressor is perceived. The paraventricular nucleus of the hypothalamus secrets corticotrophin-releasing hormone (CRH) into the hypothalamo-pituitary portal circulation and travels into the pituitary gland within seconds. CHR triggers the anterior lobe of the pituitary to release adrenocorticotropc hormone (ACTH) within 15 seconds. ACTH stimulates the release of cortisol from the cortex of the adrenal glands located on top of the kidneys. Cortisol is released within minutes. Cortisol aids in glucose metabolism, and the break down of proteins into glucose. It increases blood flow, responsiveness and also feeds back to the hypothalamus and other neurons.
The fast acting stress response begins when the brain perceives a stressor. The LC then releases norepinephrine which causes arousal and vigilance. Norepinepherine also activates the sympathetic nervous system which also releases norepinepherine that causes hypertension, hyperthermia, and tachycardia. The sympathetic NS also activates the adrenal glands. The medulla of the adrenal glands releases epinephrine into the blood stream. Epinerpherine affects glucose metabolism, causing the nutrients stored in muscles to become available to provide energy. Epinepherine as well as norepinephierin also increase blood flow to muscles by increasing the volumetric output of the heart. Blood pressure is also increased.
Other stress hormones include Beta-endorphin, prolactin, and vasopressin (ADH). All of the above hormones and pathways are STIMULATED by stress.
Some systems are INHIBITED by stress. The parasympathetic cholinergic output from the spinal cord is inhibited. Gonadotrophjic Releasing hormone (GnRH) is also inhibited. This inhibition also inhibits the anterior pituitary from releasing LH and FSH. If these are not released then there is inhibition of the Estrogen, Progesterone, and Testosterone systems and acyclicity occurs. There is also an inhibition of metabolic chemicals such as insulin and GH. The storage of energy is inhibited so that glucose can be used up immediately. Anabolic processes such as digestion, reproduction, growth, tissue repair, and the immune system are also inhibited by stress. Stress also inhibits the perception of pain and inflammation.
fast and slow stress responsee?
In the fast sympathetic NS response the medulla of the adrenal glands on top of the kidneys secrete adrenaline. In the other slower stress response the cortex of the adrenal glands secretes glucocorticoids such as cortisol or coticosterone.
The slow acting stress response begins when
a stressor is perceived. The paraventricular nucleus of the hypothalamus secrets corticotrophin-releasing hormone (CRH) into the hypothalamo-pituitary portal circulation and travels into the pituitary gland within seconds. CHR triggers the anterior lobe of the pituitary to release adrenocorticotropc hormone (ACTH) within 15 seconds. ACTH stimulates the release of cortisol from the cortex of the adrenal glands located on top of the kidneys. Cortisol is released within minutes. Cortisol aids in glucose metabolism, and the break down of proteins into glucose. It increases blood flow, responsiveness and also feeds back to the hypothalamus and other neurons.
The fast acting stress response begins when
the brain perceives a stressor. The LC then releases norepinephrine which causes arousal and vigilance. Norepinepherine also activates the sympathetic nervous system which also releases norepinepherine that causes hypertension, hyperthermia, and tachycardia. The sympathetic NS also activates the adrenal glands. The medulla of the adrenal glands releases epinephrine into the blood stream. Epinerpherine affects glucose metabolism, causing the nutrients stored in muscles to become available to provide energy. Epinepherine as well as norepinephierin also increase blood flow to muscles by increasing the volumetric output of the heart. Blood pressure is also increased.
Other stress hormones include
Beta-endorphin, prolactin, and vasopressin (ADH).
Some systems are INHIBITED by stress
The parasympathetic cholinergic output from the spinal cord is inhibited. Gonadotrophjic Releasing hormone (GnRH) is also inhibited. This inhibition also inhibits the anterior pituitary from releasing LH and FSH. If these are not released then there is inhibition of the Estrogen, Progesterone, and Testosterone systems and acyclicity occurs. There is also an inhibition of metabolic chemicals such as insulin and GH. The storage of energy is inhibited so that glucose can be used up immediately. Anabolic processes such as digestion, reproduction, growth, tissue repair, and the immune system are also inhibited by stress. Stress also inhibits the perception of pain and inflammation.
What is the dual center hypothesis in relation to food?
The dual center hypothesis to eating says that there are two parts of the brain that control eating behavior. The VMH or venromedial hypothalamus is the center that controls satiety and the LH or Lateral hypothalamus controls hunger. Lesions to the VMH cause overeating and obesity while lesions to the LH cause aphagia and weight loss.
The dual center hypothesis does not however answer how individual meals are controlled, what the role of other parts of the brain are in eating behavior, and why after a VMH or LH lesion a rat will eventually reach a new set point for body weight.
What mechanisms control hunger?
Glucoprivation is detected by the dorsomedial and ventrolteral medulla in the brain or by the liver, which sends a signal to the brain via the vagus nerve. Once activated neurons in the ventrolateral medulla release NPY (neuroppeptide Y). These neurons terminate in the in the arcuate nucleus of the hypothalamus with other NPY secreting neurons. NPY stimulates feeding (particularly of carbs), insulin, and glucocoticoid secretion. NPY does this because the NPY neurons of the arcuate n. project to MCH (melanin-concentrating hormone) and orexin neurons in the lateral hypothalamus. MCH and orexin stimulate appetite and reduces metabolic rate. Opioid peptides may play a role in stress induced feeding.
What mechanisms control satiation?
Satiation can either be a short-term or long term signal. The size of a meal and the nutirient value of the food eaten can be detected by the stomach, intestine and liver. In response to the fat content of a meal the duodenum secretes the peptide hormone CCK. CCK acts as a satiety mechanism by acting on receptors between the stomach and duodenum. These receptors transmit the signal via the vagus nerve to the brain, most likely eventually connectin gto the PVN. CCK decreases food intake. Another short term satiation mechanism involves insulin. Insulin secretion signals that the body is in the absorptive phase of metabolism (an therefore does not need more food intake). Insulin can be actively transported across the BBB and can act on cells in the hypothalamus.
A longer term satiaty mechanism comes from “Well fed” adipose tissue which secrete leptin. Leptin seems to inhibit NPY secreting neurons in the arcuate n, causing a decreases appetite and increases metabolism.
Seratonin also seems to increase immediately before the end of a meal. Injections of seratonin into the PVN decrease food intake. The seratonin in the PVN may be the molecule that coordinates the other 3 satiety signals (leptin, insulin, and PPK).
In response to the fat content of a meal
the duodenum secretes the peptide hormone CCK. CCK acts as a satiety mechanism by acting on receptors between the stomach and duodenum. These receptors transmit the signal via the vagus nerve to the brain, most likely eventually connectin gto the PVN. CCK decreases food intake
insulin
Insulin secretion signals that the body is in the absorptive phase of metabolism (an therefore does not need more food intake). Insulin can be actively transported across the BBB and can act on cells in the hypothalamus.
A longer term satiaty mechanism
comes from “Well fed” adipose tissue which secrete leptin. Leptin seems to inhibit NPY secreting neurons in the arcuate n, causing a decreases appetite and increases metabolism.
seratonin and food
Seratonin also seems to increase immediately before the end of a meal. Injections of seratonin into the PVN decrease food intake. The seratonin in the PVN may be the molecule that coordinates the other 3 satiety signals (leptin, insulin, and PPK).
What are the 3 thirst pathways of hypovolemia?
1. The sympathetic fast response: The kidney sense a decrease of blood flow because of hypovolemia. They increase the activity of JG cells and secrete rennin. Renin cleaves angiotensinogen into Angiotensin I which, becomes Angiotensin II. Angiotensin II crosses the BBB via the SFO into the POA and causes the secretion of aldosterine, vasopressin, the constriction of blood vessels, and drinking. Angiotensin also stimulates aldosterone secretion. Aldosterone causes salt to be retained by increasing the action of salt pumps in the kidneys. This causes more water to be retained and less urine volume.
2. The slow response: Blood loss is detected by atrial baroreceptors. Baroreceptors send a signal to the hypothalamus which secretes CRF (corticotrophin releasing factor). CRF goes to the anterior pituitary and stimulated the release of ACTH (adrenal cortical thropic hormone). ACTH stimulates the adrenal cortex to secrete aldosterone.
3. The CRF from the hypothalamus also acts in the posterior pitutitary which secrete ADH (anti diuretic hormone). ADH acts on the kidneys by increasing the permeability of the distal tubules to water reabsorbtion, decreasing urine volume.
What is the thirst pathway for osmotic thirst? (vasopressin)
The sympathetic fast response to thirst
The kidney sense a decrease of blood flow because of hypovolemia. They increase the activity of JG cells and secrete rennin. Renin cleaves angiotensinogen into Angiotensin I which, becomes Angiotensin II. Angiotensin II crosses the BBB via the SFO into the POA and causes the secretion of aldosterine, vasopressin, the constriction of blood vessels, and drinking. Angiotensin also stimulates aldosterone secretion. Aldosterone causes salt to be retained by increasing the action of salt pumps in the kidneys. This causes more water to be retained and less urine volume.
The slow response to thirst
Blood loss is detected by atrial baroreceptors. Baroreceptors send a signal to the hypothalamus which secretes CRF (corticotrophin releasing factor). CRF goes to the anterior pituitary and stimulated the release of ACTH (adrenal cortical thropic hormone). ACTH stimulates the adrenal cortex to secrete aldosterone.
ADH and thirst
The CRF from the hypothalamus also acts in the posterior pitutitary which secrete ADH (anti diuretic hormone). ADH acts on the kidneys by increasing the permeability of the distal tubules to water reabsorbtion, decreasing urine volume.
What is the thirst pathway for osmotic thirst? (vasopressin)
How does angiotensin get to the brain? What areas? Where does it act? How does it get there?
Angiotensin is a peptide and should not normally cross the BBB. Angiotensin seems to act on the Subfornical organ in the brain. The SFO is a circumventricular organ located in the lamina terminalis near the third ventricle. The SFO is a “leaky organ” located in the blood side of the BBB. The nerons in the SFO can detect andiotensin in the blood. The SFO neron then projects to the Median Preoptic n. that then sends signals to other parts of the brain
What is reinforcement
Reinforcement is a process in which an event that follows is contingent upon a behavior and thereby maintains or increases the probability of this behavior to occur in the future. An even can be either the presentation of an appetitive consequence (positive reinforcement or reward) or the removal of an adverse consequence (negative reinforcement) Reward also impies incentive motivation and the emotional dimension of pleasure.
What is the role of mesolimbic dopamine in natural rewards and drug seeking behavior?
The hypothesis is that naturally rewarding events can act as rewards on account of their Dopamine releasing effects in the mesolimbic system. The mesolimbic dopamine tract originates in the VTA, passes through the MFB and terminates in the olfactory tubercle, septum, n. accumbens, and amygdala. Some evidence in support of this is that:
1. Electrical Self Stimulation of the brain (ESB) increase the synthesis of dopamine, norepinepherine and tyrosine OH
2. Dopamine agonists such as cocaine increase ESB
3. Dopamine agonists also increase secondary reinforcers
4. The rate of cocaine self-administration is increased by pretreatment with a low does of a dopamine antagonist suggesting that the rat is trying to overcompensate for the effect of the antagonist and get their “dopamine fix”
5. Injections of 6-OHDA which destroys dopamine and norepinephrine neurons decreases ESB
6. There is an increase of dopamine release from the accumbens during ESB and cocaine/amphetamine self-administration.
7. Amphetamine/cocaine/opiate self administration as well as ESB can only occur when the ascending mesolimbic Dopamine tract is intact.
8. Other drugs of abuse (rewards) decrease the threshold of ESB
9. withdrawl from cocaine causes an increase in the threshold for ESB
10. 2-D Glucose injected during ESB is absorbed by the n0 of diagonal band, BNST, AHA, lateral POA, MFB, VTA. All these are part of the mesolimbic dopamine pathway.
What are the 3 major hippocampal pathways involved in LTP? Layers? Types of cells?
The hippocampal formation consists of the hippocampus, the dentate gyrus, and the subiculum. Its layers include the entohinal cortex, the parahippocampal cortex, and the perirhinal cortex. The types of cells in the hippocampus include:
1. CA1 – smaller pyramidal cells in the superior region
2. CA2 – pyramids which do not receive mossy fibers from the dentate region
3. CA3 large pyramids in the inferior region
4. CA 4- scattered pyramids inside the hillus of the dentate gyrus
The major inputs and outputs of hippocampal formation are channeled through the entorhinal cortex. Neurons in the entrothinal cortex are a part of the perforant pathway:
1. a neuron from the entorhinal cortex/subiculm follows the perforant pathway to the dentate gyrus (which consists of granule cells in hulus)
2. The mossy fiber pathway neurons generate in the granule cells in dentate region and synapse in the pyramidal cells in CA3, inferior region.
3. The Scaeffer Colleteral axon starts in the pyramidal cells in CA3 and synapses in the pyramidal cells un the superior CA1 region.
The types of cells in the hippocampus include:
1. CA1 – smaller pyramidal cells in the superior region
2. CA2 – pyramids which do not receive mossy fibers from the dentate region
3. CA3 large pyramids in the inferior region
4. CA 4- scattered pyramids inside the hillus of the dentate gyrus
pathways in the hippocampus
1. a neuron from the entorhinal cortex/subiculm follows the perforant pathway to the dentate gyrus (which consists of granule cells in hulus)
2. The mossy fiber pathway neurons generate in the granule cells in dentate region and synapse in the pyramidal cells in CA3, inferior region.
3. The Scaeffer Colleteral axon starts in the pyramidal cells in CA3 and synapses in the pyramidal cells un the superior CA1 region.
Long term potentiation and sensitization in aplesia? Mechanisms? Receptors? Presynaptic facilitation? Sensitization pathway? Calcium channels? Magnesium? Etc⬦
Long term potentiation is a long-term increase in the excitability of a neuron to a particular synaptic input caused by repeated high frequency activity of that input. Classis properties of LTP include cooperativity, associativity and input specificity. Cooperativity means that the probability of inducing LTP increases with the number of stimulated afferent inputs. Associativity means that is two distinct axonal inputs onverge onto the same post synaptic target they must be depolarized together to cause LTP. Input specificity says that LTP is restricted to only the inputs that receive stimulation.
LTP is induced when a stimulating electrode is placed on a pathway. Induction is though to involveglutamate which acts on either ionotrophic receptors such as NMDA or AMPA or metabotropic receptors that are linked with G proteins to phospholipase C activation and adenylate cyclase inhibition.
The NMDA receptor controls a calcium channel which is usually blocked by magnesium. If there is depolarizes the postsynaptic membrane and glutamate is present, the magnesium is released, the calcium channel is opened. (This only happens when there is very strong depolarization) There is Calcium influx into dendritic spines. This influx activates CaMKII enzyme that plays a role in the creation of AMPA glutamate receptors. AMPA receptors control sodium channels. When they are activated by glutamate they produce an excitatory post synaptic potential. Calcium may also act in the synthesis on NO which may be somehow released by the dendritic spine back to the terminal button and cause the release of more glutamate. These events cause structural changes to dendritic spines which may strengthen or produce additional synapses.
Sensitization occurs when:
1. seratonin is released from the shocked neuron at the head or tail
2. seratonin receptors on the sensory neurons are activated, release G protein coupled with adenyl cyclase.
3. Adenyl cyclase tuns ATP to cAMp. CAMP activates protein kinase A
Presynaptic facilitation:
1. Seratonin à G protein à PKAà
a. Phosprylates potassium chnnels à channels close
b. Acts in N type calcium influx which causes glutamate release
c. L type Calcium influx
Sensitization occurs when:
1. seratonin is released from the shocked neuron at the head or tail
2. seratonin receptors on the sensory neurons are activated, release G protein coupled with adenyl cyclase.
3. Adenyl cyclase tuns ATP to cAMp. CAMP activates protein kinase A
Presynaptic facilitation:
1. Seratonin à G protein à PKAà
a. Phosprylates potassium chnnels à channels close
b. Acts in N type calcium influx which causes glutamate release
c. L type Calcium influx
How do antiphychotics work?
Typical antipsychotics like phenothiazines, butyrophenones, and thioxantehes chemically resemble dopamine and block dopamine D2, D3, and D4 receptors in the caudate and limbic system. These receptors contribute to the extrapyramidal, parkinsonial like side effects of antipsychotic drugs (like tardive dikinesia). The mesolimbic dopamine pathways seem to coorelate with positive symptoms. This would explain why, if antipsychotics act on D2, D3, and D4 receptors of the limbic system they only treat the positive symptoms of schizophrenia. The mesocortical dopamine pathways are associated with negative symptoms and contain D1 and D5 receptos which have a low affinity for antipsychotics.
What are the genetic components to schizophrenia? Evidence and limitations?
Monozygotic twin studies have shown that if one twin is a schizophrenic, the other has a 50% chance of also being one. In dizogotic twins there is only a 17% concordance. This shows some evidence for heritability. Most likely, monozygotic twins have also been raised in the same environment so that must also be taken into account. Because schizophrenia seems to be polygenic genetic transmission models are harder.
What is the role of seratonin in depression? SSRIs? (MAOIs?) some specific drugs?
Evidence that seratonin plays a role in depression can be seen in that:
1. depressives have different seratonin transporter alleles
2. depressives have a lower amount of tryptophan (seratonin precursor) in serum after a tryptophan injection
3. In ppl who commit violent suicide there are more binding sites for seratonin in the frontal cortex.

Depression is often treated with SSRI’s such as cytolapram that specifically block the reuptake of seratonin.
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